The American journal of the medical sciences
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The serum fructosamine assay is a new commercially available test designed to measure serum glycated protein as an index of glycemic control in diabetes. The test relies on the ability of glucose bound to protein with a ketamine linkage (fructosamine) to act as a reducing agent in alkaline solution. Serum fructosamine activity was studied in 61 Type I diabetic patients attending a 2-week American Diabetes Association sponsored diabetic camp for children. ⋯ To assess if mean blood glucose correlated with these objective parameters, the authors performed capillary blood glucoses preprandially and at bedtime on all 61 diabetic campers during the 2-week period of observation and reassessed serum fructosamine activity and HgA1C on day 14 of camp. We found the HgA1C and fructosamine correlated well with the mean daily blood glucose obtained during the preceding week (r = .45, p less than .01 and r = .58, p less than .01) respectively. Our data suggest that the serum fructosamine is as effective as the HgA1C in correlating to mean blood glucose control in this cross-sectional study of Type I diabetic patients.
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Patients with documented serious infection and total bilirubin values of greater than 2 mg/dl were surveyed for serial changes in bilirubin and other laboratory and clinical features. Of 19 patients studied, 12 (Group A) had persisting or increasing hyperbilirubinemia, and 7 (Group B) had decline in bilirubin after infection onset. None demonstrated marked changes in other liver tests. ⋯ All Group A patients died because of uncontrolled infections, whereas all Group B patients survived with resolution of infection (p less than .001). Ten of 15 patients with available preinfection liver tests demonstrated serial bilirubin increases without marked changes in other liver tests prior to clinical recognition of infection. These findings demonstrate that hyperbilirubinemia disproportionate to increases in other tests may manifest before recognition of infection and that persistent or progressive hyperbilirubinemia is indicative of ongoing active infection.
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A 43-year-old woman had clinical and biochemical evidence of a secreting paraganglioma of the glomus jugulare region. Catecholamine secretion was exacerbated during embolization of the tumor before surgery and resulted in a life-threatening vasomotor attack. ⋯ This case is reported to stress the importance of adequate preoperative assessment of patients with paragangliomas of the head and neck. The extreme rarity of catecholamine-secreting tumors of this region should not lead us to underestimate the morbidity and mortality of such patients undergoing surgery or any other invasive procedure whether the diagnosis is confirmed or only suspected.
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Heme oxygenase (HO) is the rate-limiting enzyme for heme degradation, and elevated levels of HO may be associated with a variety of pathologic disturbances. A limited number of HO inhibitors such as the metalloporphyrins have been proposed as possible chemotherapeutic agents for the treatment of hyperbilirubinemia. We undertook the study of various natural newly synthesized heme analogues as possible inhibitors of HO in human adult and fetal liver microsomes. ⋯ Porphyrins with aromatic substitutions at the methene bridges (2a, 2b) did not inhibit the conversion of heme to bilirubin, even at relatively high concentrations. Furthermore, the specific activity of HO was significantly greater (5X) in fetal microsomes as contrasted with adult microsomes as contrasted with adult microsomes. Even though fetal microsomes had greater HO activity, 5 microM of compound (1b) caused a similar degree of inhibition in both adult and fetal preparations.(ABSTRACT TRUNCATED AT 250 WORDS)
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To investigate the quantitative importance of sodium balance to arterial pressure changes produced by changes in sodium intake, we studied normotensive white and black subjects and hypertensive black patients with two protocols. Protocol 1 used a 3-day control period with a 150 mEq sodium intake/day followed by 4 days of salt depletion (SD) with a diet providing 9 mEq/day of sodium and furosemide, 1 mg/kg, given the first day and then 3 days of salt loading (SL), during which 25 mL/kg of isotonic sodium chloride solution was given intravenously each day (3.88 mEq sodium/kg/day). In protocol 2, the sequence of sodium intake changes was reversed. ⋯ In protocol 1, the hypertensives had statistically significant changes in arterial pressure with changes in salt intake, and they also lost more sodium than normotensives during SD. In protocol 2, blacks, both normotensives and hypertensives, had statistically significant pressure changes with both SL and SD, and black hypertensives retained less sodium during SL than either normotensive group. Spearman correlations showed no relationship between sodium balance and mean arterial pressure, suggesting that salt-sensitive hypertension results not from the magnitude of sodium retention, but from the pressor mechanisms evoked.