[Tonsillectomy for MRSA eradication-a case report]. / Tonsillektomie zur MRSA­Sanierung ­ eine Kasuistik.

Herein is reported the case of a clinician in whom, after three unsuccessful attempts to eradicate a nasopharyngeal MRSA (methicillin resistent staphylococcus ausreus) colonization, tonsillectomy was performed with long-term success.

Screening for concomitant alcohol abuse in schizophrenia: clinical significance of the Munich Alcoholism Test and laboratory tests.

For the early and correct diagnosis of the comorbidity of schizophrenia and alcoholism, a valid laboratory marker would be most helpful in clinical practice. Seventy schizophrenics admitted to a general psychiatric unit of an urban hospital located in a large industrial area in Germany prospectively underwent a detailed addiction history, the Munich Alcoholism Test (MALT) and determinations of serum gamma-glutamyltransferase (gammaGT) and carbohydrate-deficient transferrin (CDT). Cutoff levels for laboratory tests represented the 95th percentile of data obtained from 100 matched healthy controls. Using the MALT, we found evidence of concomitant alcohol consumption in 42.8% of the study patients. The sensitivities of gammaGT and CDT for detecting alcohol abuse (confirmed using DSM III-R criteria) were 70.6 and 58.8%, respectively. Our data suggest that the MALT can be used as a reliable screening test for alcohol use in schizophrenia. In neuroleptic-treated schizophrenics with pathological gammaGT, but low MALT scores, the corresponding CDT may serve as a highly specific marker to verify a concomitant alcohol abuse.

Sensitivity of carbohydrate-deficient transferrin (CDT) in relation to age and duration of abstinence.

Carbohydrate-deficient transferrin (CDT) serum concentrations were prospectively determined in 162 subjects (alcoholics n=62, controls n=100) using three different methods of detection (IEF, CDTect, Axis%CDT). Repeated testing in alcoholics after 3 and 5 days of abstinence demonstrated a significantly higher sensitivity of CDT in patients above 40 years of age compared to younger patients.

Basal growth hormone levels in women are positively correlated with high-density lipoprotein cholesterol and apolipoprotein A-I independently of insulin-like growth factor 1 or insulin.

Previous studies in growth hormone (GH)-deficient or acromegalic patients yielded contradictory results on the effect of GH on lipoprotein metabolism. In a cross-sectional study, we analyzed the relationships between unstimulated GH, insulin-like growth factor 1 (IGF1), insulin, and lipoprotein metabolism in 44 non-obese young women. On univariate analysis, basal serum levels of GH correlated positively with triglycerides, high-density lipoprotein (HDL) cholesterol, apolipoprotein A-I (apoA-I) and apoA-II and negatively with lipoprotein lipase (LPL) activity. These associations remained significant on multivariate analyses that, in addition to GH, took into account the effects of insulin or C-peptide, as well as the effects of total, protein-bound, or free IGF1. In most cases, the relationships of these lipid parameters with insulin/C-peptide and IGF1 and its free or protein-bound subfractions were opposite of those with GH and not significant. Thus, GH appears to regulate the metabolism of HDL and triglycerides independently of IGF1 and insulin.

Basal growth hormone levels are positively correlated with high-density lipoprotein cholesterol levels in women.

Previous studies in patients with either a deficiency or an excess of growth hormone (GH) yielded contradictory results on the regulation of lipoprotein metabolism by GH. In a cross-sectional study of 563 male and 126 female participants of the Prospective Cardiovascular Münster (PROCAM) Study, we determined biometric and demographic data, serum levels of total cholesterol, triglycerides, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, apolipoprotein (apo)A-I, A-II, and B, and unstimulated GH levels. The median of basal GH levels was higher in women than in men. Moreover, 44.2% of men but only 8.7% of women had basal GH levels less than the detection limit of 0.05 microgram/L. The relationship between basal GH and lipoprotein metabolism was investigated by univariate and multivariate regression analysis of data from 315 men and 126 women with detectable basal GH levels. In men, GH correlated positively with HDL cholesterol and negatively with body mass index (BMI), age, and triglycerides. After multivariate analysis, the correlation with triglycerides remained independent of age and BMI. Among women, GH correlated positively with the use of hormonal contraception, HDL cholesterol, apoA-I, and apoA-II, and negatively with BMI, age, menopause, triglycerides, and apoB. With multivariate analysis, the positive correlations of GH with HDL cholesterol and apoA-I in women were independent of age. BMI, menopause, and oral contraception. We conclude that GH contributes to the regulation of HDL cholesterol levels. Moreover, in women the well-known effects of exogenous estrogen or estrogen loss on HDL metabolism may be partially mediated via GH.

Characterization of very low density lipoproteins and intermediate density lipoproteins of normo- and hyperlipidemic apolipoprotein E-2 homozygotes.

Triglyceride-rich lipoproteins derived from ten normo- and hyperlipidemic apoE-2 homozygotes were analyzed for their composition, beta-VLDL content, and their ability to induce cholesteryl ester storage in macrophages. In six of these probands apoE sequence analysis revealed that the cysteine residues were at positions 112 and 158 of the amino acid sequence (Rall et al. 1983. J. Clin. Invest. 71: 1023-1031). ApoE-2 of these six and the other four patients was further analyzed by SDS electrophoresis to exclude the presence of apoE-2* (Rall et al. 1982. Proc. Natl. Acad. Sci. USA. 79: 4696-4700). The relative serum concentrations of free and esterified cholesterol transported in the d less than 1.006 g/ml and d 1.006-1.019 g/ml lipoproteins of the apoE-2 homozygotes was significantly higher as compared to controls. Compositional analysis of these lipoproteins revealed a relative reduction of triglycerides and a relative increase of cholesteryl esters as compared to controls. In most patients, with increasing serum triglyceride levels the cholesteryl ester concentration increased in d less than 1.006 g/ml and d 1.006-1.019 g/ml lipoproteins. However, in three patients with a low content of beta-VLDL, the increase in the d less than 1.006 g/ml fraction cholesterol was mostly due to free cholesterol and not due to cholesteryl esters. The degree of the macrophage cholesteryl ester accumulation induced by d less than 1.006 g/ml lipoproteins was mostly dependent on the concentration of the beta-migrating fraction (beta-VLDL). The amount of beta-VLDL and pre-beta-VLDL contained in the d less than 1.006 g/ml fraction was determined densitometrically after electrophoretic separation. It could be demonstrated that the beta-VLDL content in the d less than 1.006 g/ml fraction of the apoE-2 homozygous patients was largely independent of serum triglyceride and serum cholesterol levels. When macrophages were incubated with the IDL fraction (d 1.006-1.019 g/ml) from the apoE-2 patients, no significant increase in cellular cholesteryl esters above control levels was observed. Studies with purified lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL) clearly revealed that both enzymes interacted with apoE-2 VLDL (binding, hydrolysis) to a lesser degree compared to control preparations. However, the apoE-2 VLDL preparations containing a low content of beta-VLDL were better substrates for LPL and HTGL than those containing a high beta-VLDL content. It is concluded from our studies that the plasma beta-VLDL content in apoE-2 homozygotes is a major determinant for cholesteryl ester accumulation in macrophages.(ABSTRACT TRUNCATED AT 400 WORDS)