The metabolic alterations caused by hyperaldosteronism are being increasingly recognized and have generated considerable interest among the medical fraternity. Hyperaldosteronism is suspected to have a pivotal role in the patho-physiology of congestive cardiac failure where it has been studied extensively. But its effects on calcium metabolism, parathyroid metabolism and renal handling of calcium are less well described. Recent experimental models have shed light into the roles played by previously unknown mechanisms in causing these metabolic alterations. We hereby report a case of primary hyperaldosteronism due to adrenal adenoma (Conn's syndrome) who presented with a myriad of clinical features including symptomatic hypocalcemia, significant weight loss along with uncontrolled hypertension for a prolonged period before eventually detected to have primary hyperaldosteronism. Surgical removal of the causative tumor resulted in prompt disappearance of all the symptoms and signs and regain of lost weight.
Adrenal Cortex Neoplasms/*complications/diagnosis/pathology/surgery ; Adrenocortical Adenoma/*complications/diagnosis/pathology/surgery ; Adult ; Female ; Humans ; *Hyperaldosteronism/complications/etiology/physiopathology ; Hypocalcemia/*etiology ; Pregnancy ; Treatment Outcome

We describe here the case of a 39-year-old woman with a cortisol-producing adrenal adenoma and she presented with endometrial hyperplasia and hypertension without the specific characteristics of Cushing's syndrome. The patient had consulted a gynecologist for menometrorrhagia 2 years prior to her referral and she was diagnosed with endometrial hyperplasia and hypertension. Her blood pressure and the endometrial lesion were refractory despite taking multiple antihypertensives and repetitive dilation and curettage and progestin treatment. On admission, the clinical examination revealed mild central obesity (a body mass index of 22.9 kg/m2, a waist circumference of 85 cm and a hip circumference of 94cm), but there was no hirsutism and myopathy. She showed impaired glucose tolerance on an oral glucose tolerance test. The biochemical hypercortisolemia together with the prolactin and androgen levels were evaluated to explore the cause of her anovulation. Adrenal Cushing's syndrome was confirmed on the basis of the elevated urinary free cortisol (454 microgram/24h, normal range: 20-70) with a suppressed ACTH level (2.0 pg/mL, normal range: 6.0-76.0) and the loss of circadian cortisol secretion. A CT scan revealed a 3.1 cm, hyperechoic, well-marginated mass in the left adrenal gland. Ten months post-adrenalectomy, the patient had unintentionally lost 9 kg of body weight, had regained a regular menstrual cycle and had normal thickness of her endometrium.
Adrenal Cortex Neoplasms/complications/*diagnosis/surgery ; Adrenalectomy ; Adrenocortical Adenoma/complications/*diagnosis/surgery ; Adrenocorticotropic Hormone/blood ; Adult ; Circadian Rhythm ; Cushing Syndrome/*diagnosis/etiology/physiopathology ; Diagnosis, Differential ; Endometrial Hyperplasia/*diagnosis ; Female ; Humans ; Hydrocortisone/secretion/urine

No abstract available.
Adrenal Cortex Neoplasms/*complications/diagnosis/surgery ; Adrenalectomy ; Adrenocortical Adenoma/*complications/diagnosis/surgery ; Adult ; Biopsy ; Coronary Angiography ; Drug-Eluting Stents ; Humans ; Hyperaldosteronism/diagnosis/*etiology ; Male ; Myocardial Infarction/diagnosis/*etiology/therapy ; Percutaneous Coronary Intervention/instrumentation ; Tomography, X-Ray Computed ; Treatment Outcome

OBJECTIVETo improve the diagnostic and therapeutic ability on subclinical Cushing's syndrome.

METHODSRetrospective analysis for the clinical data of 24 cases of subclinical Cushing's syndrome, the clinical and biological characters pre and post operation were compared.

RESULTSNone of the 24 cases of subclinical Cushing's syndrome had the classic symptoms and signs of Cushing's syndrome. The common symptoms of these patients were hypertension in 17 cases, diabetes mellitus in 11 cases, hyperlipidemia in 9 cases, high plasma cortisol value in 13 cases and high 24 h UFC value in 9 cases. None of patients did respond to low dose dexamethasone suppression test, but 16 cases of them did not respond to high dose dexamethasone suppression test. All the cases were found adrenal tumors by CT scan, 10 cases in left adrenal and 14 cases in right adrenal. All the patients underwent retroperitoneal laparoscopic operation and were pathologic diagnosed to adrenal adenomas. During follow-up, the symptoms of 20 cases (83.3%) were cured after surgery, and hormone supplement was required in 8 cases.

CONCLUSIONSSubclinical Cushing's syndrome may be incidentally detected on clinical manifestations, laboratory findings and imaging examinations. CT scan, assays of plasma cortisol, urinary free cortisol and dexamethasone suppression test are most useful in the diagnosis. The potential benefit of surgery should be considered in those who have a definite diagnosis of subclinical Cushing's syndrome. Hormone supplement is required in some patients. It is safe and practical to perform retroperitoneal laparoscopic surgery on the patients with subclinical Cushing's syndrome.

Adrenal Cortex Neoplasms ; complications ; surgery ; Adrenalectomy ; methods ; Adrenocortical Adenoma ; complications ; surgery ; Adult ; Cushing Syndrome ; diagnosis ; etiology ; surgery ; Female ; Follow-Up Studies ; Humans ; Laparoscopy ; Male ; Middle Aged ; Retrospective Studies ; Treatment Outcome

No abstract available.
Adrenal Cortex Function Tests ; *Adrenal Cortex Neoplasms/complications/diagnosis/metabolism/surgery ; *Adrenal Gland Neoplasms/complications/diagnosis/metabolism/surgery ; Adrenalectomy ; *Adrenocortical Adenoma/complications/diagnosis/metabolism/surgery ; Biopsy ; Cushing Syndrome/diagnosis/etiology ; Female ; Humans ; Immunohistochemistry ; *Incidental Findings ; Middle Aged ; *Neoplasms, Multiple Primary/complications/diagnosis/metabolism/surgery ; *Pheochromocytoma/complications/diagnosis/metabolism/surgery ; Predictive Value of Tests ; Tomography, X-Ray Computed ; Treatment Outcome ; Tumor Markers, Biological/metabolism