Therapy with UDCA was safe, well-tolerated, and efficacious in the short-term treatment of refractory chronic GVHD of the liver. Further investigation is needed to evaluate the long-term effects of UDCA therapy.
Hepatitis C virus (HCV) infection invariably recurs after liver transplantation (LT), and sequels of chronic hepatitis of the graft are a significant cause of morbidity and mortality. In an uncontrolled trial, 31 patients with histologically confirmed hepatitis C after LT received, sequentially, ribavirin (10 mg/kg body weight q.d.) for 12 weeks, followed by ribavirin at the same dose q.d. plus interferon-alpha (IFN-alpha) [3 million units three times a week (3 MU TIW)] for another 48 weeks. Based on an intent-to-treat analysis, the percentages of patients with undetectable HCV RNA in their serum were 0%, 38.7% and 45.2% after 12, 36 and 60 weeks of therapy, respectively. A sustained virological response, as defined by undetectable serum HCV RNA 24 weeks after the end of treatment, was observed in 9/31 patients (29%). Sustained responders had a significant improvement of their liver inflammatory activity score (P=0.025), but not of their liver fibrosis score. The chances of sustained virological response correlated with the length of treatment, but not with the HCV genotype or baseline HCV RNA level. In conclusion, patients with recurrent hepatitis C after LT might benefit from ribavirin/IFN-alpha therapy, provided that the treatment is tolerated for a sufficient duration of time.
Summary:tial role of T cells is supported by the following case report. We observed a patient who acquired celiac disease subsequent to allogeneic BMT. The donor was his HLAWe observed the occurrence of celiac disease following allogeneic bone marrow transplantation in a patient identical sister, who had suffered from celiac disease since birth. transplanted for acute leukemia. The marrow donor was his HLA-identical sister, who had suffered from celiac disease since birth. The post-transplant period was characterized by recurrent episodes of diarrhea.Case report Detailed workup showed atrophic intestinal mucosa on histology and anti-gliadin and anti-endomysium anti-A diagnosis of acute myelogenous leukemia FAB type M2 was made in a 14-year-old boy. Until then he had been bodies in the serum, features that were not present before transplantation. GVHD was absent at that time.healthy with no gastrointestinal symptoms and showed normal growth on a normal diet. Complete remission (CR) of The patient remains free of symptoms on gluten-free diet and slight immunosuppression. This case suggests AML was achieved after induction chemotherapy with Ara-C, 6-thioguanine and daunomycin. In addition, two consolitransmission of celiac disease by bone marrow transplantation and supports the T cell concept in celiac disdation cycles with Ara-C were administered. Allogeneic BMT was considered and his 3-year-older HLA-identical ease.
Summary Background The vagus nerve exerts an anti‐nociceptive effect on the viscera. Aim To investigate whether transcutaneous vagal nerve stimulation (t‐VNS) prevents the development of and/or reverses established visceral hypersensitivity in a validated model of acid‐induced oesophageal pain. Methods Before and after a 30‐minute infusion of 0.15M hydrochloric acid into the distal oesophagus, pain thresholds to electrical stimulation were determined in the proximal non‐acid exposed oesophagus. Validated sympathetic (cardiac sympathetic index) and parasympathetic (cardiac vagal tone [CVT]) nervous system measures were recorded. In study 1, 15 healthy participants were randomised in a blinded crossover design to receive either t‐VNS or sham for 30 minutes during acid infusion. In study 2, 18 different healthy participants were randomised in a blinded crossover design to receive either t‐VNS or sham, for 30 minutes after acid infusion. Results Study 1: t‐VNS increased CVT (31.6% ± 58.7 vs −9.6 ± 20.6, P = 0.02) in comparison to sham with no effect on cardiac sympathetic index. The development of acid‐induced oesophageal hypersensitivity was prevented with t‐VNS in comparison to sham (15.5 mA per unit time (95% CI 4.9 ‐ 26.2), P = 0.004). Study 2: t‐VNS increased CVT (26.3% ± 32.7 vs 3 ± 27.1, P = 0.03) in comparison to sham with no effect on cardiac sympathetic index. t‐VNS reversed established acid‐induced oesophageal hypersensitivity in comparison to sham (17.3mA/unit time (95% CI 9.8‐24.7), P = 0.0001). Conclusions t‐VNS prevents the development of, and reverses established, acid‐induced oesophageal hypersensitivity. These results have therapeutic implications for the management of visceral pain hypersensitivity.
The formation of glycogen in the liver of normal volunteers was followed noninvasively with 13C magnetic resonance spectroscopy (MRS) under two different conditions: a) intravenous infusion of [1-13C]glucose under hyperglycemic and hyperinsulinemic clamp conditions, and b) oral intake of glucose in the form of a bolus. For the intravenous infusion, [1-13C]glucose with an enrichment level of 99% was employed. The C1 signals of alpha- and beta-glucose could be detected in the human liver already after an infusion period of 8 min. However, an increase in the glycogen signal was observed only after a prolonged infusion of about 60 min. Changes in the glycogen signal correlated well with the time course of insulin and glucagon during the measurement. Experiments showed also that liver glycogen formation in man can be followed noninvasively by 13C-MRS using nonlabeled glucose or [1-13C]glucose with a low level of enrichment (6.6%). The use of nonlabeled glucose may therefore simplify the quantitation of net liver glycogen synthesis since it can be based directly on changes in the natural abundance 13C MRS glycogen signal, avoiding label dilution through the various metabolic pathways of glucose. The glucose uptake, estimated from the increase in the glycogen signal, was consistent with findings from more complex and invasive studies of glucose uptake in the liver. The average liver glycogen concentration in 12 h overnight fasted volunteers (n = 18) without any special dietary preparation was assessed to be 229 +/- 34 mM (minimum = 160 mM; maximum = 274 mM).
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