A Woman with Normotensive Primary Hyperaldosteronism.

Normotensive hyperaldosteronism is a rare disorder. It is usually diagnosed with hypokalemia or an adrenal mass. Our patient was a 27-year-old female presented with weakness. She had normal blood pressure, hypokalemia, high plasma aldosterone level and suppressed plasma renin activity. After the saline load, test aldosterone didn't show suppression. Adrenal computed tomography revealed a left adrenal mass. The patient was treated with spironolactone and potassium supplement. Surgical adrenalectomy was done. Final pathologic diagnosis was benign adrenocortical adenoma without capsular invasion. In postoperative course serum, potassium was normal.

An ectopic adreocortical adenoma of the renal sinus: a case report and literature review.

BACKGROUND: Ectopic adrenal tumors are very rare, especially in the renal sinus in adults. An unusual case of ectopic adrenal cortical adenoma in the right renal sinus is reported here. CASE PRESENTATION: This patient was a 37-year-old woman. She was admitted to our hospital for hypertension and bilateral limb weakness. Computed tomography (CT) revealed a mass in right renal sinus. It was initially considered a tumor of the renal pelvis. Further computed tomographic angiography (CTA) showed the mass to be located outside the renal pelvis. After adequate preoperative preparation (blood pressure control and serum potassium supplement), the patient underwent laparoscopic resection of retroperitoneal tumor. During the procedure, a soft tissue tumor 3.4*3.0 cm(2) in size with a golden color was found in the right renal sinus. The final immunohistochemistry examination showed an ectopic adreocortical adenoma. CONCLUSION: Ectopic adrenal tumors are rare in the renal sinus and difficult to diagnose and treat. Large and functional tumors should be treated with complete resection. The procedure is sometimes difficult for tumors located deep in the renal sinus. The decision to perform an open or minimally invasive surgery should be made according to the surgeon's experience.

Hipertensión e hipopotasemia en una mujer de 49 años / Hypertension and hypokalemia in a 49-year old woman

La hipertensión arterial secundaria a hiperaldosteronismo primario es poco frecuente,pero es una enfermedad curable, por lo que nos parece interesante presentar un caso.Se trata de una paciente que inicia un cuadro de hipertensión arterial severa y que recibetratamiento con diuréticos y fármacos inhibidores de la enzima de conversión deangiotensina (IECA) antes de ser hospitalizada. Cuando la vemos presenta hipopotasemia.A pesar de los suplementos de potasio y de retirar el tratamiento diurético y los IECA,persistía la hipocaliemia, por lo que se inició estudio de hipertensión arterial secundaria.Las concentraciones de renina estaban suprimidos con elevación de la aldosterona. Serealizó una tomografía abdominal que mostró la presencia de un tumor bien delimitadoen suprarrenal izquierda, compatible con síndrome de Conn. Tras el hallazgo se resecó eltumor por vía laparoscópica y la anatomía patológica fue de adenoma suprarrenal. Posteriormente,las cifras de potasio y presión arterial se han normalizado sin tratamiento.Nos parece importante resaltar los datos que apoyan el probable origen secundario de lahipertensión arterial, no sólo para iniciar el estudio, sino también para ajustar el tratamientoinicial, evitando los fármacos que interfieran con la evaluación, siempre que elcontrol de la presión arterial lo permita.

Primary aldosteronism resulting from an adrenocortical adenoma is an uncommon butpotentially curable form of hypertension. We present the case of a 49-year-old womanthat initiated with severe hypertension that was treated with diuretics and ACE inhibitorsbefore being hospitalized. When she came to consult, she had hypokalemia. This persistedin spite of administering potassium supplements and discontinuing the diuretics and ACE secuninhibitors.Therefore, a study was made regarding secondary arterial hypertension.Plasma renin activity was suppressed and aldosterone levels were elevated. Computedtomographic scanning detected a well-delimitated mass in left adrenal gland, suggestingConn’s syndrome. Laparoscopic adrenalectomy was performed and microscopy findingswere consistent with aldosteronoma. After surgery hypertension was resolved andpotassium levels remained normal.We consider that the data supporting the probable presence of secondary hypertensionshould be stressed, not only to perform studies but also to adjust the initial treatment,avoiding drugs that interfere with the evaluation, whenever blood pressure control allows it(AU)

Symptomatic hypercalcemia due to painless thyroiditis after unilateral adrenalectomy in a patient with Cushing's syndrome.

We report a 53-year-old woman with Cushing's syndrome due to an adrenocortical adenoma, who underwent unilateral adrenalectomy and developed symptomatic hypercalcemia during the thyrotoxic period of painless thyroiditis, while tapering off a daily supplemented dose of cortisol. A study of patients with thyrotoxicosis and hypoadrenalism at our institute revealed that mild hypercalcemia was present in 9.9% of those with thyrotoxicosis and 5.0% of those with hypoadrenalism. The present case suggests that the simultaneous occurrence of thyrotoxicosis and hypoadrenalism may lead to overt hypercalcemia due to a synergistic increase in bone resorption and impaired urinary excretion of calcium.

Unilateral adrenalectomy improves insulin resistance and polycystic ovaries in a middle-aged woman with virilizing adrenocortical adenoma complicated with Cushing's syndrome.

A benign virilizing adrenal adenoma is rare among adrenal neoplasms in middle-aged women. A 39-yr-old Japanese woman who presented with hirsutism, obesity, diabetes mellitus and hypertension was admitted. Plasma concentrations of testosterone and DHEAS were high. While the basal level of plasma ACTH was suppressed, serum cortisol level was high and its circadian rhythm was absent. Serum cortisol level was not suppressed with the low- and high-dose overnight dexamethasone suppression test. Abdominal computed tomography showed a left adrenal tumor, and an adrenocortical scintigraphy revealed uptake of the tracer on the left side. Polycystic ovaries were also found and bone mineral density revealed osteoporosis. Histopathological features of resected adrenal tumor were consistent with those of adrenocortical adenoma. Immunoreactivity of all the steroidogenic enzymes was apparent in the tumor cells and particularly dehydroepiandrosterone sulfotransferase (DHEA-ST) immunoreactivity was markedly expressed. Cortical atrophy and reduced expression of DHEA-ST were detected in the cortex of the adjacent non-neoplastic adrenal gland. Plasma testosterone, DHEAS and cortisol levels returned to normal after surgery, concomitantly with the disappearance of polycystic ovaries. This is a very rare case of virilizing adrenocortical adenoma complicated with Cushing's syndrome (CS).

Adrenocortical adenoma associated with inadequately treated congenital adrenal hyperplasia.

We report a 6 year-old boy with the simple virilizing form of 21-hydroxylase deficiency in whom an adrenal adenoma developed following 5 years of steroid treatment. Extremely high levels of basal serum 17alpha-hydroxyprogesterone as well as an exaggerated response of 17alpha-hydroxyprogesterone to adrenocorticotropic hormone confirmed congenital adrenal hyperplasia at 7 years of age. Initially elevated serum steroid levels were restrained by high dose hydrocortisone therapy, but he chronically tended to take inadequate doses of glucocorticoid. At 12 years of age an adenoma was found in the cortex of the hyperplastic right adrenal gland. The importance of early diagnosis and compliance with medication in the simple virilizing form of 21-hydroxylase deficiency is stressed.

Primary hyperaldosteronism causing posttransplantation hypertension: localization by adrenal vein sampling.

A 58 year-old man with end-stage renal disease who had received a cadaveric renal transplant presented with persistent hypertension and hypokalemia. Allograft renal artery stenosis, rejection, and cyclosporine effects were excluded. Hypokalemia persisted despite potassium supplementation and antihypertensive medications with hyperkalemic effects. The biochemical findings of primary hyperaldosteronism with a normal adrenal anatomy imaged by magnetic resonance imaging (MRI) necessitated adrenal vein sampling to lateralize a left adrenal adenoma. His hypokalemia was cured by the removal of the adenoma, and his blood pressure (BP) control was easily achieved with a less complex regimen of antihypertensives. We suggest that the concomitant existence of resistant hypokalemia and posttransplantation hypertension, especially in the cyclosporine era, should stimulate a search for hyperaldosteronism; once transplant renal artery stenosis has been excluded, the patient should be investigated for primary hyperaldosteronism. When imaging studies fail to show adrenal pathology, adrenal vein sampling will likely do so.