Clinical epidemiology of Guillain-Barré syndrome in adults in Sweden 1996-97: a prospective study.

We described clinical manifestations, outcomes, prognostic indicators and clinico-epidemiological subgroups for 53 adult patients with Guillain-Barré syndrome (GBS) in Sweden during the period 1996-97. These patients were identified from a population of 2.8 million inhabitants and prospectively followed up for one year by a network of neurologists. An additional 10 cases, of whom five were adults who had not been prospectively followed up, were not included in the analyses. At 6 months after onset 80% of the patients could walk without aid, while at 1 year 46% were fully recovered, 42% had mild residual signs or symptoms, 4% had moderate and 6% severe disabilities, and 2% had died. Intravenous human immunoglobulin or plasmapheresis were used in 72% of the patients. The sum of the Medical Research Council (MRC) score at nadir was found as the only significant predictor for residual signs at 1 year in a multivariate model. Three subgroups, with different clinico-epidemiological characteristics, were identified by using cluster analysis. In conclusion, GBS in Sweden is frequently preceded by a respiratory infection, is often treated with immunomodulatory therapies, and exhibits a high recovery rate and a low fatality rate.

Prevalence of HIV-1 infection in rural, semi-urban and urban villages in southwest Tanzania: estimates from a blood-donor study.

OBJECTIVES: To measure the prevalence of HIV-1 infection in different subgroups of blood donors and to identify groups at high risk of acquiring HIV-1. METHODS: Between March 1988 and April 1991 all blood donors at Ilembula Lutheran Hospital, Tanzania were asked about their age, marital status, home village and occupation, and tested for the presence of HIV antibodies using a first generation, whole virus lysate enzyme-linked immunosorbent assay (ELISA). Some negative (n = 265) and nearly all positive samples (439 out of 485) were subjected to confirmatory testing including recombinant and peptide-based ELISA and Western blot assays. RESULTS: A total of 3474 male and 1287 female blood donors were studied. The overall HIV-1 prevalences for men and women were 6.6 and 7.0%, respectively, with a higher prevalence in urban villages (13.6 and 15.0%, respectively), an intermediate prevalence in semi-urban villages (7.2 and 7.9%, respectively), and a lower prevalence in rural villages (3.7 and 3.0%, respectively). HIV-1 infection occurred mostly in men aged 20-44 and women aged 15-34 years. Urban donors, but not semi-urban and rural donors from the highlands, had a higher HIV-1 prevalence (21.4%) than the corresponding group from the lowlands (10.2%). Apart from area of residence, HIV-1 infection was found to be associated with occupation and marital status. There was an increase in HIV-1 prevalence, although not statistically significant, during the period studied. None of the blood donors were positive for HIV-2. CONCLUSIONS: Male and female donors from urban and semi-urban villages, non-farmers from urban villages, and unmarried donors were identified as high-risk groups, which is consistent with more extensive risk behaviour in urban communities. In addition to using an HIV test with high sensitivity, the importance of pre-donation selection of blood donors is stressed.

Abnormalities in T-lymphocyte populations in blood from patients with demyelinating polyneuropathy associated with monoclonal gammopathy.

Patients with monoclonal gammopathy secrete monoclonal antibodies (M-component), that in some patients are associated with polyneuropathy. The M-component has been shown to react with peripheral nerve myelin in some of these patients. However, it is not known whether the M-component secreting B-cells are autonomous or subject to regulation by T-cells or if other cellular abnormalities may occur. In order to define circulating lymphocyte subpopulations, flow cytometry was done on blood samples from patients with monoclonal gammopathy and demyelinating polyneuropathy (n = 13) and patients with monoclonal gammopathy without polyneuropathy (n = 11), and were compared to healthy controls. Significantly increased proportions of primed T-helper (CD4+) cells, i.e. those expressing helper/inducer function (CD29+ CD4+), providing help for antibody secretion, as well as decreased proportions of naive, unprimed suppressor/inducer (CD45RA+ CD4+) T-helper cells were found in patients with M-component associated polyneuropathy. Within the T-cytotoxic/suppressor population (CD8+) we found an increased proportion of killer/effector (S6F1+ CD8+) cells and a decreased proportion of suppressor/effector (S6F1- CD8+) cells in patients with monoclonal gammopathy and polyneuropathy. Similar findings were found in monoclonal gammopathy patients without polyneuropathy, although the deviations in general were less pronounced and did not reach statistical significance compared to the controls. The proportion of natural killer (NK) cells (CD56+) was markedly decreased in all patients with monoclonal gammopathy. In the whole group of patients with monoclonal gammopathy, we found clear proportions of interleukin-2 receptor (CD25+) expressing lymphocytes, indicating the presence of activated T-cells. No clear correlation between abberations in T-cell subtypes and clinical severity of the demyelinating polyneuropathy or titres of anti-PNM antibodies was found.(ABSTRACT TRUNCATED AT 250 WORDS)

Susceptibility to demyelinating polyneuropathy in plasma cell dyscrasia may be influenced by amino acid position 9 of the HLA-DR beta chain.

Fifty-five patients with plasma cell dyscrasias were investigated by genomic typing for HLA-DR and -DQ genes by restriction fragment length polymorphism, neurophysiology and for presence of anti-myelin-associated glycoprotein (MAG) antibodies. In 26 patients, a polyneuropathy (PN) of demyelinating type was established. Among these individuals, an association was found with the presence of a tryptophan amino acid residue at position 9 of the DR beta chain (P < 0.01). This position is part of the first hypervariable region of the DR beta chain, and may be of importance in determining preferential peptide-binding capacity of the HLA-DR molecule. The presence of anti-MAG antibodies in 15 out of 17 patients with an IgM M-component and demyelinating PN (14 of these 15 individuals carrying a tryptophan at position 9) supports the pathogenic role of an autoimmune response against MAG. The finding of an HLA class II association may indicate a pathogenic role of T cell immunity in this condition.

Influence of dietary fat, cholesterol and energy on serum lipids at vigorous physical exercise.

Seven healthy male volunteers participated in four different heavy cross-country ski trips in the mountains, 1 year apart, wearing a back-pack weighing 30 kg. Each trip lasted for 8 days covering a total distance of 160 km. Serum triglycerides and lipoprotein cholesterol were measured before and after the trip. The different experiments were carried out with the same participants and under the same conditions, but with a varying diet composition. With the four different diets used, a standard diet (3800 kcal day-1, 26% fat, 260 mg cholesterol day-1), a low-energy diet (2300 kcal day-1, 21% fat, 110 mg cholesterol day-1, a high-fat-high-cholesterol diet (3800 kcal day-1, 52% fat, 480 mg cholesterol day-1) and a high-cholesterol diet (3800 kcal day-1, 29% fat, 410 mg cholesterol day-1), a decrease in very low-density lipoprotein-low-density lipoprotein (VLDL-LDL) fraction by 38%, 50%, 41%, and 54%, respectively, was obtained. No significant increase in high-density lipoprotein (HDL) cholesterol was found in the experiments with the standard diet and the low-energy diet, but in the high-fat-high-cholesterol diet experiment the HDL cholesterol increased by 19% and the ratio HDL cholesterol:total cholesterol from 0.327 to 0.490. With the high-cholesterol diet an increase in HDL cholesterol of about the same extent was obtained. In all experiments the serum triglycerides decreased by more than 30% and no significant difference for the different diets was obtained.(ABSTRACT TRUNCATED AT 250 WORDS)

Substrate specificity of monoamine oxidase in pig liver mitochondria.

In pig liver both the A and the B form of monoamine oxidase (MAO) were found to be responsible for the oxidation of 5-hydroxytryptamine (5HT), a substrate oxidised by the A form alone in most other tissues. With increasing concentrations of this substrate, the percentage of the substrate oxidised by the B form increased. The Km value of the A and the B form of MAO for 5HT was 200 microns and 2.2 mM, respectively. It is suggested that the division of the monoamines into A and B form substrates should be done on the basis of the molecular turnover numbers rather than on their activities, and that the substrate specificities of the two forms of MAO should be determined over a large range of substrate concentrations.

Molecular turnover numbers of different forms of mitochondrial monoamine oxidase in rat.

Molecular turnover numbers of the different forms of monoamine oxidase in rat liver were estimated for serotonin, tyramine and beta-phenylethylamine by titration with irreversible inhibitors. The 'A' form was found to have a much higher turnover number for serotonin and a lower turnover number for beta-phenylethylamine than the 'B' form, while the turnover numbers for tyramine were in the same order of magnitude for both forms. The monoamine oxidase in the liver was found to have a significantly higher molecular turnover for tyramine and beta-phenylethylamine than that in the brain, heart and kidney. It was calculated that the 'A' form of monoamine oxidase amounted to about 20% and the 'B' form to about 80% of the total amount of monoamine oxidase in the rat liver mitochondrial preparation. The number of molecules per mitochondrion was also calculated.

Heterogeneity of pig liver and pig brain mitochondrial monoamine oxidase.

Pig liver and pig brain mitochondrial monoamine oxidase were inhibited by increasing concentrations of clorgyline (selective inhibitor for the "A" form of monoamine oxidase) and deprenil (selective inhibitor for the "B" form of the enzyme) and the activities were then estimated with serotonin, tyramine and beta-phenylethylamine as substrates. The results indicate that both the "A" and the "B" forms are present in these tissues. Serotonin and tyramine are shown to be oxidized by both the "A" and the "B" forms of the enzyme, whereas beta-phenylethylamine appears to be oxidized almost exclusively by the "B" form. Lipid-depletion of the mitochondrial preparation from these tissues by extraction with aqueous methyl ethyl ketone eliminated almost all of the "A" form activity while most of the "B" form activity remained.