A case was reported of a 47-year-old HIV positive woman treated with raltegravir, emtricitabine, atazanavir and ritonavir who presented after a weight gain of 20 kg in six months. She had been prescribed a combination budesonide/formoterol inhaler (160/4.5 µg/act). On examination she had a rounded face, a dorsocervical fat pad and proximal muscle weakness. She was diagnosed with iatrogenic Cushing’s syndrome. Budesonide was stopped, and her cushingoid appearance resolved and cortisol and ACTH returned to normal range. The authors hypothesise a drug-drug interaction occurred via inhibition of CYP3A4 by ritonavir.

A case report describes a 75-year-old man with a history of HIV for 27 years, hepatitis C, hypothyroidism, recurrent deep venous thrombosis, hypertension, and chronic kidney disease was admitted for treatment of worsening chronic diarrhoea and bright red blood per rectum. His antiretroviral regimen was atazanavir/ritonavir (300/100 mg daily), lamivudine (150 mg daily) and nevirapine (300 mg twice daily). Other medications included atenolol, atropine/diphenoxylate, calcitriol, cholecalciferol, fondaparinux, levothyroxine, lisinopril, loperamide, ranitidine, testosterone patch, trazodone, and vardenafil.  Colonoscopy showed lymphocytic colitis at multiple biopsy sites and oral budesonide (3 mg 3 times a day) was started. The patient's diarrhoea improved, but he was admitted 12 days later with 10.4 kg weight gain, severe leg and facial swelling, and uncontrolled hypertension.  Physical examination was notable for blood pressure 177/102 mm Hg, Cushingoid facies, and 2+ pedal and pretibial edema to the knees.  As the colitis had improved dramatically with budesonide therapy, the plan was to continue it for a full 6-week treatment course, if possible. Amlodipine, hydralazine, and furosemide were added to control the hypertension and edema, but budesonide was discontinued after 3 weeks because of persistent severe edema that was refractory to furosemide. The patient developed edema, weight gain, uncontrolled hypertension,  Cushingoid facies, hypokalemia, and metabolic alkalosis shortly after initiation of budenoside, with resolution of all symptoms soon after it was stopped.  Congestive heart failure, liver disease, and nephrotic syndrome were ruled out as causes of the edema, which supported the diagnosis of iatrogenic Cushing's syndrome. Although budesonide concentrations were not measured, the very low serum cortisol level (0.8 µg/dL) in a clinical setting of hypercortisolism provides strong indirect evidence that levels of an exogenous corticosteroid (i.e., budesonide) were high.