[Stem cell transplantation for multiple sclerosis. Hamburg experiences and state of international research]. / Stammzelltransplantation bei Multipler Sklerose. Hamburger Erfahrungen und internationaler Forschungsstand.

BACKGROUND: Autologous hematopoietic stem cell transplantation (aHSCT) is still not the standard treatment for highly inflammatory multiple sclerosis (MS). Even though randomized controlled trials are lacking, predictors for treatment response have been established. Since 2007, ten patients have received aHSCT in Hamburg. OBJECTIVE: To present observational data from patients treated in Hamburg and a review of the literature. METHODS: Descriptive statistics were used for evaluating the course of the expanded disability status scale (EDSS) as a measure for clinical outcome, magnetic resonance imaging (MRI) and neuropsychology. New gadolinium and T2-MRI uptake lesions per scan were compared. In addition, a systematic review of the currently available literature was performed. RESULTS: The Hamburg series can be divided in two groups, one group including four patients with chronic progressive MS with low inflammatory activity (median EDSS = 6.25, 0.5 relapses per year, no gadolinium-enhancing lesions) and the other group including six patients with mild to moderate disability, relapses and inflammatory activity (median EDSS = 4.25, 1 relapse per year, 2 gadolinium-enhancing lesions). The median follow-up was 2.4 years. While the first group did not seem to benefit from aHSCT, an improvement in five out of six patients was observed in the second group. New T2 lesions occurred within the first 6 months but gadolinium-enhancing lesions were not observed (p < 0.05). A systematic literature search identified a higher efficacy of aHSCT in younger, less disabled MS patients with inflammatory activity, similar to the findings from Hamburg. CONCLUSION: Cohort reports describe aHSCT as a safe and efficient treatment option in highly inflammatory MS. Based on these data aHSCT seems to be a reasonable option in selected patients with highly inflammatory MS but a randomized controlled trial is warranted.

Switch to efavirenz in a protease inhibitor-containing regimen.

PURPOSE: This report evaluated the efficacy and safety of switching from a protease inhibitor (PI)-containing HIV treatment regimen to an efavirenz (EFV)-containing regimen. METHOD: We retrospectively analyzed data from 64 patients, with a plasma viral load (VL) less than 50 copies/mL and CD4+ counts >200 cells/mL at baseline, who had been taking a regimen consisting of a PI and two nucleoside reverse transcriptase inhibitors (NRTIs; d4T/3TC [n = 45]; AZT/3TC [n = 19]) for a median of 27.5 months (range, 6-41 months) and who chose to substitute EFV for the PIs in the regimens. Statistical analyses were performed by Wilcoxon test. Fat atrophy was evaluated by physician's assessment and patients' subjective self-estimation with the criteria of well being and body state. RESULTS: 57 patients completed 36 weeks on the EFV regimen; 4 patients changed therapy but continued EFV, 2 moved to another area, and 1 discontinued EFV. During the first weeks of therapy, 56.3% of patients suffered from moderate nervous system symptoms. The plasma VL of 63 patients remained at <50 copies/mL at final analysis. Compared with time of switching to EFV, analysis at 36 weeks showed no statistically significant change from 626+/-283 to 643+/-296 cells/mL in mean absolute CD4+ cells and a statistically significant increase from 26.8+/-9.6% to 28.0+/-9.1% in relative CD4+ cells. There was a statistically significant reduction in relative CD8+CD38+ from 62.2+/-16.3% at time of switching to EFV to 55.1+/-15.0% at week 36. At baseline, 27 patients suffered from lipodystrophy, including fat atrophy and fat accumulation. After 36 weeks, nine patients showed intensified fat atrophy. In contrast, five patients improved their state concerning fat redistribution and 13 patients showed no alterations. CONCLUSION: The switch to a non-PI-containing regimen with EFV offers a good drug alternative for patients with suppressed viral load, problems of adherence, and/or adverse events due to PIs but not for patients suffering from lipoatrophy caused by nucleoside reverse transcriptase inhibitors. The intention of such a switch aims at the avoidance of fatal mutations in HIV.

[Hyper-immunoglobulin-prophylaxis and follow-up in vertical hepatitis B (author's transl)]. / Prophylaxe der vertikalen Hepatitis B durch Hyperimmun-Gammaglobulin. Verlaufskontrollen.

The vertical transmission of hepatitis-B virus from chronic HBsAg carrier mothers can cause acute even fatal hepatitis-B, or a chronic HBsAg carrier state in childhood. To prevent this vertical transmission, hepatitis-B- immunoglobulin (HB Ig) is applicated. Frequency and dosis-data are still confusing. Six children were passively immunized with HB Ig according to our schedule. Their serum was controlled for HBsAg and HBsAb with the RIA-method. None of these children became HBsAg positive.

[Hepatitis B infection of the newborn by its symptom-free mother]. / Hepatitis-B-Infektion des Neugeborenen durch seine scheinbar gesunde Mutter.

A routine screening of the serum of pregnant women for the HBs antigen in the Aachn area revealed a frequency of 1,73% symptom free carrier mothers. This proportion is three times higher as the frequency of the HBs antigen in the normal population. The risk of a vertical transmission in children born to HBs antigen positive mothers is discussed as well as extended immunological diagnosis and prophylactic use of hyperimmunglobulin.

[Treatment of haemorrhages in a haemophiliac with factor-VIII inhibitor (author's transl)]. / Zur Behandlung von Blutungen bei Hemmkörperhämophilie A.

In a 33-year-old man with haemophilia A, due to the presence of a factor VIII inhibitor, severe bleeding followed a tooth extraction. It could not be stopped by ordinary factor-VIII substitution or administration of activated prothrombin complex. Before starting substitution treatment it was necessary to decrease the inhibitor concentration in plasma. This was possible by plasma exchange with a blood-cell separator: an exchange volume of 4 litres proved to be sufficient. The inhibitor-containing plasma was replaced by fresh plasma and cryoprecipitate. It was possible to increase the haemostatic activity of the transfused factor VIII by combination with activated prothrombin complex. The inhibitor kinetics remained uninfluenced. A delayed plasmapheresis was without effect as a result of an antibody booster by previous factor-VIII substitution.