Trace element status in multiple sclerosis

We compared trace element status in multiple sclerosis (MS) patients (n = 27) with and without treatment with corticosteroids and groups of healthy subjects. Concentrations of plasma ceruloplasmin, selenium, and zinc and erythrocyte (RBC) glutathione peroxidase, Se, and Zn were similar in all groups. RBC copper concentrations were significantly lower in MS patients than in control subjects (mean +/- SEM: 0.048 +/- 0.005 vs 0.060 +/- 0.002 mumol/g Hb) because of decreased RBC Cu with steroid therapy. RBC Zn-Cu ratios were significantly higher (14.9 +/- 1.0 vs 10.1 +/- 0.3) in MS patients than in control subjects, differing in both groups of MS patients. In MS and control subjects, RBC Cu correlated significantly with RBC Zn (r = 0.56, 0.49). Disease acuity and disability had no effect on trace-mineral status. These data suggest that in MS there is altered Cu and Zn homeostasis that may cause or result from the disease and is influenced by corticosteroid therapy. Systemic trace element alterations might provide clinically useful markers of MS.     

Local hemostasis in subarachnoid hemorrhage

Fibrinopeptide A (FPA), platelet-secreted protein, platelet factor 4 and beta-thromboglobulin were determined in the cerebrospinal fluid of patients who had suffered from subarachnoid hemorrhage and were treated with 6 g tranexamic acid or 4 million KIU aprotinin to prevent rebleeding. Platelet-secreted proteins and FPA were cleared from the cerebrospinal fluid within 3 days after bleeding. Their vasoactive and thrombotic capability is limited to the initiation period of vasospasm that usually comes to clinical observation 3-8 days after bleeding. Increased thrombotic activity of the cerebrospinal fluid, as reflected by high levels of FPA and platelet-secreted protein, seemed to promote the occurrence of neurological deficits.     

Similar dose responsiveness of hepatic glycogenolysis and gluconeogenesis to glucagon in vivo

This study was undertaken to determine whether the dose-dependent effect of glucagon on gluconeogenesis parallels its effect on hepatic glycogenolysis in conscious overnight-fasted dogs. Endogenous insulin and glucagon secretion were inhibited by somatostatin (0.8 micrograms X kg-1 X min-1), and intraportal replacement infusions of insulin (213 +/- 28 microU X kg-1 X min-1) and glucagon (0.65 ng X kg-1 X min-1) were given to maintain basal hormone concentrations for 2 h (12 +/- 2 microU/ml and 108 +/- 23 pg/ml, respectively). The glucagon infusion was then increased 2-, 4-, 8-, or 12-fold for 3 h, whereas the rate of insulin infusion was left unchanged. Glucose production (GP) was determined with 3-[3H]glucose, and gluconeogenesis (GNG) was assessed with tracer (U-[14C]alanine conversion to [14C]glucose) and arteriovenous difference (hepatic fractional extraction of alanine, FEA) techniques. Increases in plasma glucagon of 53 +/- 8, 199 +/- 48, 402 +/- 28, and 697 +/- 149 pg/ml resulted in initial (15-30 min) increases in GP of 1.1 +/- 0.4 (N = 4), 4.9 +/- 0.5 (N = 4), 6.5 +/- 0.6 (N = 6), and 7.7 +/- 1.4 (N = 4) mg X kg-1 X min-1, respectively; increases in GNG (approximately 3 h) of 48 +/- 19, 151 +/- 50, 161 +/- 25, and 157 +/- 7%, respectively; and increases in FEA (3 h) of 0.14 +/- 0.07, 0.37 +/- 0.05, 0.42 +/- 0.04, and 0.40 +/- 0.17, respectively. In conclusion, GNG and glycogenolysis were similarly sensitive to stimulation by glucagon in vivo, and the dose-response curves were markedly parallel.     

General evaluation of the patient with alopecia

The evaluation of the patient with alopecia is a multistep process that comprises obtaining a good medical history, performing the clinical examination with a special emphasis on the examination of cut and plucked hair, doing a scalp biopsy, and ordering appropriate laboratory studies. Genetic counseling may be given if it is requested.     

Increased prevalence of apolipoprotein E2 in patients with retinitis pigmentosa

Apolipoprotein E isoforms were determined in 139 unrelated patients with retinitis pigmentosa (RP). When compared to prevalence rates for the general population in Germany, an increased prevalence was observed for phenotypes E2/E2: 10.1 vs. 1.0% (p less than 0.001), E2/E3: 19.4 vs. 12.0% (p less than 0.05), and E2/E4: 5.8 vs. 1.5% (n.s.), while the prevalence appeared to be reduced for phenotypes E3/E3: 48.9 vs. 59.8% (n.s.) E3/E4: 13.7 vs. 22.9% (p less than 0.05), and E4/E4: 2.2 vs. 2.8% (n.s.). These findings suggest that genetically determined abnormalities of plasma lipoprotein metabolism may be associated with some forms of RP.