Stability of the CK-MB isoenzyme on routine storage.

Unlike earlier studies on the stability of the CK-MB isoenzyme carried out on control sera and on semi-purified and purified CK isoenzymes, we have studied the stability of CK-MB measured electrophoretically in patient sera under different laboratory storage conditions. The values obtained if the test was done immediately were significantly higher than those done on stored samples. There was no difference between specimens stored at -20 degrees C overnight or kept at room temperature (RT) for a few hours, but values were significantly lower (p less than 0.005) in specimens left at RT for 6 h and then stored overnight at 4 degrees C. To determine the effects of longer storage, further specimens stored either at -20 degrees C or at 4 degrees C for up to 4 days were also tested for CK-MB stability by electrophoresis and by immunoinhibition and immunoenzymetric methods. The immunological methods were included in the study to assess method dependency of CK-MB stability. CK-MB was stable at -20 degrees C by all methods, but at 4 degrees C, CK-MB was stable only by immunological and not by electrophoretic (p less than 0.005) measurement. Specimens stored under adverse conditions (4-6 days at RT) showed 50% deterioration of CK-MB when measured electrophoretically but only about 20% when measured immunologically.

Choriogonadotropin-mediated thyrotoxicosis in a man.

A 38-year-old man with a metastatic gonadotropin-secreting tumor of unknown primary origin presented with both clinical and biochemical findings of hyperthyroidism in association with markedly increased concentrations of human choriogonadotropin (hCG) in plasma. After chemotherapy, the concentrations of both hCG and free thyroxin decreased and the patient became euthyroid. We discuss the rare occurrence of this presumably hCG-driven hyperthyroidism in men and compare it with the relatively more common eumetabolic hyperthyroidism associated with choriocarcinoma in women.

Impaired sulphation of phenol by the colonic mucosa in quiescent and active ulcerative colitis.

Substantial amounts of phenols are produced in the human colon by bacterial fermentation of protein. In the colonic mucosa of animals, phenols are inactivated predominantly by conjugation with sulphate. The purpose of this study was to confirm sulphation of phenols by isolated colonocytes from man and to evaluate mucosal sulphation in inflammatory bowel disease using the phenol, paracetamol, in rectal dialysis bags. The incubation of paracetamol with colonocytes isolated from resected colon specimens (n = 7) yielded a mean (SE) value of 7.0 (0.9) mumols/g dry weight of paracetamol sulphate after 60 minutes but virtually undetectable values of paracetamol glucuronide. Paracetamol sulphate was detected in rectal dialysates from all control subjects, with a mean (SE) value of 4.2 (0.8) nmol/hour. Sulphation was significantly impaired (p less than 0.01) in 19 patients with active ulcerative colitis (0.6 (0.2) nmol/hour) and in 17 patients with ulcerative colitis in remission (1.1 (0.4) nmol/hour). Sulphation in eight patients with Crohn's colitis (4.3 (2.1) nmol/hour) was similar to that in control subjects. Impairment of the capacity of the mucosa to sulphate phenols in quiescent and active ulcerative colitis may pose a metabolic burden on colonic epithelial cells, which are continuously exposed to endogenous phenols from the colonic lumen.

Colorimetric measurement of plasma lactate.

A rapid and simple enzymatic method for plasma lactate is proposed using stable reagents to produce the formazan color. This method agrees well with a reference kit method, r = 0.955 and the regression equation is y = 0.99x + 0.09. The over-all recovery averages 100%, with a precision ranging from 0.6 to 3.3%. No interferences have been shown with the formazan reaction. The proposed method is inexpensive, ideal for batch analyses, and is an attractive method for the busy clinical laboratory.

McArdle's disease presenting with rhabdomyolysis.

A patient with McArdle's disease is described who presented with rhabdomyolysis following severe exertion. An episode of acute renal failure four years earlier was probably secondary to a combination of myoglobinuria and an intravenous contrast agent.