Apparent Mineralocorticoid Excess in a Case of Lung Paraneoplastic Cushing Syndrome

نویسندگان

  • C. Badiu
  • Cristina Capatana
  • D. Cristofor
  • G. Mircescu
  • M. Coculescu
چکیده

Severe hypokalemia is a life threatening event, which triggers a number of therapeutic and diagnostic attitudes. In this paper we present a case of 63 years old man, who presented with progressive lassitude, edema, weight loss. The mild hypertension and hyperglycaemia were treated with spironolactone and diet. Initial evaluation showed severe hypokalemia (1.7 mmol/l), hepatomegalia, hyperplasic/nodular adrenal masses; in addition, he has developed a right middle lobe pneumonia which improved with antibiotics. Referred for the suspicion of hyperaldosteronism, aldosterone values were normal (9.3-9.5 μg/dl), but ACTH was high (725 pg/ml) and did not suppress (710.8 pg/ml) to high dose DXM, as well as cortisol: basal values 27.78 ug/dl, high dose DXM 35.06 ug/dl, showing an ACTH dependent Cushing syndrome despite lack of suggestive clinical signs. Tumor markers suggested a neuroendocrine neoplasia: carcinoembryonic antigen=101 ng/ml (normal values=0.52-6.3 ng/ml), CA 19-9= 155 ng/ml (N < 33 ng/ml). Further radiological evaluation showed a 3 cm right lobe lung tumour. Despite high potassium supplements and spironolactone, the hypokalemia remained around 3.2 mmol/l, characteristic for an apparent mineralocorticoid excess. Because of aggressive evolution of the lung tumour, he died three months after the initial admission into the hospital. Pathology report showed a lung carcinoma. ACTH immunostaining of the lung tumour was positive and revealed a paraneoplastic secretion.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

APPARENT MINERALOCORTICOID EXCESS IN THREE SIBLINGS

Three siblings (1 boy, 2 girls) with hypertension and hypokalemia are presented, two with low plasma aldosterone and suppressed renin activity and the eldest with a high renin and aldosterone level due to secondary changes in her kidneys. Urinary tetrahydrocortisol (THF) was increased relative to tetrahydrocortisone (THE). Cortisol ring A reduction constant was also lower than normal. Thes...

متن کامل

Cushing’s syndrome associated with typical, peripheral pulmonary carcinoid tumor and N2 lymph node metastasis: case report

Background: The bronchopulmonary carcinoid tumor accounts for 1-2% of all adult malignancies of the lung and 20-30% of all carcinoid tumors. Cushing’s syndrome is the result of chronic exposure to increased concentration of exogenous or endo-genus cortisol hormone, and it is generally associated with central obesity, metabolic syndrome, and hypertension. Treatment is based on decreasing cortiso...

متن کامل

Case-series of paraneoplastic Cushing syndrome in small-cell lung cancer

The objective of this study is to report three cases of paraneoplastic or ectopic Cushing syndrome, which is a rare phenomenon of the adrenocorticotropic hormone (ACTH)-dependent Cushing syndrome. Three cases are reported in respect of clinical presentation, diagnosis and treatment in addition to relevant literature review. The results showed that ectopic ACTH secretion can be associated with d...

متن کامل

Superior Vena Cava Syndrome due to Thrombosis: A Rare Paraneoplastic Presentation of Bronchogenic Carcinoma

Superior vena cava (SVC) syndrome is not an uncommon occurrence in patients with malignancy and it is often described as a medical emergency. In majority of the cases, SVC syndrome occurs due to mechanical obstruction of the SVC by extraluminal compression with primary intrathoracic malignancies. However, intraluminal obstruction due to thrombosis can also produce symptoms and signs of SVC synd...

متن کامل

Apparent mineralocorticoid excess syndrome: an overview.

Apparent mineralocorticoid excess (AME) syndrome results from defective 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2). This enzyme is co-expressed with the mineralocorticoid receptor (MR) in the kidney and converts cortisol (F) to its inactive metabolite cortisone (E). Its deficiency allows the unmetabolized cortisol to bind to the MR inducing sodium retention, hypokalemia, suppressi...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2006