Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0235394 (wasting)
 8,040 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

IN TWO PATIENTS WITH CLASSIC RENAL TUBULAR ACIDOSIS (RTA) AND IN TWO PATIENTS WITH RTA ASSOCIATED WITH THE FANCONI SYNDROME, RENAL POTASSIUM WASTING PERSISTED DESPITE SUSTAINED CORRECTION OF ACIDOSIS: (a) during moderate degrees of hypokalemia, daily urinary excretion of potassium exceeded 80 mEq in each patient; (b) during more severe degrees of hypokalemia, daily urinary excretion of potassium exceeded 40 mEq in two patients and 100 mEq in another. These urinary excretion rates of potassium are more than twice those observed in potassium-depleted normal subjects with even minimal degrees of hypokalemia. The persistence of renal potassium wasting may have resulted in part from hyperaldosteronism, since urinary aldosterone was frankly increased in two patients and was probably abnormally high in the others relative to the degree of their potassium depletion. The hyperaldosteronism persisted despite sustained correction of acidosis, a normal sodium intake, and no reduction in measured plasma volume, and was not associated with hypertension; its cause was not defined. In the two patients with classic RTA, neither renal potassium wasting nor hyperaldosteronism could be explained as a consequence of a gradient restriction on renal H(+) - Na(+) exchange because the urinary pH remained greater than, or approximately equal to, the normal arterial pH or considerably greater than the minimal urinary pH attained during acidosis. The findings provide no support for the traditional view that renal potassium wasting in either classic RTA or RTA associated with the Fanconi syndrome is predictably corrected solely by sustained correction of acidosis with alkali therapy.
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PMID:Renal potassium wasting in renal tubular acidosis (RTA): its occurrence in types 1 and 2 RTA despite sustained correction of systemic acidosis. 510 85

Congenital adrenocortical unresponsiveness to ACTH is characterized by hyperpigmentation, muscular weakness, and episodes of hypoglycemia, with lethargy or coma and convulsion, and without signs or symptoms of salt wasting. Endocrinological evaluation reveals low levels of serum and urinary glucocorticoids, elevated levels of plasma ACTH and unresponsiveness to exogenous ACTH. On the other hand, aldosterone secretion or excretion is normal and is elevated during a low sodium diet. We reported on two patients with this syndrome. Case A, a 4 year-old-girl, showed skin hyperpigmentation, hypoglycemia, convulsion and coma. She was tall wlth a marked advance of bone age. Case B, a 4 year-old-boy, showed skin hyperpigmentation, fatigability and muscular weakness. Both of them revealed low urinary excretion of THE, THF, cortolone, and beta-cortolone and low levels of plasma cortisol. The levels of urinary glucocorticoids and plasma cortisol did not respond to ACTH administration. During a low sodium diet, urinary aldosterone excretion was elevated, urinary sodium excretion ws decreased, and the patients were able to conserve sodium normally. We also summerized other reported cases and discussed the etiology of this syndrome.
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PMID:[2 cases of congenital adrenocortical unresponsiveness to ACTH (author's transl)]. 625 Sep 21

THE FOLLOWING INFERENCES MAY BE MADE FROM THE FOREGOING STUDY: 1. The lesions resulting from fat starvation, at least in the case of pigs, do not resemble or even suggest those of rickets. 2. Prolonged fat starvation leads to the entire disappearance of fat from the adipose tissues. The form of fat atrophy observed as the result of experimental fat starvation corresponds to the serous fat atrophy described by Flemming, and is essentially the same type of fat atrophy as that found in the epicardial and perirenal fat in the human subject as the result of wasting disease. 3. The. lecithins of the brain and the fat of the liver are not materially reduced by fat starvation. 4. Fat starvation does not lead to advanced serous fat atrophy of the subcutaneous fat if the animal be given a large excess of carbohydrate food or a considerable excess of the carbohydrate and proteid constituents of milk. 5. Fat starvation causes a very imperfect absorption of the salts of P(2)O(5) from the intestine.
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PMID:AN EXPERIMENTAL STUDY OF FAT STARVATION WITH ESPECIAL REFERENCE TO THE PRODUCTION OF SEROUS ATROPHY OF FAT. 1986 73