The Messy Truth On Thalidomide

As this drug does not induce adrenal hyperandrogenism, it could be an interesting option in women. Many cases of BMAH are incidentally discovered, with little or no cushingoid features despite markedly enlarged adrenals (1) (2), suggesting relatively inefficient cortisol secretion by the macronodular tissue, which might respond to lower doses of ketoconazole for steroid control. To our knowledge, only one case of successful treatment with ketoconazole has been reported in BMAH, during a 1-year therapy until adrenalectomy was performed, at doses that were not mentioned (10). We present a patient with BMAH without any evidence of illegitimate hormone dependence, treated successfully during 10 years with well-tolerated low doses Thalidomide of ketoconazole. Case FDA approval PARP inhibitor presentation A 48-year-old woman presented with sudden headaches and new-onset marked hypertension. She had no signs of Cushing's syndrome. She was known for familial (mother and brother) asymptomatic polycystic liver disease without kidney involvement. Abdominal ultrasound study showed normal kidneys, numerous hepatic cysts and unexpected large multi-lobulated bilateral adrenal masses, confirmed on CT-scan (Fig. 1A). Laboratory studies showed normal serum creatinine and urinary metanephrines; low-normal serum potassium (3.85mmol/l; normal range 3.50�C5.20mmol/l), normal plasma aldosterone concentration (62ng/l; 29�C76ng/l), PCI-32765 mw normal urine aldosterone (4.1��g/24h; 1.0�C10.0��g/24h) and suppressed plasma renin activity ( 10�C109��g/24h), corticosterone (THB, 509��g/24h; 26�C262��g/24h), cortisone (THE, 6877��g/24h; 727�C3815��g/24h) and cortisol (THF, 3031��g/24h; 458�C1907��g/24h); elevated urine free cortisol (349nmol/24h; 55�C248nmol/24h); normal plasma AM cortisol (309nmol/l; 200�C700nmol/l at 0800h) and slightly elevated PM cortisol (365nmol/l; 60�C300nmol/l, at 1700h), low ACTH (5ng/l; 10�C60ng/l) and suppressed DHEAS (