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Biomedical subjects

K Römer

Publications and source records attributed to K Römer.

9 recordsLinked to original sources

Homocysteine plasma levels are elevated in females with anorexia nervosa.

In the present pilot study significantly (T = 2.46, P = 0.018) higher levels of homocysteine were found in female anorectic patients (14.07, SD 7.3 micromol/l; n = 18) when compared with bulimic patients (10.25, SD 2.82; n = 27) or healthy controls (8.10, SD 1.79; n = 25). Since homocysteine can induce neuronal cell death leading to brain atrophy in different diseases and since it has been linked to depressive disorders these findings may have important implications for understanding common symptoms in patients suffering from anorexia.

Adolescent↗

Risk factors for the HIV-associated lipodystrophy syndrome in a cross-sectional single-centre study.

OBJECTIVE: Risk factors for the HIV-associated lipodystrophy syndrome (HALS) were studied in a single-centre, cross-sectional study. - PATIENTS AND METHODS: 278 consecutive HIV-infected outpatients at a German tertiary care centre were enrolled. Changes in body shape were quantified using linear analogue scales. Cumulative treatment duration for each antiretroviral drug, CD4 cells, viral load and age were investigated as potential risk factors for a clinical diagnosis of lipodystrophy syndrome by logistic regression. RESULTS: HALS was diagnosed in 88 patients. The risk of HALS increased significantly with longer protease inhibitor treatment (relative risk 1.61 (95% confidence interval, 1. 24 to 2.09, per year); older age and a history of low CD4 cell counts were cofactors in this multivariate model, but nucleoside analogues did not contribute significantly. Neither pattern nor severity of disease were predicted by these risk factors. Treatment durations and other risk factors were highly correlated with each other. CONCLUSIONS: These findings support a pathogenetic role for protease inhibitor toxicity, advanced HIV disease, and ageing. No evidence for an additional effect of nucleoside analogues was found. The high correlation of potential risk factors indicates that this and other available studies may be too small to detect multiple risk factors without major confounding.

Acquired Immunodeficiency Syndrome↗

Phase angle from bioelectrical impedance analysis remains an independent predictive marker in HIV-infected patients in the era of highly active antiretroviral treatment.

BACKGROUND: Highly active antiretroviral treatment (HAART) reduces the risk of wasting in HIV infection and may alter the prognostic weight of wasting. The phase angle from bioelectrical impedance analysis (BIA) can be interpreted as a surrogate marker for the catabolic reaction to chronic HIV infection and opportunistic disease. OBJECTIVE: Our objective was to assess the prognostic ability of the phase angle in HIV-infected patients in the era of HAART. DESIGN: Two cross-sectional observation studies were conducted in 1996 and 1997 at a German university outpatient HIV clinic. In the 1996 and 1997 cohorts, HAART was prescribed to 17 of 212 and 168 of 257 patients at baseline and to 179 of 212 and 234 of 257 patients during observation, respectively. Whole-body BIA was assessed at 50 KHz. Time to clinical progression and survival were calculated by using Cox proportional hazard models with time-dependent covariates. Median observation times were 1000 and 515 d for the 1996 and 1997 cohorts, respectively. RESULTS: Higher phase angle was associated with a lower relative mortality risk, adjusted for viral load and CD4(+) cell count, of 0.49 (95% CI: 0.30, 0.81) per degree in 1996 and of 0.33 (95% CI: 0.18, 0.61) in 1997. The influence of phase angle on time to clinical progression, adjusted for viral load and CD4(+) cell count, was not significant in 1996 but the relative risk was 0.58 (0.36, 0.83) in 1997. CONCLUSION: Despite the favorable effects of HAART on the nutritional status of HIV-infected persons, low phase angle remains an independent adverse prognostic marker of clinical progression and survival.

Adult↗

Lack of in vitro synergy of clinically used antibodies specific for ICAM-1 and LFA-1.

Antibodies blocking adhesion molecules such as leucocyte function antigen (LFA)-1 (CD11a) and intercellular adhesion molecule (ICAM)-1 (CD54) are currently under clinical investigation for rejection prophylaxis in organ transplantation. In a murine model a combined though not a single application of antibodies against LFA-1 and ICAM-1 can induce tolerance towards heart transplants. No information regarding a possible synergistic action in man is as yet available. To fill this blank we tested the immunosuppressive capacity of ANTILFA (alpha-LFA-1)- and BIRR1 (alpha-ICAM-1) on human cells in vitro alone and in combination. Allogeneic venous endothelial cells, the lymphoblastoid cell line MSAB or peripheral blood mononuclear cells were used as stimulation. DNA synthesis, IL-2 production and cytotoxic T cell lysis were measured to assess T cell response. The strongest antibody effects were seen when endothelial cells were used as stimulators with the T cell response being assessed by IL-2 production. Most assays showed a similar immunosuppressive effect of LFA-1 and ICAM-1 blocking while the combination of both antibodies was not significantly more effective than each antibody alone. Thus our data do not provide a rationale for clinical trials using a combination of these antibodies.

Antibodies, Blocking↗

DNA polymorphism of the major histocompatibility class I genes and their association with serologically defined haplotypes.

DNA of unrelated persons as well as members of families that were totally or partially homozygous or completely heterozygous on the loci of the major histocompatibility class I genes has been isolated from peripheral blood lymphocytes and blot hybridized with the class I pseudogene pHLA 12.4 probe. The autoradiographic DNA patterns were discussed and compared with well-defined serological features. Positive associations with serologically typed alleles had been demonstrated for HLA-A1,11; -A2; -A3; -B7; -B14; -B35; -Bw41; and -Cw5.

Alleles↗