Proctocort

DRUG IMAGES

PROCTOCORT 1% CREAM
PROCTOCORT 30 MG SUPPOSITORY

The following indications for PROCTOCORT (hydrocortisone) have been approved by the FDA:

Indications:
Allergic dermatitis
Atopic dermatitis
Contact dermatitis
Cutaneous T-cell lymphoma
Discoid lupus erythematosus
Genital organ pruritus
Granuloma annulare
Hemorrhoids
Lichen simplex chronicus
Plaque psoriasis
Proctitis
Pruritus ani
Pruritus of skin
Pyoderma gangrenosum
Scalp psoriasis
Seborrheic dermatitis
Skin inflammation

Professional Synonyms:
Atopic eczema
Circumscribed neurodermatitis
Dermatitis seborrheica
Dermatitis venenata
Dermatitis
Disseminated neurodermatitis
Dyssebacea
Dyssebacia
Genital pruritus
Itchy skin eruption
Lichen annularis
Primary cutaneous T-cell lymphoma
Pruritic dermatitis
Rectitis
Seborrhea corporis
Seborrheic eczema
Small cerebriform cell lymphoma
Unna's disease
Vidal's disease

The following dosing information is available for PROCTOCORT (hydrocortisone):

Dosing
Administration
PROCTOCORT
HYDROCORTISONE

Hydrocortisone and its acetate, buteprate, butyrate, and valerate esters are applied topically. Dermatologic preparations of the drugs are applied sparingly in thin films and are rubbed gently into the affected area 1-4 times daily. Rectal creams and ointments of the drugs are applied externally to the anal area.

Some commercially available creams may be applied externally to the anogenital areas. Nonprescription preparations of the drugs should not be used for self-medication for longer than 7 days; if the condition worsens or symptoms persist, the drug should be discontinued and a physician consulted. Nonprescription preparations of the drugs should not be used in children younger than 2 years of age unless directed and supervised by a physician.

For dermatoses of the scalp, the hair may be parted and a small amount of lotion applied directly to the affected area and rubbed gently into the scalp. Usual hair care should be maintained, but the lotion should not be washed out immediately after application. Alternatively, for dermatoses of the scalp, hydrocortisone aerosol is applied to the dry scalp after shampooing.

When the aerosol is used for other dermatoses, each 10-cm2 of affected area is sprayed for 1-2 seconds from a distance of about 15 cm 2 or 3 times daily.

Occlusive dressings may be used for severe or resistant dermatoses.

For use in the mouth, a small amount of 0.5% hydrocortisone acetate paste is pressed to the lesion without rubbing until a thin film develops. The paste is applied 2 or 3 times daily after meals and at bedtime.

If substantial regeneration or repair of the oral tissues does not occur after 7 days of treatment, further investigation of the etiology of the oral lesions should be undertaken.

Hydrocortisone is administered rectally as a retention enema, and hydrocortisone acetate is given rectally as a suppository or an aerosol foam suspension according to the manufacturers' instructions. Patients should be advised that hydrocortisone acetate suppositories may stain fabric so that they can take appropriate precautionary measures. For the adjunctive treatment of ulcerative colitis, 100 mg of hydrocortisone is administered nightly as a retention enema.

The patient should lie on his left side during and for 30 minutes after administration of the retention enema so that the drug will distribute throughout the left colon; the enema should be retained for at least 1 hour and preferably all night. Some clinicians administer 100 mg as a retention enema twice daily followed by 100 mg nightly when improvement occurs. The drug is usually given for 21 days or until clinical and proctologic remissions are achieved.

Clinical symptoms may improve in 3-5 days, followed by proctologic improvement; in some cases, 2-3 months of therapy may be required to attain a proctologic remission. Therapy with hydrocortisone retention enema should be discontinued if clinical or proctologic improvement does not occur within 2-3 weeks. Following treatment for longer than 21 days, therapy with hydrocortisone enema should be withdrawn gradually by giving the drug every other night for 2-3 weeks and then discontinuing it.

In patients with ulcerative proctitis of the distal rectum who cannot retain corticosteroid enemas, 90 mg of hydrocortisone acetate (1 applicatorful of a 10% aerosol foam suspension) may be given rectally 1 or 2 times daily for 2-3 weeks and then, if necessary, every other day until clinical and proctologic improvements occur; symptoms may improve within 5-7 days. For the adjunctive treatment of ulcerative colitis of the rectum and other inflammatory conditions of the anorectum, 25 mg of hydrocortisone acetate as a suppository may be administered rectally in the morning and at night for 2 weeks; in severe proctitis, 25 mg may be given 3 times daily or 50 mg may be given twice daily. For the adjunctive treatment of postirradiation or factitial proctitis, therapy is generally continued for 6-8 weeks or less if an adequate response is attained. Alternatively, for the symptomatic treatment of internal hemorrhoids and the adjunctive treatment of other inflammatory conditions of the anorectum, 10 mg of hydrocortisone acetate as a suppository may be administered rectally in the morning and at night for 2-6 days.

No enhanced Administration information available for this drug.

Dosing information for PROCTOCORT
DRUG LABEL	DOSING TYPE	DOSING INSTRUCTIONS
PROCTOCORT 1% CREAM	Maintenance	Adults apply a thin layer to the affected area(s) by topical route 2 times per day
PROCTOCORT 30 MG SUPPOSITORY	Maintenance	Adults insert 1 suppository (30 mg) by rectal route 2 times per day as needed

Generic dosing information for HYDROCORTISONE
DRUG LABEL	DOSING TYPE	DOSING INSTRUCTIONS
HYDROCORTISONE 1% CREAM	Maintenance	Adults apply a thin layer to the affected area(s) by topical route 2 times per day
HYDROCORTISONE AC 30 MG SUPP	Maintenance	Adults insert 1 suppository (30 mg) by rectal route 2 times per day as needed
RA HYDROCORTISONE 1% CREAM	Maintenance	Adults apply a thin layer to the affected area(s) by topical route 2 times per day
KRO HYDROCORTISONE 1% CREAM	Maintenance	Adults apply a thin layer to the affected area(s) by topical route 2 times per day
EQ HYDROCORTISONE 1% CREAM	Maintenance	Adults apply a thin layer to the affected area(s) by topical route 2 times per day
CVS HYDROCORTISONE 1% CREAM	Maintenance	Adults apply a thin layer to the affected area(s) by topical route 2 times per day
HM HYDROCORTISONE 1% CREAM	Maintenance	Adults apply a thin layer to the affected area(s) by topical route 2 times per day
QC HYDROCORTISONE 1% CREAM	Maintenance	Adults apply a thin layer to the affected area(s) by topical route 2 times per day
GNP HYDROCORTISONE 1% CREAM	Maintenance	Adults apply a thin layer to the affected area(s) by topical route 2 times per day

The following drug interaction information is available for PROCTOCORT (hydrocortisone):

Contraindicated
Severe
Moderate

There are 2 contraindications. These drug combinations generally should not be dispensed or administered to the same patient. A manufacturer label warning that indicates the contraindication warrants inclusion of a drug combination in this category, regardless of clinical evidence or lack of clinical evidence to support the contraindication.

Drug Interaction	Drug Names
Efalizumab; Natalizumab/Immunosuppressives; Immunomodulators SEVERITY LEVEL: 1-Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient. MECHANISM OF ACTION: Natalizumab,(1-3) efalizumab,(4) immunosuppressives, and immunomodulators all suppress the immune system. CLINICAL EFFECTS: Concurrent use of natalizumab(1-3) or efalizumab(4) with immunosuppressives or immunomodulators may result in an increased risk of infections, including progressive multifocal leukoencephalopathy (PML), an opportunistic infection caused by the JC virus (JCV). PREDISPOSING FACTORS: Previous JCV infection, longer duration of natalizumab treatment - especially if greater than 2 years, and prior or concomitant treatment with immunosuppressant medication are all independent risk factors which increase the risk for PML.(1,5) The FDA has estimated PML incidence stratified by risk factors: If anti-JCV antibody positive, no prior immunosuppressant use and natalizumab treatment less than 25 months, incidence <1/1,000. If anti-JCV antibody positive, history of prior immunosuppressant use and natalizumab treatment less than 25 months, incidence 2/1,000 If anti-JCV antibody positive, no prior immunosuppressant use and natalizumab treatment 25-48 months, incidence 4/1,000 If anti-JCV antibody positive, history of prior immunosuppressant use and natalizumab treatment 25-48 months, incidence 11/1,000. PATIENT MANAGEMENT: The US manufacturer of natalizumab states patients with Crohn's disease should not receive concurrent immunosuppressants, with the exception of limited overlap of corticosteroids, due to the increased risk for PML. For new natalizumab patients currently receiving chronic oral corticosteroids for Crohn's Disease, begin corticosteroid taper when therapeutic response to natalizumab has occurred. If corticosteroids cannot be discontinued within six months of starting natalizumab, discontinue natalizumab.(3) The US manufacturer of natalizumab states that natalizumab should not ordinarily be used in multiple sclerosis patients receiving immunosuppressants or immunomodulators due to the increased risk for PML. Immunosuppressives include, but are not limited to azathioprine, cyclophosphamide, cyclosporine, mercaptopurine, methotrexate, mitoxantrone, mycophenolate, and corticosteroids.(3,6) The UK manufacturer of natalizumab states that concurrent use with immunosuppressives or antineoplastic agents is contraindicated.(1) The Canadian manufacturer of natalizumab states that natalizumab should not be used with immunosuppressive or immunomodulatory agents.(2) The US manufacturer of certolizumab states that concurrent therapy with natalizumab is not recommended.(7) DISCUSSION: Progressive multifocal leukoencephalopathy has been reported in patients receiving concurrent natalizumab were recently or concomitantly taking immunomodulators or immunosuppressants.(1-5,8,9) In a retrospective cohort study of multiple sclerosis patients newly initiated on a disease-modifying therapy, use of high-efficacy agents (alemtuzumab, natalizumab, or ocrelizumab) resulted in the same risk of overall infections as moderate-efficacy agents, but there was an elevated risk of serious infections (adjusted hazard ratio [aHR] = 1.24, 95% confidence interval (CI) = 1.06-1.44) and UTIs (aHR = 1.21, 95% CI = 1.14-1.30).(10)	TYSABRI
Desmopressin/Glucocorticoids SEVERITY LEVEL: 1-Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient. MECHANISM OF ACTION: Glucocorticoids increase the risk of hyponatremia.(1-4) CLINICAL EFFECTS: Concurrent use of glucocorticoids may increase the risk of hyponatremia with desmopressin.(1-4) PREDISPOSING FACTORS: Predisposing factors for hyponatremia include: polydipsia, renal impairment (eGFR < 50 ml/min/1.73m2), illnesses that can cause fluid/electrolyte imbalances, age >=65, medications that cause water retention and/or increase the risk of hyponatremia (carbamazepine, chlorpromazine, lamotrigine, loop diuretics, NSAIDs, opioids, SSRIs, thiazide diuretics, and/or tricyclic antidepressants). PATIENT MANAGEMENT: The concurrent use of systemic or inhaled glucocorticoids with desmopressin is contraindicated.(1-4) Desmopressin may be initiated 3 days or 5 half-lives after glucocorticoid discontinuation, whichever is longer. If concurrent use is deemed medically necessary, make sure serum sodium levels are normal before beginning therapy and consider using the desmopressin nasal 0.83 mcg dose. Consider measuring serum sodium levels more frequently than the recommended intervals of: within 7 days of concurrent therapy initiation, one month after concurrent therapy initiation and periodically during treatment. Counsel patients to report symptoms of hyponatremia, which may include: headache, nausea/vomiting, feeling restless, fatigue, drowsiness, dizziness, muscle cramps, changes in mental state (confusion, decreased awareness/alertness), seizures, coma, and trouble breathing. Counsel patients to limit the amount of fluids they drink in the evening and night-time and to stop taking desmopressin if they develop a stomach/intestinal virus with nausea/vomiting or any nose problems (blockage, stuffy/runny nose, drainage).(1) DISCUSSION: In clinical trials of desmopressin for the treatment of nocturia, 4 of 5 patients who developed severe hyponatremia (serum sodium <= 125 mmol/L) were taking systemic or inhaled glucocorticoids. Three of these patients were also taking NSAIDs and one was receiving a thiazide diuretic.(2) Drugs associated with hyponatremia may increase the risk, including loop diuretics, carbamazepine, chlorpromazine, glucocorticoids, lamotrigine, NSAIDs, opioids, SSRIs, thiazide diuretics, and/or tricyclic antidepressants.(1,3-4)	DDAVP, DESMOPRESSIN ACETATE, NOCDURNA

Drug Interaction

Drug Names

Efalizumab; Natalizumab/Immunosuppressives; Immunomodulators

SEVERITY LEVEL: 1-Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient.

MECHANISM OF ACTION: Natalizumab,(1-3) efalizumab,(4) immunosuppressives, and immunomodulators all suppress the immune system.

CLINICAL EFFECTS: Concurrent use of natalizumab(1-3) or efalizumab(4) with immunosuppressives or immunomodulators may result in an increased risk of infections, including progressive multifocal leukoencephalopathy (PML), an opportunistic infection caused by the JC virus (JCV).

PREDISPOSING FACTORS: Previous JCV infection, longer duration of natalizumab treatment - especially if greater than 2 years, and prior or concomitant treatment with immunosuppressant medication are all independent risk factors which increase the risk for PML.(1,5) The FDA has estimated PML incidence stratified by risk factors: If anti-JCV antibody positive, no prior immunosuppressant use and natalizumab treatment less than 25 months, incidence <1/1,000. If anti-JCV antibody positive, history of prior immunosuppressant use and natalizumab treatment less than 25 months, incidence 2/1,000 If anti-JCV antibody positive, no prior immunosuppressant use and natalizumab treatment 25-48 months, incidence 4/1,000 If anti-JCV antibody positive, history of prior immunosuppressant use and natalizumab treatment 25-48 months, incidence 11/1,000.

PATIENT MANAGEMENT: The US manufacturer of natalizumab states patients with Crohn's disease should not receive concurrent immunosuppressants, with the exception of limited overlap of corticosteroids, due to the increased risk for PML. For new natalizumab patients currently receiving chronic oral corticosteroids for Crohn's Disease, begin corticosteroid taper when therapeutic response to natalizumab has occurred. If corticosteroids cannot be discontinued within six months of starting natalizumab, discontinue natalizumab.(3)

The US manufacturer of natalizumab states that natalizumab should not ordinarily be used in multiple sclerosis patients receiving immunosuppressants or immunomodulators due to the increased risk for PML. Immunosuppressives include, but are not limited to azathioprine, cyclophosphamide, cyclosporine, mercaptopurine, methotrexate, mitoxantrone, mycophenolate, and corticosteroids.(3,6) The UK manufacturer of natalizumab states that concurrent use with immunosuppressives or antineoplastic agents is contraindicated.(1)

The Canadian manufacturer of natalizumab states that natalizumab should not be used with immunosuppressive or immunomodulatory agents.(2) The US manufacturer of certolizumab states that concurrent therapy with natalizumab is not recommended.(7)

DISCUSSION: Progressive multifocal leukoencephalopathy has been reported in patients receiving concurrent natalizumab were recently or concomitantly taking immunomodulators or immunosuppressants.(1-5,8,9) In a retrospective cohort study of multiple sclerosis patients newly initiated on a disease-modifying therapy, use of high-efficacy agents (alemtuzumab, natalizumab, or ocrelizumab) resulted in the same risk of overall infections as moderate-efficacy agents, but there was an elevated risk of serious infections (adjusted hazard ratio [aHR] = 1.24, 95% confidence interval (CI) = 1.06-1.44)

and UTIs (aHR = 1.21, 95% CI = 1.14-1.30).(10)

TYSABRI

Desmopressin/Glucocorticoids

SEVERITY LEVEL: 1-Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient.

MECHANISM OF ACTION: Glucocorticoids increase the risk of hyponatremia.(1-4)

CLINICAL EFFECTS: Concurrent use of glucocorticoids may increase the risk of hyponatremia with desmopressin.(1-4)

PREDISPOSING FACTORS: Predisposing factors for hyponatremia include: polydipsia, renal impairment (eGFR < 50 ml/min/1.73m2), illnesses that can cause fluid/electrolyte imbalances, age >=65, medications that cause water retention and/or increase the risk of hyponatremia (carbamazepine, chlorpromazine, lamotrigine, loop diuretics, NSAIDs, opioids, SSRIs, thiazide diuretics, and/or tricyclic antidepressants).

PATIENT MANAGEMENT: The concurrent use of systemic or inhaled glucocorticoids with desmopressin is contraindicated.(1-4) Desmopressin may be initiated 3 days or 5 half-lives after glucocorticoid discontinuation, whichever is longer. If concurrent use is deemed medically necessary, make sure serum sodium levels are normal before beginning therapy and consider using the desmopressin nasal 0.83

mcg dose. Consider measuring serum sodium levels more frequently than the recommended intervals of: within 7 days of concurrent therapy initiation, one month after concurrent therapy initiation and periodically during treatment. Counsel patients to report symptoms of hyponatremia, which may include: headache, nausea/vomiting, feeling restless, fatigue, drowsiness, dizziness, muscle cramps, changes in mental state (confusion, decreased awareness/alertness), seizures, coma, and trouble breathing. Counsel patients to limit the amount of fluids they drink in the evening and night-time and to stop taking desmopressin if they develop a stomach/intestinal virus with nausea/vomiting or any nose problems (blockage, stuffy/runny nose, drainage).(1)

DISCUSSION: In clinical trials of desmopressin for the treatment of nocturia, 4 of 5 patients who developed severe hyponatremia (serum sodium <= 125 mmol/L) were taking systemic or inhaled glucocorticoids. Three of these patients were also taking NSAIDs and one was receiving a thiazide diuretic.(2) Drugs associated with hyponatremia may increase the risk, including loop diuretics, carbamazepine, chlorpromazine, glucocorticoids, lamotrigine, NSAIDs, opioids, SSRIs, thiazide diuretics, and/or tricyclic antidepressants.(1,3-4)

DDAVP, DESMOPRESSIN ACETATE, NOCDURNA

There are 20 severe interactions. These drug interactions can produce serious consequences in most patients. Actions required for severe interactions include, but are not limited to, discontinuing one or both agents, adjusting dosage, altering administration scheduling, and providing additional patient monitoring. Review the full interaction monograph for more information.

Drug Interaction	Drug Names
Selected Anticholinesterase/Corticosteroids SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: The mechanism of this interaction is unknown. CLINICAL EFFECTS: Concurrent use of these agents may contribute to increased muscle weakness and decreased response to anticholinesterases shortly after onset of corticosteroid therapy in the treatment of myasthenia gravis. Deterioration in muscle strength, including severe muscular depression, has been documented in patients with myasthenia gravis while receiving corticosteroids and anticholinesterases. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: If possible, hold anticholinesterase agents at least 24 hours before initiating corticosteroid therapy. If concurrent use is necessary, close observation of the patient is indicated and life support systems should be available. DISCUSSION: Decreased effectiveness of anticholinesterases during the period of corticosteroid-induced increased weakness probably reflects a temporary increase in the severity of the disease process itself rather than a specific, direct interaction between the two drugs. Despite the initial adverse effect, glucocorticoid (or ACTH) therapy subsequently produces improvement, beyond pre-therapy muscle strength, in most myasthenia gravis patients. In an uncontrolled study involving nine patients receiving therapeutic doses of pyridostigmine, the concurrent administration of methylprednisolone resulted in a decrease in muscle strength in 71% of treatment courses. During 57% of treatment courses, severe muscle weakness occurred, necessitating mechanical ventilation. Improvement in muscle strength and response to pyridostigmine above baseline levels occurred after methylprednisolone was discontinued. Other clinical observations have indicated that the concomitant use of these agents can affect muscle strength, although each agent alone has been used successfully in treating myasthenia gravis.	ANTICHOLIUM, BLOXIVERZ, DEMECARIUM BROMIDE, EDROPHONIUM CHLORIDE, MESTINON, NEOSTIGMINE METHYLSULFATE, NEOSTIGMINE-STERILE WATER, PREVDUO, PYRIDOSTIGMINE BROMIDE, PYRIDOSTIGMINE BROMIDE ER, REGONOL
Mifepristone/Corticosteroids SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Mifepristone is an antagonist of the progesterone and glucocorticoid (GR-II) receptors, but has little effect at the mineralocorticoid (GR-I) receptor. Mifepristone has a higher affinity for the glucocorticoid receptor than either dexamethasone or cortisol and will displace both endogenous and exogenous glucocorticoids from their binding sites. CLINICAL EFFECTS: Although serum cortisol levels rise, antagonism of the glucocorticoid receptor may lead to adrenal insufficiency. Efficacy of locally administered corticosteroids may be diminished. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The manufacturers of mifepristone states that mifepristone is contraindicated in patients receiving concurrent long-term corticosteroid therapy.(1-2) Due to its long mean half-life of 85 hours(2), even short term mifepristone use may have an extended duration of effect. DISCUSSION: The manufacturers of mifepristone states that mifepristone is contraindicated in patients receiving concurrent long-term corticosteroid therapy.(1-2)	KORLYM, MIFEPREX, MIFEPRISTONE
Aldesleukin/Glucocorticoids SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Corticosteroids may suppress interleukin-2-induced tumor necrosis factor (TNF) synthesis.(1) CLINICAL EFFECTS: Concurrent use of corticosteroids may reduce the antitumor effectiveness of aldesleukin.(2) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The manufacturer of aldesleukin states that concurrent administration of corticosteroids and aldesleukin should be avoided.(2) DISCUSSION: Corticosteroids have been shown to reduce aldesleukin-related side effects such as fever, renal insufficiency, hyperbilirubinemia, confusion, and dyspnea.(1,2) However, dexamethasone has been shown to reduce aldesleukin-induced TNF synthesis.(1)	PROLEUKIN
Systemic Corticosteroids; Corticotropin (ACTH)/Live Vaccines SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Corticosteroids and corticotropin suppress the immune system. In severely immunocompromised patients, virus replication after administration of live, attenuated-virus vaccines can be enhanced and/or the immune response to the vaccine may be decreased.(1) CLINICAL EFFECTS: The expected serum antibody response may not be obtained and/or the vaccine may result in illness.(1) PREDISPOSING FACTORS: Patients receiving immunosuppressive doses of corticosteroids or corticotropin for equal to or greater than 14 consecutive days.(1) PATIENT MANAGEMENT: The Centers for Disease Control's (CDC) Advisory Committee on Immunization Practices (ACIP) states that live-virus and live, attenuated vaccines should not be administered to patients who are severely immunosuppressed, including those who are receiving or have received high-dose, systemic steroids for greater than or equal to 14 consecutive days. Live vaccines should be deferred for at least 1 month after discontinuation of high-dose systemic steroids administered for 14 consecutive days. When initiating immunosuppressives doses of corticosteroids, wait 4 weeks after a live vaccines is administered. However, if patients require therapy for chronic inflammatory conditions, do not delay therapy due to past vaccines. Patients who are vaccinated within the 14 days prior to initiating immunosuppressive therapy should be considered unvaccinated and should be revaccinated at least 3 months after immunosuppressive therapy is discontinued.(1) The US manufacturer of corticotropin(2) and triamcinolone(3) and the Australian manufacturer of dexamethasone(4) state that administration of live or live-attenuated vaccines is contraindicated in patients receiving immunosuppressive doses of corticosteroids or corticotropin. The manufacturer of deflazacort states that live or live-attenuated vaccines should be administered at least 4 to 6 weeks prior to initiation of therapy with deflazacort.(5) DISCUSSION: Many clinicians consider a dose equivalent to either 2 mg/kg of body weight or a total of 20 mg/day of prednisone as sufficiently immunosuppressive to raise safety concerns about live-virus vaccines.(1) Immunization procedures may be undertaken in patients receiving corticosteroids when the therapy is short term (less than 2 weeks); low to moderate dose; long-term, alternate-day treatment with short-acting preparations; maintenance physiologic doses (replacement therapy); or administered topically (skin or eyes), by aerosol, or by intra-articular, bursal, or tendon injection.(1) Killed or inactivated vaccines do not pose a danger to immunocompromised patients.(1)	ACAM2000 (NATIONAL STOCKPILE), ADENOVIRUS TYPE 4, ADENOVIRUS TYPE 4 AND TYPE 7, ADENOVIRUS TYPE 7, BCG (TICE STRAIN), BCG VACCINE (TICE STRAIN), DENGVAXIA, ERVEBO (NATIONAL STOCKPILE), FLUMIST TRIVALENT 2024-2025, IXCHIQ, M-M-R II VACCINE, PRIORIX, PROQUAD, ROTARIX, ROTATEQ, STAMARIL, VARIVAX VACCINE, VAXCHORA ACTIVE COMPONENT, VAXCHORA VACCINE, VIVOTIF, YF-VAX
Amphotericin B/Corticosteroids; Corticotropin (ACTH) SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Corticosteroids and corticotropin may potentiate potassium excretion and overload salt and water retention.(1) CLINICAL EFFECTS: Concurrent use of amphotericin b with corticosteroids or corticotropin may potentiate amphotericin b-induced hypokalemia, thereby predisposing patients to cardiac dysfunction.(1-2) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The US manufacturer of amphotericin b states that concurrent use of corticosteroids or corticotropin should be avoided unless absolutely necessary to avoid side effects. If concurrent use is necessary, serum electrolytes and cardiac function must be monitored closely.(1) DISCUSSION: There are four case reports of cardiac enlargement, hypokalemia, and hypernatremia from concurrent use of amphotericin b and corticosteroids.(2)	ABELCET, AMBISOME, AMPHOTERICIN B, AMPHOTERICIN B LIPOSOME
Tofacitinib/Immunosuppressives; Immunomodulators SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Concurrent use of tofacitinib and azathioprine, other biologic disease-modifying antirheumatic drugs (DMARDs), or potent immunosuppressants may result in additive or synergistic effects on the immune system.(1) CLINICAL EFFECTS: Concurrent use of tofacitinib and azathioprine, other biologic DMARDs, or potent immunosuppressants use may increase the risk of serious infections.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Tofacitinib should not be used concurrently with azathioprine, other biologic DMARDs, or cyclosporine.(1) Patient should be monitored for decreases in lymphocytes and neutrophils. Therapy should be adjusted based on the indication. - For all indications: If absolute neutrophil count (ANC) or lymphocyte count is less than 500 cells/mm3, discontinue tofacitinib. - For rheumatoid arthritis or psoriatic arthritis and absolute neutrophil count (ANC) 500 to 1000 cells/mm3: interrupt dosing. When ANC is greater than 1000 cells/mm3, resume Xeljanz 5 mg twice daily or Xeljanz XR 11 mg once daily. - For ulcerative colitis and ANC 500 to 1000 cells/mm3: -If taking Xeljanz 10 mg twice daily, decrease to 5 mg twice daily. When ANC is greater than 1000 cells/mm3, increase to 10 mg twice daily based on clinical response. -If taking Xeljanz 5 mg twice daily, interrupt dosing. When ANC is greater than 1000 cells/mm3, resume 5 mg twice daily. -If taking Xeljanz XR 22 mg once daily, decrease to 11 mg once daily. When ANC is greater than 1000 cells/mm3, increase to 22 mg once daily based on clinical response. -If taking Xeljanz XR 11 mg once daily, interrupt dosing. When ANC is greater than 1000 cells/mm3, resume 11 mg once daily. - For polyarticular course juvenile idiopathic arthritis (pcJIA) and ANC 500 to 1000 cells/mm3: interrupt dosing until ANC is greater than 1000 cells/mm3.(1) DISCUSSION: Concurrent use of tofacitinib and azathioprine, other biologic DMARDs, or potent immunosuppressants may increase the risk of infection.(1)	TOFACITINIB CITRATE, XELJANZ, XELJANZ XR
Selected Multiple Sclerosis Agents/Immunosuppressants; Immunomodulators SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Ocrelizumab or ofatumumab in combination with immunosuppressives and immune-modulators all suppress the immune system.(1,2) CLINICAL EFFECTS: Concurrent use of ocrelizumab or ofatumumab with immunosuppressive or immune-modulating agents may result in an increased risk of serious infections, such as disseminated herpetic infection or progressive multifocal leukoencephalopathy (PML), an opportunistic infection caused by the JC virus (JCV).(1,2) PREDISPOSING FACTORS: Incomplete washout of previously prescribed immunosuppressive or immune-modulating medications. PATIENT MANAGEMENT: The ocrelizumab US prescribing information states: - Ocrelizumab and other immune-modulating or immunosuppressive therapies, (including immunosuppressant doses of corticosteroids) are expected to increase the risk of immunosuppression, and the risk of additive immune system effects must be considered if these therapies are coadministered with ocrelizumab. When switching from drugs with prolonged immune effects, such as daclizumab, fingolimod, natalizumab, teriflunomide, or mitoxantrone, the duration and mode of action of these drugs must be considered to avoid unintended additive immunosuppressive effects when initiating ocrelizumab.(1) The ofatumumab US prescribing information states: - Ofatumumab and other immunosuppressive therapies (including systemic corticosteroids) may have the potential for increased immunosuppressive effects and increase the risk of infection. When switching between therapies, the duration and mechanism of action of each therapy should be considered due to the potential for additive immunosuppressive effects. Ofatumumab for MS therapy has not been studied in combination with other MS agents that suppress the immune system.(2) DISCUSSION: Fatal disseminated herpes zoster and herpes simplex infections and cases of progressive multifocal leukoencephalopathy (PML) have been reported in patients who previously received immunomodulators or immunosuppressants.(1,2) In a retrospective cohort study of multiple sclerosis patients newly initiated on a disease-modifying therapy, use of high-efficacy agents (alemtuzumab, natalizumab, or ocrelizumab) resulted in the same risk of overall infections as moderate-efficacy agents, but there was an elevated risk of serious infections (adjusted hazard ratio [aHR] = 1.24, 95% confidence interval (CI) = 1.06-1.44) and UTIs (aHR = 1.21, 95% CI = 1.14-1.30).(3)	KESIMPTA PEN, OCREVUS, OCREVUS ZUNOVO
T Cell Immunotherapies/Corticosteroids SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Corticosteroids suppress the immune system. Concurrent use or premedication with a prophylactic corticosteroid may interfere with the activity of CAR-T cell immunotherapies.(1-6) CLINICAL EFFECTS: Corticosteroids may decrease the efficacy of CAR-T cell immunotherapies.(1-6) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The manufacturers recommend avoiding concurrent or prophylactic use of corticosteroids as a premedication prior to infusion of CAR-T cell immunotherapy. Corticosteroids may be used and are recommended in the case of a life-threatening emergency, including the management of cytokine release syndrome or neurological toxicities.(1-6) DISCUSSION: Corticosteroids may decrease the efficacy of CAR-T cell immunotherapy.(1-6) The manufacturers recommend avoiding concurrent or prophylactic use of corticosteroids as a premedication prior to infusion of CAR-T cell immunotherapy.(1-6) Corticosteroids may be used and are recommended in the case of a life-threatening emergency, including the management of cytokine release syndrome or neurological toxicities.(1-6)	ABECMA, AMTAGVI, AUCATZYL, BREYANZI, BREYANZI CD4 COMPONENT, BREYANZI CD8 COMPONENT, CARVYKTI, KYMRIAH, TECARTUS, TECELRA, YESCARTA
Upadacitinib/Immunosuppressives; Immunomodulators SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Upadacitinib, immunosuppressives, and immunomodulators all suppress the immune system. CLINICAL EFFECTS: Concurrent use of upadacitinib with immunosuppressives or immunomodulators may result in an increased risk of serious infections. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The US manufacturer of upadacitinib states that concurrent use of upadacitinib with immunosuppressives or immunomodulators is not recommended. DISCUSSION: Serious infections have been reported in patients receiving upadacitinib. Reported infections included pneumonia, cellulitis, tuberculosis, multidermatomal herpes zoster, oral/esophageal candidiasis, cryptococcosis. Reports of viral reactivation, including herpes virus reactivation and hepatitis B reactivation, were reported in clinical studies with upadacitinib.(1)	RINVOQ, RINVOQ LQ
Inebilizumab/Immunosuppressives; Immunomodulators SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Inebilizumab, immunosuppressives, and immunomodulators all suppress the immune system.(1) CLINICAL EFFECTS: Concurrent use of inebilizumab with immunosuppressive or immunomodulating agents may result in myelosuppression including neutropenia resulting in an increased risk for serious infections.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The US manufacturer of inebilizumab states that the concurrent use of inebilizumab with immunosuppressive agents, including systemic corticosteroids, may increase the risk of infection. If concurrent therapy is warranted, consider the risk of additive immune suppression and monitor based on prescribing information for both agents.(1) DISCUSSION: Inebilizumab has not been studied in combination with other immunosuppressants. If concurrent therapy is warranted, consider the potential for increased immunosuppressive risks from both agents. The most common infections reported by inebilizumab treated patients in the randomized and open-label clinical trial periods included urinary tract infections (20%), nasopharyngitis (13%), upper respiratory tract infections (8%), and influenza (7%). Although there been no cases of Hepatitis B virus reactivation or progressive multifocal leukoencephalopathy reported in patients taking inebilizumab, these infections have been observed in patients taking other B-cell-depleting antibodies.(1)	UPLIZNA
Baricitinib/Immunosuppressives; Immunomodulators SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Concurrent use of baricitinib with other biologic disease-modifying antirheumatic drugs (DMARDs) or potent immunosuppressants such as azathioprine or cyclosporine may result in additive or synergistic effects on the immune system. CLINICAL EFFECTS: Concurrent use of baricitinib with other biologic DMARDs or potent immunosuppressants such as azathioprine or cyclosporine may increase the risk of serious infections.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The US manufacturer of baricitinib states that concurrent use of baricitinib with biologic DMARDs or potent immunosuppressants is not recommended.(1) DISCUSSION: Most patients who developed serious infections while being treated with baricitinib were on concomitant immunosuppressants like methotrexate and corticosteroids. The combination of baricitinib with other biologic DMARDs has not been studied.(1)	OLUMIANT
Ponesimod/Immunosuppressives; Immunomodulators SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Ponesimod in combination with immunosuppressives and immune-modulators all suppress the immune system.(1) CLINICAL EFFECTS: Concurrent use of ponesimod with immunosuppressive or immune-modulating agents may result in an increased risk of serious infections, such as disseminated herpetic infection, cryptococcal infection, or progressive multifocal leukoencephalopathy (PML), an opportunistic infection caused by the JC virus (JCV).(1) PREDISPOSING FACTORS: Incomplete washout of previously prescribed immunosuppressive or immune-modulating medications. PATIENT MANAGEMENT: The ponesimod US prescribing information states ponesimod has not been studied in combination with anti-neoplastic, immune-modulating, or immunosuppressive therapies. Caution should be used during concomitant administration because of the risk of additive immune effects during therapy and in the weeks following administration. When switching from drugs with prolonged immune effects, the half-life and mode of action of these drugs must be considered in order to avoid unintended additive immunosuppressive effects. Initiating treatment with ponesimod after alemtuzumab is not recommended. However, ponesimod can generally be started immediately after discontinuation of beta interferon or glatiramer acetate.(1) DISCUSSION: Fatal disseminated herpes zoster and herpes simplex infections, cryptococcal meningitis, disseminated cryptococcal infections, and cases of progressive multifocal leukoencephalopathy (PML) have been reported in patients who previously received immunomodulators or immunosuppressants.(1)	PONVORY
Fingolimod/Immunosuppressives; Immunomodulators SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Fingolimod in combination with immunosuppressives and immune-modulators all suppress the immune system.(1-3) CLINICAL EFFECTS: Concurrent use of fingolimod with immunosuppressive or immune-modulating agents may result in an increased risk of serious infections, such as disseminated herpetic infection or progressive multifocal leukoencephalopathy (PML), an opportunistic infection caused by the JC virus (JCV).(1-3) PREDISPOSING FACTORS: Incomplete washout of previously prescribed immunosuppressive or immune-modulating medications. PATIENT MANAGEMENT: Recommendations for fingolimod regarding this interaction differ between regulatory approving agencies. The fingolimod US prescribing information states: - Antineoplastic, immune-modulating, or immunosuppressive therapies, (including corticosteroids) are expected to increase the risk of immunosuppression, and the risk of additive immune system effects must be considered if these therapies are coadministered with fingolimod. When switching from drugs with prolonged immune effects, such as natalizumab, teriflunomide or mitoxantrone, the duration and mode of action of these drugs must be considered to avoid unintended additive immunosuppressive effects when initiating fingolimod.(1) The fingolimod Canadian prescribing information states: - Concurrent use with immunosuppressive or immunomodulatory agents is contraindicated due to the risk of additive immune system effects. However, co-administration of a short course of corticosteroids (up to 5 days) did not increase the overall rate of infection in patients participating Phase III clinical trials.(2) The fingolimod UK specific product characteristics states: - Fingolimod is contraindicated in patients currently receiving immunosuppressive therapies or those immunocompromised by prior therapies. When switching patients from another disease modifying therapy to Gilenya, the half-life and mode of action of the other therapy must be considered in order to avoid an additive immune effect whilst at the same time minimizing the risk of disease activation.(3) DISCUSSION: Fatal disseminated herpes zoster and herpes simplex infections and cases of progressive multifocal leukoencephalopathy (PML) have been reported in patients who previously received immunomodulators or immunosuppressants.(1-3)	FINGOLIMOD, GILENYA, TASCENSO ODT
Ozanimod/Immunosuppressives; Immunomodulators SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Ozanimod in combination with immunosuppressives and immune-modulators all suppress the immune system.(1) CLINICAL EFFECTS: Concurrent use of ozanimod with immunosuppressive or immune-modulating agents may result in an increased risk of serious infections, such as disseminated herpetic infection or progressive multifocal leukoencephalopathy (PML), an opportunistic infection caused by the JC virus (JCV).(1) PREDISPOSING FACTORS: Incomplete washout of previously prescribed immunosuppressive or immune-modulating medications. PATIENT MANAGEMENT: The ozanimod US prescribing information state this information regarding this interaction: -Ozanimod has not been studied in combination with anti-neoplastic, immune-modulating, or immunosuppressive therapies. Caution should be used during concomitant administration because of the risk of additive immune effects during therapy and in the week following administration. When switching from drugs with prolonged immune effects, the half-life and mode of action of these drugs must be considered in order to avoid unintended additive immunosuppressive effects. Initiating treatment with ozanimod after alemtuzumab is not recommended. However, ozanimod can generally be started immediately after discontinuation of beta interferon or glatiramer acetate.(1) DISCUSSION: Fatal disseminated herpes zoster and herpes simplex infections and cases of progressive multifocal leukoencephalopathy (PML) have been reported in patients who previously received immunomodulators or immunosuppressants.(1)	ZEPOSIA
Siponimod/Immunosuppressives; Immunomodulators SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Siponimod in combination with immunosuppressives and immune-modulators all suppress the immune system.(1) CLINICAL EFFECTS: Concurrent use of siponimod with immunosuppressive or immune-modulating agents may result in an increased risk of serious infections, such as disseminated herpetic infection or progressive multifocal leukoencephalopathy (PML), an opportunistic infection caused by the JC virus (JCV).(1) PREDISPOSING FACTORS: Incomplete washout of previously prescribed immunosuppressive or immune-modulating medications. PATIENT MANAGEMENT: The siponimod US prescribing information state this information regarding this interaction: -Siponimod has not been studied in combination with anti-neoplastic, immune-modulating, or immunosuppressive therapies. Caution should be used during concomitant administration because of the risk of additive immune effects during therapy and in the week following administration. When switching from drugs with prolonged immune effects, the half-life and mode of action of these drugs must be considered in order to avoid unintended additive immunosuppressive effects. Initiating treatment with siponimod after alemtuzumab is not recommended. However, siponimod can generally be started immediately after discontinuation of beta interferon or glatiramer acetate.(1) DISCUSSION: Fatal disseminated herpes zoster and herpes simplex infections and cases of progressive multifocal leukoencephalopathy (PML) have been reported in patients who previously received immunomodulators or immunosuppressants.(1)	MAYZENT
Cladribine/Immunosuppressives; Immunomodulators SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Cladribine in combination with immunosuppressives and immune-modulators all suppress the immune system.(1-2) CLINICAL EFFECTS: Concurrent use of cladribine with immunosuppressive or immune-modulating agents may result in an increased risk of serious infections, such as disseminated herpetic infection or progressive multifocal leukoencephalopathy (PML), an opportunistic infection caused by the JC virus (JCV).(1-2) PREDISPOSING FACTORS: Incomplete washout of previously prescribed immunosuppressive or immune-modulating medications. PATIENT MANAGEMENT: Recommendations for cladribine regarding this interaction differ between regulatory approving agencies. The cladribine US prescribing information states: -Concomitant use with myelosuppressive or other immunosuppressive drugs is not recommended. Acute short-term therapy with corticosteroids can be administered. In patients who have previously been treated with immunomodulatory or immunosuppressive drugs, consider potential additive effect, the mode of action, and duration of effect of the other drugs prior to initiation of cladribine.(1) The cladribine Canadian prescribing information states: -Use of cladribine in immunocompromised patients is contraindicated because of a risk of additive effects on the immune system. Acute short-term therapy with corticosteroids can be administered during cladribine treatment.(2) DISCUSSION: Fatal disseminated herpes zoster and herpes simplex infections and cases of progressive multifocal leukoencephalopathy (PML) have been reported in patients who previously received immunomodulators or immunosuppressants.(1-2)	CLADRIBINE, MAVENCLAD
Ritlecitinib/Immunosuppressives; Immunomodulators SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Ritlecitinib, immunosuppressives, and immunomodulators all suppress the immune system. CLINICAL EFFECTS: Concurrent use of ritlecitinib with immunosuppressives or immunomodulators may result in an increased risk of serious infections. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The US manufacturer of ritlecitinib states that concurrent use of ritlecitinib with other JAK inhibitors, biologic immunomodulators, cyclosporine or other potent immunosuppressants is not recommended.(1) DISCUSSION: Serious infections have been reported in patients receiving ritlecitinib. Reported infections included appendicitis, COVID-19 infection (including pneumonia), and sepsis. Reports of viral reactivation, including herpes virus reactivation was reported in clinical studies with ritlecitinib.(1)	LITFULO
Etrasimod/Immunosuppressives; Immunomodulators SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Etrasimod causes reversible sequestration of lymphocytes in lymphoid tissues, resulting in a mean 55% decrease in peripheral blood lymphocyte count at 52 weeks.(1) Other immunosuppressives and immune-modulators also suppress the immune system. CLINICAL EFFECTS: Concurrent use of etrasimod with immunosuppressive or immune-modulating agents may result in an increased risk of serious and fatal infections, such as disseminated herpetic infection, cryptococcal infection, or progressive multifocal leukoencephalopathy (PML).(1) PREDISPOSING FACTORS: Incomplete washout of previously prescribed immunosuppressive or immune-modulating medications increases the risk of adverse effects. PATIENT MANAGEMENT: The etrasimod US prescribing information states etrasimod has not been studied in combination with anti-neoplastic, immune-modulating, or immunosuppressive therapies. Concomitant administration of these therapies with etrasimod should be avoided because of the risk of additive immune effects during therapy and in the weeks following administration. Etrasimod's effect on peripheral lymphocytes may persist for up to 5 weeks after discontinuation.(1) When switching from drugs with prolonged immune effects, the half-life and mode of action of these drugs must be considered in order to avoid unintended additive immunosuppressive effects.(1) DISCUSSION: Fatal disseminated herpes zoster and herpes simplex infections, cryptococcal meningitis, disseminated cryptococcal infections, and cases of progressive multifocal leukoencephalopathy (PML) have been reported in patients treated with other sphingosine-1 phosphate receptor modulators.(1)	VELSIPITY
Ropeginterferon alfa-2b/Slt Immunosuppress; Immunomodulator SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Ropeginterferon alfa-2b and immunosuppressives both suppress the immune system. CLINICAL EFFECTS: Concurrent use of ropeginterferon alfa-2b with immunosuppressives may result in an increased risk of serious infections. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Avoid concurrent use of myelosuppressive agents.(1-2) If concurrent use cannot be avoided, monitor for effects of excessive immunosuppression. DISCUSSION: In clinical trials, 20% of patients experienced leukopenia. Interferon alfa products may cause fatal or life-threatening infections.(1-2)	BESREMI
Sodium Iodide I 131/Myelosuppressives that affect Iodide SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Sodium iodide I 131 can cause depression of the hematopoetic system. Myelosuppressives and immunomodulators also suppress the immune system.(1) Many compounds can affect iodide protein binding and alter iodide pharmacokinetics and pharmacodynamics. CLINICAL EFFECTS: Concurrent use of sodium iodide I 131 with agents that cause bone marrow depression, including myelosuppressives or immunomodulators, may result in an enhanced risk of hematologic disorders, including anemia, blood dyscrasias, bone marrow depression, leukopenia, and thrombocytopenia. Bone marrow depression may increase the risk of serious infections and bleeding.(1) Compounds that affect iodide pharmacokinetics and pharmacodynamics may impact the effectiveness of radioactive iodide.(1,2) PREDISPOSING FACTORS: Compounds that affect iodide pharmacokinetics and pharmacodynamics are expected to have the most impact during therapy using radioactive iodide. Diagnostic procedures would be expected to be impacted less. PATIENT MANAGEMENT: The US manufacturer of sodium iodide I 131 states that concurrent use with bone marrow depressants may enhance the depression of the hematopoetic system caused by large doses of sodium iodide I 131.(1) Sodium iodide I 131 causes a dose-dependent bone marrow suppression, including neutropenia or thrombocytopenia, in the 3 to 5 weeks following administration. Patients may be at increased risk of infections or bleeding during this time. Monitor complete blood counts within one month of therapy. If results indicate leukopenia or thrombocytopenia, dosimetry should be used to determine a safe sodium iodide I 131 activity.(1) Discuss the use of agents that affect iodide pharmacokinetics and pharmacodynamics with the patient's oncologist.(1,2) DISCUSSION: Hematologic disorders including death have been reported with sodium iodide I 131. The most common hematologic disorders reported include anemia, blood dyscrasias, bone marrow depression, leukopenia, and thrombocytopenia.(1) Many agents interact with radioactive iodine. The average duration of effect is: anticoagulants - 1 week antihistamines - 1 week anti-thyroid drugs, e.g: carbimazole, methimazole, propylthiouracil - 3-5 days corticosteroids - 1 week iodide-containing medications, e.g: amiodarone - 1-6 months expectorants - 2 weeks Lugol solution - 3 weeks saturated solution of potassium iodine - 3 weeks vitamins - 10-14 days iodide-containing X-ray contrast agents - up to 1 year lithium - 4 weeks phenylbutazone - 1-2 weeks sulfonamides - 1 week thyroid hormones (natural or synthetic), e.g.: thyroxine - 4 weeks tri-iodothyronine - 2 weeks tolbutamide - 1 week topical iodide - 1-9 months (1,2)	HICON, SODIUM IODIDE I-131

There are 13 moderate interactions. The clinician should assess the patient’s characteristics and take action as needed. Actions required for moderate interactions include, but are not limited to, discontinuing one or both agents, adjusting dosage, altering administration.

Drug Interaction	Drug Names
Corticosteroids/Hormonal Contraceptives; Estrogens SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: It is speculated that hormonal contraceptives and estrogens inhibit hepatic metabolism of some corticosteroids as well as endogenous cortisol. Competitive protein binding may also contribute to elevations in serum corticosteroids. CLINICAL EFFECTS: Concurrent use of hormonal contraceptives or estrogens may result in an increase in the therapeutic and toxic effects of corticosteroids. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Patients receiving concurrent hormonal contraceptives or estrogen should be observed for symptoms of corticosteroid toxicity. A lower corticosteroid dose may be required. DISCUSSION: In a study in 6 healthy females controlled on long-term oral contraceptives, subjects received either a placebo or high and low-dose prednisolone (0.53 and 0.14 mg/Kg iv). Both dosages of prednisolone decreased the total clearance, unbound clearance, and volume of distribution (Vd) at maximum concentration (Cmax) of total drug. Significant increases in half-life for free and unbound prednisolone and hydrocortisone concentrations were also observed in comparison to the placebo group. In a study in 8 females controlled on oral contraceptive therapy, 8 females not receiving contraceptive therapy, and 8 males, each subject received prednisolone 40 mg iv. The plasma clearance of total prednisolone in females on OC was 96 ml/min, which was significantly lower than those in both the male and female (205 and 187 ml/min, respectively) control groups. Prednisolone half-life and mean residence times were increased. The oral contraceptive group had a significantly higher (2-fold) concentration of transcortin, resulting in lower clearance, decreased Vd, and a 2-fold increase in the area-under-curve (AUC) for prednisolone. A clinical trial demonstrated the interaction between prednisolone (20 mg) and oral contraceptives containing ethinyl estradiol (30 mcg). The oral contraceptive users had an average plasma concentration of prednisolone 131% higher compared to the control group, and plasma cortisol levels were suppressed by approximately 90%. No differences were reported for ethinyl estradiol levels. In a study in 8 females taking oral contraceptives and 8 females who were were not, subjects received IV doses of prednisolone at 0.1 mg/Kg and 1.0 mg/Kg. Free prednisolone clearance was reduced by approximately 30% in the contraceptive receiving subjects compared to the control group, and plasma cortisol concentrations were reduced 2-fold compared to the control group. One or more of the drug pairs linked to this monograph have been included in a list of interactions that could be considered for classification as "non-interruptive" in EHR systems. This DDI subset was vetted by an expert panel commissioned by the U.S. Office of the National Coordinator (ONC) for Health Information Technology.	2-METHOXYESTRADIOL, ACTIVELLA, AFIRMELLE, ALTAVERA, ALYACEN, AMETHIA, AMETHYST, ANGELIQ, ANNOVERA, APRI, ARANELLE, ASHLYNA, AUBRA, AUBRA EQ, AUROVELA, AUROVELA 24 FE, AUROVELA FE, AVIANE, AYUNA, AZURETTE, BALCOLTRA, BALZIVA, BEYAZ, BIJUVA, BLISOVI 24 FE, BLISOVI FE, BRIELLYN, CAMRESE, CAMRESE LO, CAZIANT, CHARLOTTE 24 FE, CHATEAL EQ, CLIMARA, CLIMARA PRO, COMBIPATCH, COVARYX, COVARYX H.S., CRYSELLE, CYRED, CYRED EQ, DASETTA, DAYSEE, DELESTROGEN, DEPO-ESTRADIOL, DESOGESTR-ETH ESTRAD ETH ESTRA, DIETHYLSTILBESTROL, DIVIGEL, DOLISHALE, DOTTI, DROSPIRENONE-ETH ESTRA-LEVOMEF, DROSPIRENONE-ETHINYL ESTRADIOL, DUAVEE, EEMT, EEMT H.S., ELESTRIN, ELINEST, ELURYNG, ENILLORING, ENPRESSE, ENSKYCE, ESTARYLLA, ESTRACE, ESTRADIOL, ESTRADIOL (ONCE WEEKLY), ESTRADIOL (TWICE WEEKLY), ESTRADIOL BENZOATE, ESTRADIOL CYPIONATE, ESTRADIOL HEMIHYDRATE, ESTRADIOL HEMIHYDRATE MICRO, ESTRADIOL MICRONIZED, ESTRADIOL VALERATE, ESTRADIOL-NORETHINDRONE ACETAT, ESTRATEST F.S., ESTRATEST H.S., ESTRING, ESTRIOL, ESTRIOL MICRONIZED, ESTROGEL, ESTROGEN-METHYLTESTOSTERONE, ESTRONE, ETHINYL ESTRADIOL, ETHYNODIOL-ETHINYL ESTRADIOL, ETONOGESTREL-ETHINYL ESTRADIOL, EVAMIST, FALMINA, FEIRZA, FEMLYV, FEMRING, FINZALA, FYAVOLV, GEMMILY, HAILEY, HAILEY 24 FE, HAILEY FE, HALOETTE, ICLEVIA, ISIBLOOM, JAIMIESS, JASMIEL, JINTELI, JOLESSA, JOYEAUX, JULEBER, JUNEL, JUNEL FE, JUNEL FE 24, KAITLIB FE, KALLIGA, KARIVA, KELNOR 1-35, KELNOR 1-50, KURVELO, LARIN, LARIN 24 FE, LARIN FE, LAYOLIS FE, LEENA, LESSINA, LEVONEST, LEVONORG-ETH ESTRAD ETH ESTRAD, LEVONORG-ETH ESTRAD-FE BISGLYC, LEVONORGESTREL-ETH ESTRADIOL, LEVORA-28, LO LOESTRIN FE, LO-ZUMANDIMINE, LOESTRIN, LOESTRIN FE, LOJAIMIESS, LORYNA, LOW-OGESTREL, LUTERA, LYLLANA, MARLISSA, MENEST, MENOSTAR, MERZEE, MIBELAS 24 FE, MICROGESTIN, MICROGESTIN FE, MILI, MIMVEY, MINIVELLE, MINZOYA, MONO-LINYAH, MYFEMBREE, NATAZIA, NECON, NEXTSTELLIS, NIKKI, NORELGESTROMIN-ETH ESTRADIOL, NORETHIN-ETH ESTRA-FERROUS FUM, NORETHINDRON-ETHINYL ESTRADIOL, NORETHINDRONE-E.ESTRADIOL-IRON, NORGESTIMATE-ETHINYL ESTRADIOL, NORTREL, NUVARING, NYLIA, OCELLA, ORIAHNN, ORTHO TRI-CYCLEN, ORTHO-NOVUM, PHILITH, PIMTREA, PORTIA, PREMARIN, PREMPHASE, PREMPRO, RECLIPSEN, RIVELSA, SAFYRAL, SETLAKIN, SIMLIYA, SIMPESSE, SLYND, SPRINTEC, SRONYX, SYEDA, TARINA 24 FE, TARINA FE, TARINA FE 1-20 EQ, TAYTULLA, TILIA FE, TRI-ESTARYLLA, TRI-LEGEST FE, TRI-LINYAH, TRI-LO-ESTARYLLA, TRI-LO-MARZIA, TRI-LO-MILI, TRI-LO-SPRINTEC, TRI-MILI, TRI-SPRINTEC, TRI-VYLIBRA, TRI-VYLIBRA LO, TRIVORA-28, TURQOZ, TWIRLA, TYBLUME, VAGIFEM, VALTYA, VELIVET, VESTURA, VIENVA, VIORELE, VIVELLE-DOT, VOLNEA, VYFEMLA, VYLIBRA, WERA, WYMZYA FE, XARAH FE, XELRIA FE, XULANE, YASMIN 28, YAZ, YUVAFEM, ZAFEMY, ZARAH, ZOVIA 1-35, ZUMANDIMINE
Corticosteroids/Selected Strong CYP3A4 Inducers SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Strong CYP3A4 inducers may induce the metabolism of corticosteroids. Corticosteroids may affect the metabolism of phenytoin. CLINICAL EFFECTS: Concurrent or recent use of strong CYP3A4 inducers may result in decreased levels and effectiveness of corticosteroids. Dexamethasone has been shown to increase and decrease phenytoin levels. PREDISPOSING FACTORS: Induction effects may be more likely with regular use of the inducer for longer than 1-2 weeks. PATIENT MANAGEMENT: Patients receiving concurrent therapy with a strong CYP3A4 inducer should be monitored for decreased effectiveness of their corticosteroid. Increased dosage of corticosteroid may be required during concurrent therapy and for several weeks after completing concurrent therapy. If concurrent therapy is discontinued, the dosage of the corticosteroid may need to be adjusted. Phenytoin levels should be closely monitored in patients receiving corticosteroids. The dosage of phenytoin may need to be adjusted if corticosteroids are initiated or discontinued. DISCUSSION: Carbamazepine has been shown to increase the metabolism of methylprednisolone, prednisolone, and prednisone, resulting in decreased levels and effectiveness of these agents. Phenobarbital has been shown to increase the metabolism of dexamethasone, methylprednisolone, and prednisolone. Primidone is metabolized to phenobarbital. Phenytoin has been shown to increase the metabolism of dexamethasone, hydrocortisone, methylprednisolone, prednisolone, and prednisone, resulting in decreased levels and effectiveness of these agents Rifampin has been shown to increase the metabolism of cortisol, dexamethasone, methylprednisolone, prednisolone, and prednisone. Strong CYP3A4 inducers linked to this monograph include: apalutamide, barbiturates, carbamazepine, encorafenib, enzalutamide, fosphenytoin, ivosidenib, lumacaftor, mitotane, phenobarbital, phenytoin, primidone, rifabutin, rifapentine, rifampin, and St. John's wort.	ASA-BUTALB-CAFFEINE-CODEINE, ASCOMP WITH CODEINE, BRAFTOVI, BUTALB-ACETAMINOPH-CAFF-CODEIN, BUTALBITAL, BUTALBITAL-ACETAMINOPHEN, BUTALBITAL-ACETAMINOPHEN-CAFFE, BUTALBITAL-ASPIRIN-CAFFEINE, CARBAMAZEPINE, CARBAMAZEPINE ER, CARBATROL, CEREBYX, DILANTIN, DILANTIN-125, DONNATAL, EPITOL, EQUETRO, ERLEADA, FIORICET, FIORICET WITH CODEINE, FOSPHENYTOIN SODIUM, LYSODREN, MITOTANE, MYSOLINE, ORKAMBI, PENTOBARBITAL SODIUM, PHENOBARBITAL, PHENOBARBITAL SODIUM, PHENOBARBITAL-BELLADONNA, PHENOBARBITAL-HYOSC-ATROP-SCOP, PHENOHYTRO, PHENYTEK, PHENYTOIN, PHENYTOIN SODIUM, PHENYTOIN SODIUM EXTENDED, PRIFTIN, PRIMIDONE, RIFABUTIN, RIFADIN, RIFAMPIN, SEZABY, TALICIA, TEGRETOL, TEGRETOL XR, TENCON, TIBSOVO, XTANDI
NSAIDs/Corticosteroids SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Concurrent use of NSAIDs and corticosteroids result in additive risk of GI ulceration. CLINICAL EFFECTS: Concurrent use of NSAIDs and corticosteroids may increase the incidence and/or severity of GI irritation or ulceration, including increasing the risk for bleeding. PREDISPOSING FACTORS: Risk of GI bleed may be increased in patients who are of older age, in poor health status, or who use alcohol or smoke. Risk may also be increased by concurrent use of anticoagulants, antiplatelets, selective serotonin reuptake inhibitors (SSRIs) or serotonin-norepinephrine reuptake inhibitors (SNRIs); with longer duration of NSAID use; and with prior history of peptic ulcer disease and/or GI bleeding. The risk for bleeding episodes may be greater in patients with disease-associated factors (e.g. thrombocytopenia, advanced liver disease). PATIENT MANAGEMENT: Monitor patients receiving concurrent therapy carefully for signs of gastrointestinal ulceration. Use the lowest effective NSAID dose for the shortest duration possible. If concurrent therapy is warranted, monitor patients receiving concurrent therapy for signs of blood loss, including decreased hemoglobin, hematocrit, fecal occult blood, and/or decreased blood pressure and promptly evaluate patients with any symptoms. Instruct patients to report signs of GI bleeding such as black, tarry stools; "coffee ground" vomit; nausea; or stomach/abdominal pain. DISCUSSION: Concurrent use of NSAIDs and corticosteroids increase the risk of GI bleeding.	ANAPROX DS, ANJESO, ARTHROTEC 50, ARTHROTEC 75, BROMFENAC SODIUM, BUPIVACAINE-KETOROLAC-KETAMINE, CALDOLOR, CAMBIA, CELEBREX, CELECOXIB, COMBOGESIC, COMBOGESIC IV, CONSENSI, COXANTO, DAYPRO, DICLOFENAC, DICLOFENAC POTASSIUM, DICLOFENAC SODIUM, DICLOFENAC SODIUM ER, DICLOFENAC SODIUM MICRONIZED, DICLOFENAC SODIUM-MISOPROSTOL, EC-NAPROSYN, ELYXYB, ETODOLAC, ETODOLAC ER, FELDENE, FENOPROFEN CALCIUM, FENOPRON, FLURBIPROFEN, HYDROCODONE-IBUPROFEN, IBU, IBUPAK, IBUPROFEN, IBUPROFEN LYSINE, IBUPROFEN-FAMOTIDINE, INDOCIN, INDOMETHACIN, INDOMETHACIN ER, INFLAMMACIN, INFLATHERM(DICLOFENAC-MENTHOL), KETOPROFEN, KETOPROFEN MICRONIZED, KETOROLAC TROMETHAMINE, KIPROFEN, LODINE, LOFENA, LURBIPR, MECLOFENAMATE SODIUM, MEFENAMIC ACID, MELOXICAM, NABUMETONE, NABUMETONE MICRONIZED, NALFON, NAPRELAN, NAPROSYN, NAPROTIN, NAPROXEN, NAPROXEN SODIUM, NAPROXEN SODIUM CR, NAPROXEN SODIUM ER, NAPROXEN-ESOMEPRAZOLE MAG, NEOPROFEN, OXAPROZIN, PHENYLBUTAZONE, PIROXICAM, R.E.C.K.(ROPIV-EPI-CLON-KETOR), RELAFEN DS, ROPIVACAINE-CLONIDINE-KETOROLC, ROPIVACAINE-KETOROLAC-KETAMINE, SULINDAC, SUMATRIPTAN SUCC-NAPROXEN SOD, SYMBRAVO, TOLECTIN 600, TOLMETIN SODIUM, TORONOVA II SUIK, TORONOVA SUIK, TOXICOLOGY SALIVA COLLECTION, TRESNI, TREXIMET, VIMOVO, VIVLODEX, ZIPSOR, ZORVOLEX
Corticosteroids/Selected Macrolide Antibiotics SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Some macrolide antibiotics may inhibit the metabolism of corticosteroids. CLINICAL EFFECTS: Concurrent use of some macrolide antibiotics may result in elevated levels and clinical effects of corticosteroids. Immunosuppression and Cushing's syndrome have been reported during concurrent therapy, including therapy with inhaled corticosteroids. PREDISPOSING FACTORS: Concurrent administration of enzyme inducing drugs. PATIENT MANAGEMENT: Patients receiving concurrent therapy with corticosteroids and macrolide antibiotics should be monitored for increased corticosteroid affects. The dosage of the corticosteroid may need to be adjusted or the macrolide antibiotic may need to be discontinued. One US manufacturer of inhaled fluticasone states that the concurrent use of macrolide antibiotics is not recommended.(1) DISCUSSION: In a study in 10 steroid-dependent asthmatics, concurrent troleandomycin (1 gram/day) decreased methylprednisolone clearance by 60%. All subjects developed adverse effects typical of excessive corticosteroid use such as weight gain, fluid retention, and cushingoid features.(2) Other studies and reports have shown increased methylprednisolone levels with concurrent troleandomycin,(3-10) in some of these reports, the interaction was used to lower steroid dosages.(6-10) There is one report of fatal varicella infection in a patient receiving concurrent therapy with methylprednisolone and troleandomycin.(11) Cushing's syndrome has been reported with concurrent inhaled budesonide and clarithromycin.(12) Psychosis(13) and mania(14) have been reported with concurrent prednisone and clarithromycin. Erythromycin(3-9) and troleandomycin(9) have also been reported to interact with methylprednisolone.	CLARITHROMYCIN, CLARITHROMYCIN ER, E.E.S. 200, E.E.S. 400, ERY-TAB, ERYPED 200, ERYPED 400, ERYTHROCIN LACTOBIONATE, ERYTHROCIN STEARATE, ERYTHROMYCIN, ERYTHROMYCIN ESTOLATE, ERYTHROMYCIN ETHYLSUCCINATE, ERYTHROMYCIN LACTOBIONATE, LANSOPRAZOL-AMOXICIL-CLARITHRO, OMECLAMOX-PAK, VOQUEZNA TRIPLE PAK
Anticoagulants/Corticosteroids SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Corticosteroids may increase the coagulability of blood, thus decreasing the effect of the anticoagulant.(1,2) Corticosteroids may also lower vascular integrity, which could increase the risk of hemorrhage.(3,4) CLINICAL EFFECTS: Concurrent use of corticosteroids may result in either increased (increased risk of bleeding) or decreased effects (increased risk of treatment failure) of anticoagulants. PREDISPOSING FACTORS: The risk for bleeding episodes may be greater in patients with disease-associated factors (e.g. thrombocytopenia). Drug associated risk factors include concurrent use of multiple drugs which inhibit anticoagulant/antiplatelet metabolism and/or have an inherent risk for bleeding (e.g. NSAIDs). PATIENT MANAGEMENT: The patient's clotting times should be monitored closely, along with any clinical signs of hemorrhage or clot formation. The dosage of the anticoagulant may need to be adjusted accordingly. If concurrent therapy is warranted, monitor patients receiving concurrent therapy for signs of blood loss, including decreased hemoglobin, hematocrit, fecal occult blood, and/or decreased blood pressure and promptly evaluate patients with any symptoms. When applicable, perform agent-specific laboratory test (e.g. INR, aPTT) to monitor efficacy and safety of anticoagulation. Discontinue anticoagulation in patients with active pathologic bleeding. Instruct patients to report any signs and symptoms of bleeding, such as unusual bleeding from the gums or nose; unusual bruising; red or black, tarry stools; red, pink or dark brown urine; acute abdominal or joint pain and/or swelling. The time of highest risk for a coumarin-type drug interaction is when the precipitant drug is initiated or discontinued. Contact the prescriber before initiating, altering the dose or discontinuing either drug. DISCUSSION: Corticotropin and other corticosteroids have been shown to both increase (3,5-11) and decrease (1,12,13) the effects of acenocoumarol, dicumarol, fluindione, and warfarin. Hemorrhagic episodes have been associated with concurrent use of these medications.(3,5) One or more of the drug pairs linked to this monograph have been included in a list of interactions that could be considered for classification as "non-interruptive" in EHR systems. This DDI subset was vetted by an expert panel commissioned by the U.S. Office of the National Coordinator (ONC) for Health Information Technology.	ANISINDIONE, DICUMAROL, ELMIRON, JANTOVEN, PENTOSAN POLYSULFATE SODIUM, PHENINDIONE, WARFARIN SODIUM
Bupropion/Steroids SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Both bupropion and systemic steroids are known to lower the seizure threshold.(1,2) CLINICAL EFFECTS: Concurrent use of bupropion and systemic steroids may result in additive effects on the seizure threshold, increasing the risk of seizures.(1,2) PREDISPOSING FACTORS: The risk of seizures may be increased in patients with a history of head trauma or prior seizure; CNS tumor; severe hepatic cirrhosis; excessive use of alcohol or sedatives; addiction to opiates, cocaine, or stimulants; use of over-the-counter stimulants an anorectics; a total daily dose of bupropion greater than 450 mg or single doses greater than 150 mg; rapid escalation of bupropion dosage; diabetics treated with oral hypoglycemics or insulin; or with concomitant medications known to lower seizure threshold (antidepressants, antipsychotics, theophylline).(1,2) PATIENT MANAGEMENT: The concurrent use of bupropion and systemic steroids should be undertaken only with extreme caution and with low initial bupropion dosing and small gradual dosage increases.(1,2) Single doses should not exceed 150 mg.(1,2) The maximum daily dose of bupropion should not exceed 300 mg for smoking cessation(2) or 450 mg for depression.(1) DISCUSSION: Because of the risk of seizure from concurrent bupropion and other agents that lower seizure threshold, the manufacturer of bupropion states that the concurrent use of bupropion and systemic steroids should be undertaken only with extreme caution and with low initial bupropion dosing and small gradual dosage increases.(1,2)	APLENZIN, AUVELITY, BUPROPION HCL, BUPROPION HCL SR, BUPROPION XL, CONTRAVE, FORFIVO XL, WELLBUTRIN SR, WELLBUTRIN XL
Quinolones/Corticosteroids SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Quinolone-induced arthropathy is a class effect of the quinolones.(1) Exactly how corticosteroid use increases the risk of tendon rupture is unknown. CLINICAL EFFECTS: Concurrent use of quinolones and corticosteroids may increase the risk of tendonitis and/or tendon rupture. This affect is most common in the Achilles tendon, but has been reported in the rotator cuff (shoulder), hand, biceps, thumb, and other tendons.(2-9) PREDISPOSING FACTORS: Risk factors for tendinitis and tendon rupture include age greater than 60; a history of kidney, heart, or lung transplantation, strenuous physical activity, renal failure, and previous tendon disorders such as rheumatoid arthritis. PATIENT MANAGEMENT: Quinolone use should be discontinued if the patient experiences pain, inflammation, or rupture of a tendon. Patients should be instructed to rest and refrain from exercise until the diagnosis of tendonitis tendon rupture has been excluded.(2-9) DISCUSSION: Ruptures of the shoulder, hand, Achilles tendon, or other tendons that required surgical repair or resulted in prolonged disability have been reported in patients receiving ciprofloxacin,(2) gatifloxacin,(3) levofloxacin,(4) lomefloxacin,(5) moxifloxacin,(6) nalidixic acid,(7) norfloxacin,(8) and ofloxacin.(9) A retrospective review of the IMS Health database examined quinolone use use from July 1, 1992 to June 30, 1998. The adjusted relative risk of tendon disorder with concurrent quinolone use was 1.9. Relative risk increased to 3.2 in patients aged 60 or older compared to 0.9 in patients aged less than 60. In patients aged 60 or older who used corticosteroids and quinolones concurrently, relative risk increased to 6.2.(10) In contrast, another retrospective review examined patients from a health insurance claims database and found no apparent effect from concurrent quinolone and corticosteroid use.(11) In a review of the follow-up to 42 spontaneously reported case of quinolone-associated tendon disorders in the Netherlands between January, 1988 and January, 1998, risk factors for tendon disorders included age older than 60, oral corticosteroid use, and existing joint problems.(12) In a review of the Swiss Drug Monitoring system, four of seven cases of levofloxacin-associated tendon problems also involved concurrent oral or inhaled corticosteroids.(13) In a review of the Medline database from 1966-2001, 98 case reports of tendinopathy associated with quinolones were located. Thirty-two (32.7%) of the patients had received systemic or inhaled corticosteroids before and during quinolone therapy. Of the 40 patients who suffered a tendon rupture, 21 (52.5%) were receiving corticosteroids.(14) Other authors have reported cases of tendon disorders in patients receiving concurrent corticosteroids and ciprofloxacin,(15) levofloxacin, (16-20) and ofloxacin.(21)	AVELOX IV, BAXDELA, CIPRO, CIPROFLOXACIN, CIPROFLOXACIN HCL, CIPROFLOXACIN-D5W, GATIFLOXACIN SESQUIHYDRATE, LEVOFLOXACIN, LEVOFLOXACIN HEMIHYDRATE, LEVOFLOXACIN-D5W, MOXIFLOXACIN, MOXIFLOXACIN HCL, NALIDIXIC ACID, OFLOXACIN
Selected Corticosteroids/Selected Azole Antifungal Agents SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Itraconazole, ketoconazole, posaconazole, and voriconazole may inhibit the CYP3A4 mediated metabolism of some corticosteroids, resulting in increased systemic exposure. Itraconazole and ketoconazole may also suppress endogenous cortisol output. CLINICAL EFFECTS: Concurrent use of itraconazole, ketoconazole, posaconazole, or voriconazole may result in elevated levels of and effects from the corticosteroid, including Cushing syndrome. These effects have been seen with systemic as well as inhaled corticosteroids. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Patients should be carefully monitored with concurrent administration of these agents, or when itraconazole, ketoconazole, posaconazole, or voriconazole is added to corticosteroid therapy. The dose of the corticosteroid may need to be adjusted or alternative therapy considered. DISCUSSION: In a randomized, double-blind, cross-over study in 10 healthy subjects, pretreatment with itraconazole (200 mg daily for 5 days) increased the area-under-curve (AUC) and maximum concentration (Cmax) of a single inhaled dose of budesonide (1000 mcg) by 4.2-fold and 1.6-fold, respectively. Suppression of cortisol production was increased 43%.(1) A study examined adrenal insufficiency in 25 cystic fibrosis patients treated with itraconazole and inhaled budesonide and in 12 patients receiving itraconazole alone. Eleven of the 25 patients receiving concurrent itraconazole and budesonide and none of the patients receiving only itraconazole had adrenal insufficiency.(2) There are case reports of Cushing syndrome in patients receiving concurrent itraconazole (range 200 mg to 800 mg daily) and inhaled budesonide (range 400 mcg to 1400 mcg daily).(3-5) The concurrent use of ketoconazole has been shown to increase budesonide area-under-curve (AUC) by eight-fold.(6) In a study in eight healthy subjects, the simultaneous administration of ketoconazole increased budesonide AUC by 6.5-fold. Administering the two agents 12 hours apart increased budesonide AUC by 3.8-fold.(7) There are case reports of Cushing syndrome in patients receiving concurrent itraconazole (range 100 mg to 400 mg daily) and inhaled fluticasone (range 250 mcg to 1.5 mg daily).(8,9) In a randomized, placebo-controlled, crossover, four phase study in 8 healthy subjects, itraconazole decreased the systemic clearance of intravenous dexamethasone by 68%, increased the area-under-curve (AUC) of dexamethasone by 3.3-fold, and prolonged its half-life by 3.2-fold. The AUC of oral dexamethasone was increased 3.7-fold, maximum concentration (Cmax) was increased by 1.7-fold, and the elimination half-life was prolonged 2.8-fold by itraconazole.(10) In a randomized, cross-over study in 14 healthy subjects, pretreatment with itraconazole (400 mg Day 1, 200 mg Days 2-4) increased the AUC of a single oral dose of methylprednisolone by 1.5-fold. Cortisol levels were significantly lower after concurrent therapy than with methylprednisolone alone.(11) There is a case report of Cushing syndrome following the addition of itraconazole (400 mg daily) to methylprednisolone (12 mg/day).(12) In a study in 6 healthy subjects, pretreatment with ketoconazole (200 mg daily) increased the AUC of a single intravenous dose of methylprednisolone (20 mg) by 135% and decreased its clearance by 60%. Concurrent ketoconazole also increased the reduction in 24-hour cortisol AUC and suppressed morning cortisol concentrations.(13) In a study in 8 healthy subjects, ketoconazole decreased the clearance of methylprednisolone by 46% and increased mean residence time by 37%.(14) In a randomized, cross-over study in 14 healthy subjects, pretreatment with itraconazole (400 mg Day 1, 200 mg Days 2-4) had no effect on the pharmacokinetics of a single oral dose of prednisone (60 mg).(11) In a randomized, cross-over study in 6 healthy subjects, pretreatment with ketoconazole (200 mg daily for 6 days) had no effect on the pharmacokinetics of a single intravenous dose of prednisolone (14.8 mg).(15) In a randomized, double-blind, cross-over study in 10 healthy subjects, pretreatment with itraconazole (200 mg daily for 4 days) increased the AUC and half-life of a single oral dose of prednisolone (20 mg) by 24% and 29%, respectively.(16) In a study, concurrent oral ketoconazole increased the AUC of des-ciclesonide from orally inhaled ciclesonide by 3.6-fold. There were no changes in ciclesonide levels.(17) In a study in 24 healthy subjects, subjects were randomized to receive either ketoconazole (200 mg BID) or placebo on Days 4-9 of a a 9 day course of mometasone (400 mcg BID). No subject had mometasone levels greater than 150 pcg/ml on Day 3. Four of 12 subjects who received ketoconazole had mometasone Cmax levels greater than 200 mcg/ml on Day 9. Plasma cortisol levels appeared to decrease as well.(18) In a cross-over study in 15 healthy subjects, subjects were randomized to receive fluticasone furoate and vilanterol on days 5-11 with either ketoconazole (200mg once daily) or placebo for days 1-11 with a washout period of 7-14 days. Fluticasone furoate AUC was increased by 36%, Cmax was increased by 33%, and decreased systemic cortisol levels by 27%. There were no effects on heart rate and blood potassium levels. There was a small increase in QTc which was 7.6ms greater when compared to placebo; however, ketoconazole has been reported to increase QTc by 5-6ms. Vilanterol AUC was increased by 65% and Cmax was increased by 22%. There were no effects on heart rate and blood potassium levels. No serious adverse events occurred and no subjects withdrew from the study due to adverse events. The most common adverse event reported was headache. (19) Coadministration of orally inhaled fluticasone (1000 mcg) and ketoconazole (200 mg once daily) resulted in a 1.9-fold increase in plasma fluticasone exposure and a 45% decrease in plasma cortisol AUC.(20) There is a case report of Cushing syndrome following the addition of voriconazole (200 mg twice daily for 21 days for 2 courses) to budesonide,(21) as well as voriconazole added to intranasal mometasone(22) and inhaled fluticasone.(22) There is a case report of Cushing syndrome following the addition of posaconazole (200 mg three times daily) to inhaled fluticasone.(23)	ITRACONAZOLE, ITRACONAZOLE MICRONIZED, KETOCONAZOLE, NOXAFIL, POSACONAZOLE, SPORANOX, TOLSURA, VFEND, VFEND IV, VORICONAZOLE
Erlotinib/Corticosteroids SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: The exact mechanism is unknown. CLINICAL EFFECTS: Concurrent use of corticosteroids may increase the risk of gastrointestinal perforation in patients receiving erlotinib. Fatalities have been reported.(1) PREDISPOSING FACTORS: Patients with a history of peptic ulceration or diverticular disease or who are receiving concomitant anti-angiogenic, NSAIDs, and/or taxane-based chemotherapy may be an increased risk of gastrointestinal perforation.(1) PATIENT MANAGEMENT: Monitor patients receiving concurrent therapy for signs of gastrointestinal perforation. Discontinue erlotinib in patients who develop gastrointestinal perforation.(1) DISCUSSION: In a phase II trial of concurrent bevacizumab plus erlotinib, 2 of 13 patients suffered fatal gastrointestinal perforations.(2) In another phase II trial of concurrent bevacizumab with erlotinib, 1 of 104 patients died of gastrointestinal perforation.(3) Two patients developed gastrointestinal perforations while taking erlotinib, corticosteroids, and ciprofloxacin.(3)	ERLOTINIB HCL, TARCEVA
Gallium Ga 68 Dotatate/Corticosteroids SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: High-dose corticosteroids may down-regulate somatostatin subtype 2 receptors, the main binding site for gallium Ga 68 dotatate.(1) CLINICAL EFFECTS: Repeated use of high doses of corticosteroids before use of gallium Ga 68 dotatate may result in false negative imaging results.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: In patients receiving high-dose corticosteroids prior to use of gallium Ga 68 dotatate, interpret imaging results with caution and in the context of the patient's clinical presentation. DISCUSSION: Repeated use of high doses of corticosteroids before use of gallium Ga 68 dotatate may result in false negative imaging results due to down-regulation of the somatostatin subtype 2 receptor.(1)	GALLIUM GA-68 DOTATOC, NETSPOT
Selected Corticosteroids/Levoketoconazole SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Levoketoconazole may inhibit the CYP3A4 mediated metabolism of some corticosteroids, resulting in increased systemic exposure. Levoketoconazole may also suppress endogenous cortisol output. Levoketoconazole is the enantiomer of ketoconazole. CLINICAL EFFECTS: Concurrent use of levoketoconazole may result in elevated levels of and effects from the corticosteroid, including Cushing syndrome. These effects have been seen with systemic as well as inhaled corticosteroids. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Patients should be carefully monitored with concurrent administration of these agents, or when levoketoconazole is added to corticosteroid therapy. The dose of the corticosteroid may need to be adjusted or alternative therapy considered. DISCUSSION: The concurrent use of ketoconazole has been shown to increase budesonide area-under-curve (AUC) by eight-fold. In a study in eight healthy subjects, the simultaneous administration of ketoconazole increased budesonide AUC by 6.5-fold. Administering the two agents 12 hours apart increased budesonide AUC by 3.8-fold. In a study in 6 healthy subjects, pretreatment with ketoconazole (200 mg daily) increased the AUC of a single intravenous dose of methylprednisolone (20 mg) by 135% and decreased its clearance by 60%. Concurrent ketoconazole also increased the reduction in 24-hour cortisol AUC and suppressed morning cortisol concentrations. In a study in 8 healthy subjects, ketoconazole decreased the clearance of methylprednisolone by 46% and increased mean residence time by 37%. In a randomized, cross-over study in 6 healthy subjects, pretreatment with ketoconazole (200 mg daily for 6 days) had no effect on the pharmacokinetics of a single intravenous dose of prednisolone (14.8 mg). In a study, concurrent oral ketoconazole increased the AUC of des-ciclesonide from orally inhaled ciclesonide by 3.6-fold. There were no changes in ciclesonide levels. In a study in 24 healthy subjects, subjects were randomized to receive either ketoconazole (200 mg BID) or placebo on Days 4-9 of a a 9 day course of mometasone (400 mcg BID). No subject had mometasone levels greater than 150 pcg/ml on Day 3. Four of 12 subjects who received ketoconazole had mometasone Cmax levels greater than 200 mcg/ml on Day 9. Plasma cortisol levels appeared to decrease as well. In a cross-over study in 15 healthy subjects, subjects were randomized to receive fluticasone furoate and vilanterol on days 5-11 with either ketoconazole (200mg once daily) or placebo for days 1-11 with a washout period of 7-14 days. Fluticasone furoate AUC was increased by 36%, Cmax was increased by 33%, and decreased systemic cortisol levels by 27%. There were no effects on heart rate and blood potassium levels. There was a small increase in QTc which was 7.6ms greater when compared to placebo; however, ketoconazole has been reported to increase QTc by 5-6ms. Vilanterol AUC was increased by 65% and Cmax was increased by 22%. There were no effects on heart rate and blood potassium levels. No serious adverse events occurred and no subjects withdrew from the study due to adverse events. The most common adverse event reported was headache. Coadministration of orally inhaled fluticasone (1000 mcg) and ketoconazole (200 mg once daily) resulted in a 1.9-fold increase in plasma fluticasone exposure and a 45% decrease in plasma cortisol AUC.	RECORLEV
Systemic Corticosteroids; Corticotropin/Non-Live or Non-Replicating Vaccines SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Corticosteroids and corticotropin suppress the immune system and may alter the immune system's response to vaccines.(1) CLINICAL EFFECTS: Vaccines administered during or within 2 weeks prior to therapy with corticosteroids or corticotropin may result in decreased effectiveness of the vaccine.(1) PREDISPOSING FACTORS: Patients receiving immunosuppressive doses of corticosteroids or corticotropin for equal to or greater than 14 consecutive days.(1) PATIENT MANAGEMENT: The Centers for Disease Control's (CDC) Advisory Committee on Immunization Practices (ACIP) states that non-live vaccines should be used with caution in patients who are severely immunosuppressed, including those who are receiving or have received high-dose, systemic steroids for greater than or equal to 14 consecutive days. When initiating immunosuppressives doses of corticosteroids, wait 2 weeks after a non-live vaccines is administered. However, if patients require therapy for chronic inflammatory conditions, do not delay therapy due to past vaccines.(1) The immune response to non-live vaccines should be monitored in patients receiving corticosteroids. Vaccinations given during corticosteroid therapy may need to be repeated.(1) Patients who are vaccinated within the 14 days prior to initiating immunosuppressive therapy should be considered unvaccinated and should be revaccinated at least 3 months after immunosuppressive therapy is discontinued when immune competence is restored.(1) DISCUSSION: Vaccinations given during and within 2 weeks prior to corticosteroid therapy may be less effective. However they are considered safe to administer.(1) Many clinicians consider a dose equivalent to either 2 mg/kg of body weight or a total of 20 mg/day of prednisone as sufficiently immunosuppressive to raise safety concerns about live-virus vaccines.(1) Immunization procedures may be undertaken in patients receiving corticosteroids when the therapy is short term (less than 2 weeks); low to moderate dose; long-term, alternate-day treatment with short-acting preparations; maintenance physiologic doses (replacement therapy); or administered topically (skin or eyes), by aerosol, or by intra-articular, bursal, or tendon injection.(1)	ACTHIB, ADACEL TDAP, AREXVY, AREXVY ANTIGEN COMPONENT, BEXSERO, BIOTHRAX, BOOSTRIX TDAP, CAPVAXIVE, COMIRNATY 2024-2025, CYFENDUS (NATIONAL STOCKPILE), DAPTACEL DTAP, ENGERIX-B ADULT, ENGERIX-B PEDIATRIC-ADOLESCENT, GARDASIL 9, HAVRIX, HEPLISAV-B, HIBERIX, IMOVAX RABIES VACCINE, INFANRIX DTAP, IPOL, IXIARO, JYNNEOS, JYNNEOS (NATIONAL STOCKPILE), KINRIX, MENQUADFI, MENVEO A-C-Y-W-135-DIP, MENVEO MENA COMPONENT, MENVEO MENCYW-135 COMPONENT, MODERNA COVID 24-25(6M-11Y)EUA, MRESVIA, NOVAVAX COVID 2024-2025 (EUA), PEDIARIX, PEDVAXHIB, PENBRAYA, PENBRAYA MENACWY COMPONENT, PENBRAYA MENB COMPONENT, PENTACEL, PENTACEL ACTHIB COMPONENT, PENTACEL DTAP-IPV COMPONENT, PFIZER COVID 2024-25(5-11Y)EUA, PFIZER COVID 2024-25(6M-4Y)EUA, PNEUMOVAX 23, PREVNAR 20, QUADRACEL DTAP-IPV, RABAVERT, RECOMBIVAX HB, SHINGRIX, SHINGRIX GE ANTIGEN COMPONENT, SPIKEVAX 2024-2025, TDVAX, TENIVAC, TICOVAC, TRUMENBA, TWINRIX, TYPHIM VI, VAQTA, VAXELIS, VAXNEUVANCE, VIMKUNYA
Capivasertib/Corticosteroids SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Capivasertib may cause severe hyperglycemia. Corticosteroids also cause hyperglycemia.(1) CLINICAL EFFECTS: Concurrent use of capivasertib with corticosteroids may cause severe hyperglycemia.(1) PREDISPOSING FACTORS: Patients with a medical history of diabetes mellitus and in patients with risk factors for hyperglycemia, such as obesity (BMI >= 30), elevated fasting glucose of > 160 mg/dL, HbA1c at or above the upper limit of normal, or intercurrent infections, may be at increased risk for hyperglycemia.(1) PATIENT MANAGEMENT: The US manufacturer of capivasertib recommends monitoring fasting blood glucose more frequently in patients on concomitant systemic corticosteroids.(1) If hyperglycemia occurs after starting capivasertib, monitor fasting glucose as clinically indicated and at least twice weekly until fasting glucose returns to normal.(1) DISCUSSION: Because capivasertib has been associated with severe hyperglycemia, fasting blood glucose should be monitored closely during the concurrent use of corticosteroids with capivasertib therapy.(1) In clinical studies, hyperglycemia occurred in 18% of patients treated with capivasertib. Grade 3 (insulin therapy initiated; hospitalization indicated) or Grade 4 (life-threatening consequences; urgent intervention indicated) hyperglycemia occurred in 2.8% of patients. Diabetic ketoacidosis occurred in 0.3% of patients and diabetic metabolic decompensation in 0.6% of patients. Dose reduction for hyperglycemia was required in 0.6% of patients and permanent discontinuation was required in 0.6% of patients. The median time to first occurrence of hyperglycemia was 15 days (range: 1 to 367).(1) In the 65 patients with hyperglycemia, 45% required treatment with anti-hyperglycemic medication (insulin in 15%, and metformin in 29%). Of the 29 patients who required anti-hyperglycemic medication during treatment with capivasertib, 66% (19/29) remained on these medications at treatment discontinuation or last follow up.(1)	TRUQAP

The following contraindication information is available for PROCTOCORT (hydrocortisone):

Overview
Contraindicated
Severe
Moderate

Drug contraindication overview.

No enhanced Contraindications information available for this drug.

There are 0 contraindications.

There are 7 severe contraindications. Adequate patient monitoring is recommended for safer drug use.

Severe List
Active tuberculosis
Diabetes mellitus
Fungal infection
Infection
Intestinal anastomosis
Ocular herpes simplex
Ocular hypertension

There are 15 moderate contraindications. Clinically significant contraindication, where the condition can be managed or treated before the drug may be given safely.

Moderate List
Chronic heart failure
Diverticulitis of gastrointestinal tract
Gastrointestinal fistula
Herpes simplex infection
Hypertension
Hyperthyroidism
Hypothalamic-pituitary insufficiency
Hypothyroidism
Intestinal abscess
Kidney disease with reduction in glomerular filtration rate (GFr)
Measles
Open angle glaucoma
Osteoporosis
Psychotic disorder
Varicella zoster virus infection

The following adverse reaction information is available for PROCTOCORT (hydrocortisone):

Overview
Severe
Less Severe

Adverse reaction overview.

No enhanced Common Adverse Effects information available for this drug.

There are 45 severe adverse reactions.

More Frequent	Less Frequent
Infection	Adrenocortical insufficiency Folliculitis Hypercortisolism Purpura Skin and skin structure infection Skin atrophy

Rare/Very Rare
Abdominal distension Abnormal hepatic function tests Acute cognitive impairment Adrenocortical insufficiency Anaphylaxis Body fluid retention Bradycardia Bullous dermatitis Cataracts Central serous chorioretinopathy Chronic heart failure Delirium Drug-induced psychosis Dyspnea Excitement Gastrointestinal hemorrhage Glaucoma Glycosuria Hallucinations Hepatomegaly Hyperglycemia Hypertension Hypothalamic-pituitary insufficiency Idiopathic intracranial hypertension Impaired wound healing Intestinal perforation Myopathy Ocular hypertension Osteoporosis Paranoid disorder Peptic ulcer Personality disorders Pulmonary edema Skin hypopigmentation Skin striae Skin ulcer Thromboembolic disorder Urticaria

Rare/Very Rare

Abdominal distension
Abnormal hepatic function tests
Acute cognitive impairment
Adrenocortical insufficiency
Anaphylaxis
Body fluid retention
Bradycardia
Bullous dermatitis
Cataracts
Central serous chorioretinopathy
Chronic heart failure
Delirium
Drug-induced psychosis
Dyspnea
Excitement
Gastrointestinal hemorrhage
Glaucoma
Glycosuria
Hallucinations
Hepatomegaly
Hyperglycemia
Hypertension
Hypothalamic-pituitary insufficiency
Idiopathic intracranial hypertension
Impaired wound healing
Intestinal perforation
Myopathy
Ocular hypertension
Osteoporosis
Paranoid disorder
Peptic ulcer
Personality disorders
Pulmonary edema
Skin hypopigmentation
Skin striae
Skin ulcer
Thromboembolic disorder
Urticaria

There are 42 less severe adverse reactions.

More Frequent	Less Frequent
Erythema Increased appetite Stinging of skin	Acute pain at drug application site Blurred vision Headache disorder Irregular menstrual periods Nausea Paresthesia Pruritus of skin Skin rash Telangiectasia Treatment site sequelae

Rare/Very Rare
Acne vulgaris Acneiform eruption Allergic dermatitis Alopecia Blistering skin Contact dermatitis Depression Dizziness Dry skin Dyschromia Euphoria Exophthalmos Flushing Glycosuria Hirsutism Hypercortisolism Hyperesthesia Hyperglycemia Insomnia Lipodystrophy Miliaria Mood changes Nervousness Perioral dermatitis Rectal irritation Skin irritation Skin rash Sleep disorder Urticaria

The following precautions are available for PROCTOCORT (hydrocortisone):

Pediatric
Pregnant
Lactation
Geriatric

No enhanced Pediatric Use information available for this drug.

Contraindicated

None

Severe Precaution

None

Management or Monitoring Precaution

None

No enhanced Pregnancy information available for this drug.

No enhanced Lactation information available for this drug.

No enhanced Geriatric Use information available for this drug.

The following icd codes are available for PROCTOCORT (hydrocortisone)'s list of indications:

Allergic dermatitis
L20	Atopic dermatitis
L20.0	Besnier's prurigo
L20.8	Other atopic dermatitis
L20.81	Atopic neurodermatitis
L20.82	Flexural eczema
L20.83	Infantile (acute) (chronic) eczema
L20.84	Intrinsic (allergic) eczema
L20.89	Other atopic dermatitis
L20.9	Atopic dermatitis, unspecified
L23	Allergic contact dermatitis
L23.0	Allergic contact dermatitis due to metals
L23.1	Allergic contact dermatitis due to adhesives
L23.2	Allergic contact dermatitis due to cosmetics
L23.3	Allergic contact dermatitis due to drugs in contact with skin
L23.4	Allergic contact dermatitis due to dyes
L23.5	Allergic contact dermatitis due to other chemical products
L23.6	Allergic contact dermatitis due to food in contact with the skin
L23.7	Allergic contact dermatitis due to plants, except food
L23.8	Allergic contact dermatitis due to other agents
L23.81	Allergic contact dermatitis due to animal (cat) (dog) dander
L23.89	Allergic contact dermatitis due to other agents
L23.9	Allergic contact dermatitis, unspecified cause
Atopic dermatitis
L20	Atopic dermatitis
L20.0	Besnier's prurigo
L20.8	Other atopic dermatitis
L20.81	Atopic neurodermatitis
L20.82	Flexural eczema
L20.84	Intrinsic (allergic) eczema
L20.89	Other atopic dermatitis
L20.9	Atopic dermatitis, unspecified
Contact dermatitis
L23	Allergic contact dermatitis
L23.0	Allergic contact dermatitis due to metals
L23.1	Allergic contact dermatitis due to adhesives
L23.2	Allergic contact dermatitis due to cosmetics
L23.3	Allergic contact dermatitis due to drugs in contact with skin
L23.4	Allergic contact dermatitis due to dyes
L23.5	Allergic contact dermatitis due to other chemical products
L23.6	Allergic contact dermatitis due to food in contact with the skin
L23.7	Allergic contact dermatitis due to plants, except food
L23.8	Allergic contact dermatitis due to other agents
L23.81	Allergic contact dermatitis due to animal (cat) (dog) dander
L23.89	Allergic contact dermatitis due to other agents
L23.9	Allergic contact dermatitis, unspecified cause
L24	Irritant contact dermatitis
L24.0	Irritant contact dermatitis due to detergents
L24.1	Irritant contact dermatitis due to oils and greases
L24.2	Irritant contact dermatitis due to solvents
L24.3	Irritant contact dermatitis due to cosmetics
L24.4	Irritant contact dermatitis due to drugs in contact with skin
L24.5	Irritant contact dermatitis due to other chemical products
L24.6	Irritant contact dermatitis due to food in contact with skin
L24.7	Irritant contact dermatitis due to plants, except food
L24.8	Irritant contact dermatitis due to other agents
L24.81	Irritant contact dermatitis due to metals
L24.89	Irritant contact dermatitis due to other agents
L24.9	Irritant contact dermatitis, unspecified cause
L24.A0	Irritant contact dermatitis due to friction or contact with body fluids, unspecified
L24.A1	Irritant contact dermatitis due to saliva
L24.A2	Irritant contact dermatitis due to fecal, urinary or dual incontinence
L24.A9	Irritant contact dermatitis due friction or contact with other specified body fluids
L24.B	Irritant contact dermatitis related to stoma or fistula
L24.B0	Irritant contact dermatitis related to unspecified stoma or fistula
L24.B1	Irritant contact dermatitis related to digestive stoma or fistula
L24.B2	Irritant contact dermatitis related to respiratory stoma or fistula
L24.B3	Irritant contact dermatitis related to fecal or urinary stoma or fistula
L25	Unspecified contact dermatitis
L25.0	Unspecified contact dermatitis due to cosmetics
L25.1	Unspecified contact dermatitis due to drugs in contact with skin
L25.2	Unspecified contact dermatitis due to dyes
L25.3	Unspecified contact dermatitis due to other chemical products
L25.4	Unspecified contact dermatitis due to food in contact with skin
L25.5	Unspecified contact dermatitis due to plants, except food
L25.8	Unspecified contact dermatitis due to other agents
L25.9	Unspecified contact dermatitis, unspecified cause
Cutaneous t-cell lymphoma
C84.0	Mycosis fungoides
C84.A	Cutaneous t-cell lymphoma, unspecified
C84.A0	Cutaneous t-cell lymphoma, unspecified, unspecified site
C84.A1	Cutaneous t-cell lymphoma, unspecified lymph nodes of head, face, and neck
C84.A2	Cutaneous t-cell lymphoma, unspecified, intrathoracic lymph nodes
C84.A3	Cutaneous t-cell lymphoma, unspecified, intra-abdominal lymph nodes
C84.A4	Cutaneous t-cell lymphoma, unspecified, lymph nodes of axilla and upper limb
C84.A5	Cutaneous t-cell lymphoma, unspecified, lymph nodes of inguinal region and lower limb
C84.A6	Cutaneous t-cell lymphoma, unspecified, intrapelvic lymph nodes
C84.A7	Cutaneous t-cell lymphoma, unspecified, spleen
C84.A8	Cutaneous t-cell lymphoma, unspecified, lymph nodes of multiple sites
C84.A9	Cutaneous t-cell lymphoma, unspecified, extranodal and solid organ sites
Discoid lupus erythematosus
H01.12	Discoid lupus erythematosus of eyelid
H01.121	Discoid lupus erythematosus of right upper eyelid
H01.122	Discoid lupus erythematosus of right lower eyelid
H01.123	Discoid lupus erythematosus of right eye, unspecified eyelid
H01.124	Discoid lupus erythematosus of left upper eyelid
H01.125	Discoid lupus erythematosus of left lower eyelid
H01.126	Discoid lupus erythematosus of left eye, unspecified eyelid
H01.129	Discoid lupus erythematosus of unspecified eye, unspecified eyelid
L93.0	Discoid lupus erythematosus
Genital organ pruritus
L29.2	Pruritus vulvae
L29.3	Anogenital pruritus, unspecified
Granuloma annulare
L92.0	Granuloma annulare
Hemorrhoids
K64.0	First degree hemorrhoids
K64.8	Other hemorrhoids
K64.9	Unspecified hemorrhoids
O22.4	Hemorrhoids in pregnancy
O22.40	Hemorrhoids in pregnancy, unspecified trimester
O22.41	Hemorrhoids in pregnancy, first trimester
O22.42	Hemorrhoids in pregnancy, second trimester
O22.43	Hemorrhoids in pregnancy, third trimester
O87.2	Hemorrhoids in the puerperium
Lichen simplex chronicus
L28.0	Lichen simplex chronicus
Plaque psoriasis
L40.0	Psoriasis vulgaris
L40.9	Psoriasis, unspecified
Proctitis
K62.7	Radiation proctitis
K62.89	Other specified diseases of anus and rectum
Pruritus ani
L29.0	Pruritus ani
L29.3	Anogenital pruritus, unspecified
Pruritus of skin
L29.8	Other pruritus
L29.81	Cholestatic pruritus
L29.89	Other pruritus
L29.9	Pruritus, unspecified
Pyoderma gangrenosum
L88	Pyoderma gangrenosum
Scalp psoriasis
L40.0	Psoriasis vulgaris
L40.1	Generalized pustular psoriasis
L40.4	Guttate psoriasis
L40.8	Other psoriasis
L40.9	Psoriasis, unspecified
Seborrheic dermatitis
L21	Seborrheic dermatitis
L21.0	Seborrhea capitis
L21.1	Seborrheic infantile dermatitis
L21.8	Other seborrheic dermatitis
L21.9	Seborrheic dermatitis, unspecified
Skin inflammation
L20	Atopic dermatitis
L20.8	Other atopic dermatitis
L20.89	Other atopic dermatitis
L20.9	Atopic dermatitis, unspecified
L21	Seborrheic dermatitis
L21.8	Other seborrheic dermatitis
L21.9	Seborrheic dermatitis, unspecified
L25	Unspecified contact dermatitis
L30.8	Other specified dermatitis
L30.9	Dermatitis, unspecified
L40	Psoriasis
L40.1	Generalized pustular psoriasis
L40.8	Other psoriasis
L40.9	Psoriasis, unspecified
R21	Rash and other nonspecific skin eruption