1/38. A case of severe hypertension caused by ACTH-independent macronodular adrenal hyperplasia.This report describes a rare case of ACTH-independent macronodular adrenal hyperplasia (AIMAH) arisen with symptomatic severe hypertension and hypokaliemia. A 55-year-old man was admitted to hospital with a clinical picture characterized by several episodes of transient ischemic attacks (TIA) and right hemiplegia, related to severe arterial hypertension. Laboratory tests showed urinary levels of catecholamines, metanephrines and vanillylmandelic acid (VMA) in normal range; high urinary free cortisol excretion, elevated serum cortisol with loss of the circadian rhythm and low ACTH plasma levels. ACTH failed to respond to CRH administration. serum cortisol levels were not modified after high doses of dexamethasone. MRI showed bilateral macronodular hyperplasia of adrenal glands, whereas pituitary-MRI did not show tumoral lesions. Therefore, ACTH-independent macronodular hyperplasia was suspected. Though obese, the patient had no typical Cushing habit, and symptomatic hypertension with hypokaliemia was the only clinical evidence for this rare kind of Cushing's syndrome. After obtaining a satisfactory control of blood pressure, the patient was successfully submitted to laparoscopic bilateral adrenalectomy and underwent complete clinical remission. The histology showed adrenal macronodular hyperplasia. During the twenty-four month follow-up, the patient had no further transient ischemic attacks or need of glucocorticoid replacement therapy and withdrew the antihypertensive drugs.- - - - - - - - - - ranking = 1keywords = gland (Clic here for more details about this article) |
2/38. Preclinical Cushing's syndrome due to ACTH-independent bilateral macronodular adrenocortical hyperplasia with excessive secretion of 18-hydroxydeoxycorticosterone and corticosterone.A 64-year-old woman developed hypertension and hypokalemia, due to ACTH-independent bilateral macronodular adrenocortical hyperplasia (AIMAH) with excessive secretion of 18-hydroxydeoxycorticosterone and corticosterone. plasma cortisol did not show a diurnal rhythm, and was not suppressed by dexamethasone (8 mg). plasma cortisol responded to ACTH and was increased by hypoglycemia without modifying ACTH levels. Radiological studies demonstrated that adrenal glands were enlarged with macronodules. Although the patient exhibited a low plasma renin activity and aldosterone levels, hypokalemia and hypertension were observed. Hormonal findings would support the hypothesis that the tumor of AIMAH originated from cells of the upper zona fasciculata.- - - - - - - - - - ranking = 1keywords = gland (Clic here for more details about this article) |
3/38. Hypokalemic metabolic alkalosis--three case reports.The two most common forms of inherited normotensive hypokalemic metabolic alkalosis are Bartter's and Gitelman's syndromes. Bartter's syndrome typically present with normal or increased calcium excretion. Hypomagnesemia occurs in only one third of affected individuals. In contrast, hypomagnesemia and hypocalciuria are considered hallmarks of Gitelman's syndrome. In most patients, the symptom of muscle weakness and polyuria occur early in life, which may be attributed to potassium depletion. Despite hyperaldosteronism, the patients tend to be normotensive, which is at least explained by vascular hyperresponsiveness to prostaglandins. Therapeutic approaches to Bartter's and Gitelman's syndromes include potassium supplementation, prostaglandin synthesis inhibitors (nonsteroid anti-inflammatory agents), aldosterone antagonists and converting enzyme inhibitors. Three patients with hypokalemia, normal blood pressure, metabolic alkalosis, hyperreninemia and hyperaldosteronism are described. Two patients had Bartter's syndrome and one patients had Gitelman's syndrome.- - - - - - - - - - ranking = 2keywords = gland (Clic here for more details about this article) |
4/38. respiratory paralysis in Sjogren syndrome with normal renal function.We report a 28-year-old woman who presented with quadriparesis and respiratory failure, and had severe hypokalaemia and distal renal tubular acidosis. She recovered completely on potassium and alkali supplementation. biopsy and scintigraphy of the minor salivary glands confirmed the presence of Sjogren syndrome. A 6-month course of prednisolone did not correct the distal renal tubular acidosis.- - - - - - - - - - ranking = 1keywords = gland (Clic here for more details about this article) |
5/38. Diagnosing bulimia nervosa with parotid gland swelling.BACKGROUND: The authors describe bulimia nervosa, or BN, and its effect on the parotid gland. The associated asymptomatic bilaterally enlarged parotid glands often present a diagnostic dilemma. CASE DESCRIPTION: The authors present a case of a 22-year-old woman with BN who had bilateral parotid gland swelling, serum electrolyte alteration and no dental stigmata. Her principal concern was the associated cosmetic deformity. CLINICAL IMPLICATIONS: Because patients with BN who have parotid gland swelling usually are secretive about their purging, the diagnosis may be confirmed by conducting a clinical examination and a serum electrolyte study. Prompt diagnosis can avoid serious medical complications.- - - - - - - - - - ranking = 8keywords = gland (Clic here for more details about this article) |
6/38. Primary hyperaldosteronism treated by radiofrequency ablation.This is a report of a 57-year-old Jordanian man who had uncontrolled hypertension and hypokalemia. He was diagnosed to have primary hyperaldosteronism with left adrenal adenoma. Traditionally, surgical resection of the adrenal gland whether by laparotomy or laparoscopic procedures would have been considered at this point. However, the treating team elected radiofrequency ablation of the left adrenal in view of the fact that this facility and the expertise was available in the hospital; in addition, this procedure required a shorter duration of hospitalization, was less expensive, and was less invasive. Subsequently, the patients blood pressure improved to 120/75 mm Hg and his anti-hypertensive medications were reduced. serum aldosterone and computed tomography scan of adrenals improved. We are reporting this case as it is the first time such modalities in the treatment of adrenal adenoma was used.- - - - - - - - - - ranking = 1keywords = gland (Clic here for more details about this article) |
7/38. diagnosis of adenomatous primary aldosteronism in a patient with severe hypertension.BACKGROUND: A 27-year-old woman presented to her primary-care physician with severe hypertension after complaining of fatigue over the preceding months. She was otherwise asymptomatic. She was referred to a hypertension clinic and was found to be hypokalemic. She was immediately commenced on amlodipine, with atenolol added 2 weeks later. After 4 weeks of this drug therapy, her hypertension persisted and investigations to exclude secondary causes of hypertension were performed. INVESTIGATIONS: aldosterone and renin levels were measured under controlled conditions and the results expressed as an aldosterone-to-renin ratio. CT of the adrenal glands was also performed. diagnosis: Adenomatous primary aldosteronism (Conn's syndrome). MANAGEMENT: The patient was initially treated with spironolactone before undergoing a laparoscopic left adrenalectomy.- - - - - - - - - - ranking = 1keywords = gland (Clic here for more details about this article) |
8/38. Bartter's syndrome and diabetes mellitus.We here report a case of Bartter's syndrome occurring in association with diabetes mellitus. The patient, an insulin-dependent diabetic, presented with hypokalaemia, inappropriate kaliuresis and metabolic alkalosis. He had high plasma renin activity, relatively low plasma aldosterone, and resistance to infused angiotensin ii. A high potassium diet raised total body potassium and serum potassium, did not affect plasma renin activity, but raised plasma aldosterone significantly and did not alter the resistance to angiotensin ii. indomethacin administered acutely reduced urinary potassium and kallikrein excretion and, on chronic administration, lowered plasma renin activity, urinary chloride excretion, and raised serum potassium. Salt restriction resulted in a prompt and significant reduction in urinary sodium and chloride excretion. Urinary kallikrein excretion was very high throughout, increased with sodium restriction, and decreased with sodium loading. Oral potassium supplementation partially corrected the hypokalaemia, but did not affect blood sugar control. In this patient the primary defect appears to have been primary urinary potassium wasting, rather than sodium or chloride wasting. The striking effects of indomethacin suggest that prostaglandins may play a fundamental role in the genesis of the syndrome.- - - - - - - - - - ranking = 1keywords = gland (Clic here for more details about this article) |
9/38. Normotensive glucocorticoid-suppressible hyperaldosteronism in adult.A 40 year-old man was admitted to our hospital for detailed examination of hypokalemia (2.7 mEq/l). His blood pressure was normal. Metabolic alkalosis, ACTH dependent hyperaldosteronism (18 ng/dl) and over-response to synthetic ACTH were observed. plasma renin activity, on the other hand, was within the normal range (1.7 ng/ml/hr). serum potassium was normalized to 4.1 mEq/l and the responsiveness of the renin-angiotensin-aldosterone system was recovered after the administration of dexamethasone. These results led us to suggest that this case might be normotensive glucocorticoid-suppressible hyperaldosteronism. The etiology which was not associated with hypertension and low plasma renin activity has not been clarified but may be related to the shortness of duration of this disease. Our case was also afflicted with mild hypercortisolemia and excessive excretion of urinary 17-hydroxycorticosteroid and 17-ketosteroid which was suppressed by the administration of dexamethasone (2 mg/day). These findings may be related to hypersensitivity of the fascicular zone of the adrenal gland to ACTH.- - - - - - - - - - ranking = 1keywords = gland (Clic here for more details about this article) |
10/38. On the pathogenetic role of prostaglandins in Bartter's syndrome.Two patients, one with Bartter's syndrome and one with severe abuse of diuretics, were investigated before and after indomethacin treatment. Before indomethacin the two patients showed a similar pattern of hypokalaemic alcalosis, secondary hyperaldosteronism, and increased urinary excretion of PGE2 and kallikrein. After a few days on peroral indomethacin medication the hypokalaemia was significantly improved, the plasma renin activity, and the urinary excretion of aldosterone, PGE2 and kallikrein were normalized in both patients. It is concluded that the beneficial effect of indomethacin cannot be used as a proof of prostaglandin overproduction as the primary defect in Bartter's syndrome.- - - - - - - - - - ranking = 5keywords = gland (Clic here for more details about this article) |
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