Rhabdomyolysis is occasionally associated with metabolic disorders such as diabetic coma, severe electrolyte disturbances and myxedema coma. We describe rhabdomyolysis accom panying thyroid crisis. A 50-year-old man with Graves' disease developed rhabdomyolysis, congestive heart failure and hepatic failure during the course of thyroid crisis and then died of acute renal failure. Postmortem examination revealed rhabdomyolysis in the cardiac and psoas muscles, old myocardial infarction, hepatic centrilobular necrosis, renal cortical necrosis, and follicular hyperplasia in the thyroid. Circulatory collapse and dehydration under excessive hypermetabolic state presumably suppressed the source of energy and oxygen for muscle cells, leading to cellular damage.
A human pituitary cell line (18-54, SF) grows in serum-free medium and secretes prolactin (PRL). Autoregulation of pituitary cell growth and PRL production by exogenously supplied ovine PRL (oPRL) was investigated. Human PRL (hPRL) and oPRL stimulated pituitary cell growth up to 92% and 85%, respectively, at hPRL and oPRL additions of 100-1,000 ng/ml. Short-term (1 h) incubation of the cells with oPRL decreased hPRL secretion from the cells by 72% at 10 ng/ml addition. Intracellular hPRL was stimulated under the same conditions by 50-275% at oPRL concentrations of 10-1,000 ng/ml. Long-term (10 days) incubation of the cells with oPRL had no significant effect on extracellular or intracellular hPRL production. These data suggest that the pituitary gland can serve as a primary feedback site and that PRL can autoregulate its own production as well as affect the growth of pituitary cells.
Twenty-four-hour urinary excretion of angiotensin-converting enzyme (ACE) was investigated in relation to that of albumin and beta 2-microglobulin (beta 2M) in 25 non-insulin-dependent diabetes mellitus (NIDDM) patients without nephropathy, 13 NIDDM patients with incipient nephropathy, 18 NIDDM patients with overt nephropathy, and 14 nondiabetic subjects. NIDDM patients without nephropathy and nondiabetic subjects were similar in albumin, beta 2M, and ACE excretion. NIDDM patients with incipient nephropathy had elevated albumin excretion (P less than .01) and similar beta 2M and ACE excretion compared with nondiabetic subjects. On the other hand, NIDDM patients with overt nephropathy had elevated albumin, beta 2M, and ACE excretion compared with nondiabetic subjects (P less than .01). In all NIDDM patients studied, a positive correlation was found between ACE excretion and albumin excretion (r = 0.76, P less than .001) or beta 2M excretion (r = 0.52, P less than .01). These data suggest that elevated ACE excretion in NIDDM patients with overt nephropathy may be reflective of renal tubular damage.
Urinary angiotensin-converting enzyme (ACE) and urinary N-acetyl-beta-D-glucosaminidase (NAG) were measured after a 5-year interval in 38 non-azotemic type 2 diabetic patients. Of these patients at baseline, 16 had nil nephropathy, 15 had incipient nephropathy, and 7 had overt nephropathy. During the follow-up, 6 and 1 of the 16 patients with nil nephropathy developed incipient and overt nephropathy, respectively. Four of the 15 patients with incipient nephropathy progressed to overt nephropathy. The 7 patients with overt nephropathy continued to have overt nephropathy, with slight azotemia in one. Urinary ACE and NAG levels were normal at baseline and showed no significant elevations at follow-up in the patients with nil nephropathy, no significant changes in baseline and modest elevations at follow-up in the patients with incipient nephropathy, and high at baseline and marked elevations at follow-up in the patients with overt nephropathy. In all patients, urinary ACE during the follow-up was positively correlated with urinary albumin or NAG, but not with glomerular filtration rate. Urinary ACE may be of poor prognostic value for the follow-up of diabetic patients, which is at variance with urinary albumin.
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