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Biomedical subjects

A Ganguly

Publications and source records attributed to A Ganguly.

At least 109 records · Page 6Linked to original sources
PubMed1981

Hyperaldosteronism due to unsuspected adrenal carcinoma: discovery during investigation of hypertension in a young woman.

During investigation for hypertension a 19-year-old black woman was found to have an unsuspected adrenal carcinoma. Hyperaldosteronism was established as the cause of the hypertension by observing suppressed plasma renin activity and nonsuppressible plasma aldosterone concentration. The causal relationship was confirmed by a cure of the hypertension and a return in the responsiveness of the renin-angiotensin-aldosterone axis to normal after removal of the carcinoma. This report emphasizes the value of a comprehensive investigation of hypertension, especially in young patients.

Adrenal Gland Neoplasms↗
PubMed1981

Triamterene-thiazide combination: alternative therapy for primary aldosteronism.

The hypertension and hypokalemia of primary aldosteronism are related to excessive aldosterone secretion. Spironolactone, an aldosterone antagonist, is used in high doses to treat the disorder, but it may induce a number of side effects that can limit its use. We investigated the feasibility of treating a group of eight patients with hyperaldosteronism with a triamterene-thiazide combination to induce volume depletion and increase serum potassium concentration. All patients responded with normalization or near normalization of blood pressure. Serum potassium could be maintained within the normal range with or without potassium supplements in all but one patient. The effectiveness of the therapy suggests that thiazide-triamterene treatment may offer an alternative in some patients with primary aldosteronism who do not tolerate spironolactone.

Adenoma↗
PubMed1981

Genetic and pathophysiologic studies of a new kindred with glucocorticoid-suppressible hyperaldosteronism manifest in three generations.

This report describes investigations in a new kindred with dexamethasone-suppressible hyperaldosteronism affecting three successive generations. The presumptive diagnosis was first made in a 7-yr-old boy and led to the identification of the disorder in his mother and grandmother. Several other members of the family were investigated. Genotyping and HLA typing were also performed. To further explore the nature of this unusual disorder, urine from the three patients documented to have the syndrome was assayed for an aldosterone-stimulating factor recently reported to be found in patients with idiopathic aldosteronism. None of these patients showed measurable activity of such a urinary factor. The identification of members in three generations strongly supports the heritable nature of the disorder and probable autosomal dominant type of transmission. The absence of urinary aldosterone-stimulating factor in these patients further supports the tenet that the disorder is pathogenetically distinct from idiopathic aldosteronism, since both disorders are usually associated with bilateral adrenal hyperplasia.

Adult↗
PubMed1980

Differences between adrenal adenoma causing primary aldosteronism and other adrenal tissues in the incorporation of labeled steroid precursors into their products.

The incorporation and conversion of several labeled steroid precursors into their products were examined in slices of adrenal tissue from two patients with primary aldosteronism and compared with that in "normal" adrenal tissue and adrenal tissues from a patient with Cushing's syndrome. The products of the incorporation were separated by Sephadex LH-20 column chromatography. The major products of conversion in the adenomatous tissue of primary aldosteronism were 18-hydroxycorticosterone and lesser amounts of aldosterone. Smaller amounts of 18-hydroxycorticosterone were isolated from all other adrenal tissues studied. No aldosterone could be recovered after incubating any of the adrenal tissue studied with labeled 18-hydroxy-11-deoxycorticosterone or 18-hydroxycorticosterone as precursor steroid. These in vitro results seem to suggest that there is increased 18-hydroxylation in the adenoma of primary aldosteronism compared with other tissues and that relatively more 18-hydroxycorticosterone is produced in such tissue than aldosterone.

Adenoma↗
PubMed1980

Primary aldosteronism due to unilateral adrenal hyperplasia.

A 45-yr-old man with hypertension, hypokalemia, low plasma renin, and hyperaldosteronism was studied. Plasma and urine aldosterone were consistently above normal, remaining abnormally high even on a 300-meq sodium intake. Plasma aldosterone had a marked circadian rhythm, which was correlated with plasma cortisol. Aldosterone secretion was temporarily suppressed after dexamethasone administration and was stimulated by exogenous ACTH. The effect of posture was variable in the eight studies performed, possible due to episodic secretion of aldosterone observed near the sampling times of 0800 and 1200 h. Blood from the right adrenal vein contained 50--100 times more aldosterone than the left adrenal venous samples. The right adrenal gland was excised and found to contain many microscopic subcapsular nests of clear cells. Plasma aldosterone, renin, and potassium returned to normal after surgery, and blood pressure fell to 120/75 over the next 8 months. Three years later, the patient is normotensive without drugs.

Adrenalectomy↗
PubMed1980

Childhood primary aldosteronism due to an adrenal adenoma: preoperative localization by adrenal vein catheterization.

Primary aldosteronism resulting from an adrenal adenoma is rare in children. An 8 1/2-year-old girl was found to have hypertension and spontaneous hypokalemia, both detected as incidental findings. Subsequent investigations revealed inappropriately elevated levels of plasma and urinary aldosterone with suppressed plasma renin activity. Adrenal vein blood sampling and venography suggested the presence of left adrenal adenoma which was confirmed at surgical exploration and pathologic examination. All the clinical and biochemical abnormalities were corrected by the adrenalectomy. The differential diagnoses of various types of hyperaldosteronism and/or hypokalemia in such a clinical setting are discussed.

Adenoma↗
PubMed1979

Diagnosis and localization of pheochromocytoma. Detection by measurement of urinary norepinephrine excretion during sleep, plasma norepinephrine concentration and computerized axial tomography (CT-scan).

The feasibility of differentiating patients with pheochromocytoma from other hypertensive patients by measuring urinary excretion rates of norepinephrine during sleep, a period of physiologic suppression of norepinephrine release, was investigated. The mean excretion rates of norepinephrine in 248 normal subjects and in 109 patients with essential hypertension were 1.03 +/- 0.03 and 1.12 +/- 0.06 (SEM) micrograms/hour, respectively, whereas the lowest excretion rate among the six patients with pheochromocytoma was about seven times higher. Plasma norepinephrine concentration in patients with pheochromocytoma was also consistently above the range observed in both normotensive and hypertensive subjects. CT scan correctly identified the same tumors visualized by selective arteriography. It is suggested that the usefulness of these approaches will provide simpler means of screening and detecting pheochromocytoma.

Adolescent↗
PubMed1979

Primary aldosteronism: diagnosis, localization, and treatment.

New diagnostic techniques have enhanced the detection of primary aldosteronism. However, the response of blood pressure after operation in unilateral and bilateral adrenal disease is different. We have compared four localizing techniques--adrenal venography, adrenal isotopic scanning, a modified adrenal venous sampling for steroid measurements, and the anomalous postural decrease in plasma aldosterone concentration--in 51 patients with primary aldosteronism, all of whom had undergone operative confirmation. Adrenalectomy resulted in normal blood pressure in 59%, improvement in 25%, and no change in 16%. Correct localization of the lesion was obtained in 47% by the adrenal isotopic scan, in 66% by adrenal venography, and in 91% by the modified adrenal venous hormone technique despite four false-positives. Of the 26 patients with an anomalous postural decrease in plasma aldosterone, 88% had a unilateral lesion.

Adenoma↗
PubMed1979

Detection of adrenal tumors by computerized tomographic scan in endocrine hypertension.

Localization of adrenal lesions in various adrenal disorders can be difficult. An attempt to identify the adrenal tumors in ten patients with pheochromocytoma, Cushing's syndrome, or primary aldosteronism was made using computerized tomographic (CT) scans. The adrenal tumor was visualized in eight patients. The CT scan appears to be a promising noninvasive technique for localization of adrenal tumors.

Adrenal Gland Neoplasms↗
PubMed1977

Assessment of 11beta-hydroxylase activity with plasma corticosterone, deoxycorticosterone, cortisol, and deoxycortisol: role of ACTH and angiotensin.

UNLABELLED: In this study we evaluated the role of ACTH and angiotensin on regulation of activities of 11beta-hydroxylases of the adrenal cortex. The ratio of the plasma concentrations of 11 deoxycorticosterone (DOC) to plasma corticosterone (B) reflected the activity of the enzyme of the B and/or aldosterone pathways, and the ratio of plasma 11-deoxycortisol (S) to plasma cortisol (F) as the activity of the enzyme in the F pathway. In normal subjects, both ratios were significantly lower at 0800-0900 h (Doc to B, .01+/-.004, mean+/-SE, n=10; and S to F, .01+/-.003) than at 2000 h (DOC to B, .028+/-.024 and S to F, .015+/-.005). The plasma levels of DOC, B, S and F were all significantly lower at 2000-2100 h than at 0800-0900 h. In contrast 9 patients with Cushing's syndrome exhibited no diurnal change in the ratios. The ratios increased substantially following dexamethasone or metyrapone administration. A high or low salt diet and an angiotensin infusion produced no significant effect on the ratios. The plasma concentration of all four steroids was increased by more than 50% by an infusion of angiotensin. Four hours after administration of 80 mg of Lasix at 0800 h to 10 normal subjects, the ratios of DOC to B and S to F increased significantly (P less than .02), an effect possibly related to a decreased secretion of ACTH. CONCLUSIONS: 1) 11beta-hydroxylase activity of the B and/or aldosterone and F pathways appears to change in parallel with ACTH secretion, and 2) although angiotensin stimulates steroidogenesis of the pathways, it has no apparent effect on 11beta-hydroxylase activity.

17-Hydroxycorticosteroids↗
PubMed1977

The effects of temperature and plasma cortisol on distribution of aldosterone between plasma and red blood cells: influence on metabolic clearance rate and on hepatic and renal extraction of aldosterone.

Aldosterone enters red blood cells (RBC) to a greater extent at 37 C than at lower temperatures. The ratio of 3H-aldosterone concentration in RBC to that in plasma increases from 0.2 at 4 C to 0.7 at 37 C when cortisol concentration is low. Increasing plasma cortisol increases the RBC/plasma aldosterone ratio. When plasma transcortin (CBG) is saturated with cortisol, the RBC/plasma ratio of 3H-aldosterone approaches 0.93, the ratio observed in RBC incubated in 4% albumin solution. The effects of plasma cortisol and temperature on the RBC/plasma ratio reflect an affinity of aldosterone for plasma CBG greater than the affinity for plasma albumin or RBC. Hepatic extraction averages 92% of plasma and RBC aldosterone. Neither hepatic extraction nor renal extraction (less than or equal to 20%) is significantly altered by changing plasma cortisol concentration. Whole blood MCR of aldosterone is unaffected by redistribution of aldosterone from plasma to RBC when plasma cortisol increases, but both plasma cortisol and the temperature at which blood is separated affect the RBC/plasma ratio of 3H-aldosterone and thus change the calculated plasma MCR. The RBC transport of aldosterone, and its dependence on temperature and plasma cortisol, must be taken into account in the evaluation of plasma aldosterone concentration.

Aldosterone↗
PubMed1977

Transient fall and subsequent return of high aldosterone secretion by adrenal adenoma during continued dexamethasone administration.

Plasma aldosterone concentration was consistently decreased by 50% or more in 6 patients with aldosterone-producing adenoma on the first day of dexamethasone administration, only to rise subsequently with continued use of dexamethasone while plasma cortisol concentration remained suppressed. The secondary rise in plasma aldosterone was not related to measured changes in known stimuli of aldosterone secretion. It is probable that the observations result from intrinsic alteration of aldosterone synthesis in the adenoma during prolonged ACTH suppression.

Adenoma↗