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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.

Changes in TSH-receptor antibody (TR-Ab) and thyroid stimulating antibody (TS-Ab) after thyroidectomy were examined in seventeen thyrotoxic patients (3 males and 14 females, 40.0 +/- 3.4 yr) with positive TR-Ab and TS-Ab. They were subjected to thyroid surgery because of suspected malignancy, methymazol induced agranulocytosis, cardiac failure, recurrent gastric ulcer or emotional instability. Of these patients, 3 were totally thyroidectomized, 11 were subtotally thyroidectomized and 3 were unilaterally lobectomized. Histological findings in these patients showed diffuse hyperplasia in 8 cases, an adenomatous goiter in 3, diffuse hyperplasia plus follicular adenomas in 5, and Hashitoxicosis in one. Their thyroid function before surgery was as follows: T3 level, 3.9 +/- 0.7 ng/ml; T4, 19.5 +/- 3.3 micrograms/dl; free T3, 11.9 +/- 1.2 pg/ml; free T4, 4.9 +/- 1.0 ng/dl; and TSH, 0.9 +/- 0.1 microU/ml. Mean levels of TR-Ab and TS-Ab before surgery were 56.8 +/- 4.6% and 1,218.6 +/- 262.4%, respectively. Positive anti-thyroid antibody (TGHA) was 47.0%, positive anti-microsomal antibody (MCHA) was 88.2% in these thyrotoxic patients, and mean levels of TGHA and MCHA were 1,688 +/- 715 and 89,280 +/- 34,717 times, respectively. After the operation, these parameters were decreased and their thyroid functions became an euthyroid or a hypothyroid state one month later. The incidence of post-operative hypothyroidism was 45.5% in subtotally thyroidectomized patients, 33.3% in unilaterally lobectomized patients and 100% in totally thyroidectomized patients. TR-Ab levels decreased from 56.2 +/- 6.5% before surgery to 24.5 +/- 12.2% 12 months after surgery, but increased again to 35.0 +/- 15.7% 24 months after surgery in subtotally thyroidectomized patients. These levels also decreased from 50.4 +/- 11.0% before surgery to 37.8 +/- 11.4% 12 months after surgery, and remained unchanged to 38.2 +/- 10.4% 24 months after surgery in unilaterally lobectomized patients. On the other hand, in totally thyroidectomized patients, TR-Ab levels decreased and normalized 12 months after surgery. One of subtotally thyroidectomized or unilaterally lobectomized patients developed recurrent thyrotoxicosis with an increased positive TR-Ab. Mean levels of TS-Ab decreased to 28.3 +/- 181.3% and 152.5 +/- 47.9% 12 and 24 months after surgery, respectively, in subtotally thyroidectomized patients. These levels decreased 12 months after surgery and then increased again to 303.6 +/- 130.6% in unilaterally lobectomized patients. On the other hand, TS-Ab levels decreased and normalized to 94.3 +/- 3.9% 6 months after surgery in totally thyroidectomized patients.(ABSTRACT TRUNCATED AT 400 WORDS)

To assess the nature of the heparin-induced aldosterone deficiency, we investigated the stimulatory effect of angiotensin II (All) on aldosterone and its precursor steroids in adrenal zona glomerulosa cells from heparin-treated rats compared with those in the cells from vehicle-treated rats. Heparin-treated rats had low plasma aldosterone levels, high plasma renin activity and plasma All levels, and normal plasma corticosterone level 6 weeks after the treatment (1500 IU/kg, twice daily). Basal aldosterone production, when corrected to a uniform number of cells per group, was similar in the cells from heparin-and vehicle-treated rats. The cells from heparin-treated rats had a less sensitive and lower response of aldosterone production to All; an increase by 4 orders of magnitude in the threshold dose for All and a decrease in the maximum All-stimulated level.The maximum All-stimulated levels, but not the basal levels, of pregnenolone, corticosterone and 18-OHB production were low in the cells from heparin-treated rats.ACTH caused a similar stimulatory effect on aldosterone production in the cells from heparin-and vehicle-treated rats. The cells from heparin-treated rats had a less sensitive and lower response of aldosterone production to potassium; an increase by one order of magnitude in the threshold dose for potassium and a decrease in the maximum potassium-stimulated level, presumably because of the glomerulosa hyporesponsivness to AII. These results suggest that our heparin-treated rats have selective impairment of adrenal zona glomerulosa cells, involving the specific receptors and the aldosterone bio¬ synthesis, to AIL

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