Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020639 (hypoproteinemia)
 1,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We analyzed the serum anion gap (AG = sodium plus potassium minus chloride plus bicarbonate, N = 11-21 mEq/l), serum uric acid and urea concentrations in hyponatremia of various origins. We found that characteristic chemical patterns emerged in association with different hypotonic states: Low uric acid concentration was typically observed in the SIADH and in hyponatremia related to hypopituitarism. The same observation was also frequently noted in hyponatremia secondary to diuretics or to polydypsia. In the SIADH, we observed a decrease in the AG but to a greater extent (-26%) than one would expect from the simple dilutional effect (-16%). Fifty percent of the patients presented an AG lower than 11 mEq/l. In patients with diuretic-related hyponatremia, one group presented an hypouricemia and a low AG as in SIADH (reflecting volume expansion), in the other group the AG was normal or increased as was uric acid concentration (reflecting volume depletion). In adrenocorticotropin deficiency, hyponatremia was typically associated with a low bicarbonate concentration, a normal AG and hypouricemia. In polydypsic patients with hyponatremia, the AG was usually normal or increased despite sometimes very low sodium levels. Uric acid levels were highly variable, most often decreased. We also noted in these patients that the serum urea levels were correlated with urine osmolality (R = +0.8; p < 0.001), and in 40% of them we observed very low blood urea concentration (0.5-2 mmol/l) at the admission time. In hyponatremia related to cardiac failure or cirrhosis, the AG was usually normal despite mild hypoproteinemia.
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PMID:Uric acid, anion gap and urea concentration in the diagnostic approach to hyponatremia. 852 2

We herein describe a rare case of hyponatremia that was aggravated by a burn injury. The patient was also found to have hypothyroidism, followed by SIADH, and finally CSWS, which showed complicated clinical features. A 68-year-old man was admitted for evaluation and treatment of a thermal burn. On admission, the patient was dehydrated, which was evidenced by physical signs. The patient had hyponatremia (serum Na 123 mmol/L) with high excretion of urinary sodium. Plasma AVP levels related to plasma osmolality were high. Plasma levels of renin and aldosterone were low, while the plasma ANP level was normal. However, there was no deficiency of mineralocorticoid or glucocorticoid. After admission, the hyponatremia worsened, and edema with hypoproteinemia developed. The patient was found to have hypothyroidism due to chronic thyroiditis. However, hyponatremia was not completely recovered with replacement of thyroid hormone. The hyponatremia was normalized by administration of DMC. The skin injury was treated with a skin graft. After DMC was discontinued, hyponatremia developed once again. However, this time, there was no inappropriate antidiuresis and the hyponatremia was normalized with the administration of fludrocortisone. These findings revealed that the hyponatremia in this patient may have been primarily due to CSWS. It was most likely exacerbated by hypothyroidism, burn injury, and SIADH caused by the infection. The patient showed physical signs of dehydration and edema. Furthermore, biochemical laboratory data were unable to distinguish between hypovolemia and non-hypovolemia. These complicated features were explained by multiple disorders
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PMID:Hyponatremia secondary to multiple etiologies: a case report. 1808 71