Avoiding "Rash" Conclusions: Challenge of IgA Vasculitis in Adults.

IgA vasculitis is primarily a pediatric disease that is rarely encountered in adults. With adults, gastrointestinal manifestations are quite common, yet are nonspecific and may overlap with other diseases, particularly Crohn's disease, which can make the diagnosis a challenging task. Treatment is controversial given the disease course is usually self-limited with few serious complications. We present a case of IgA vasculitis in an adult patient with limited extraintestinal findings illustrating the complexity of arriving at the correct diagnosis.

Amelioration of endotoxin-induced acute lung injury in pigs by HWA 138 and A 80 2715: new analogs of pentoxifylline.

We have evaluated the potential therapeutic effects of the xanthine derivatives HWA 138 (1-(5 hydroxy-5-methylhexyl)-3-methylxanthine) and A 80,2715 (1-(5 hydroxy-5-methylhexyl)-3-methyl-7-propylxanthine) on acute lung injury in endotoxemic pigs when administered following the septic insult. Salmonella abortus equi endotoxin (LPS) was given as a continuous intravenous infusion of 2 micrograms/kg/h over a period of 8 h. 1 h after the start of the LPS infusion the animals received a bolus injection followed by continuous infusion of A 80,2715 (3 mg/kg + 1.5 mg/kg/h; n = 6), HWA 138 (3 mg/kg + 1.5 mg/kg/h; n = 6), or saline (LPS control; n = 6). Treatment with A 80,2715 or HWA 138 inhibited the LPS-induced increases in the pulmonary artery pressure (p < .05; ANOVA) and in lung wet/dry weight ratio (p < .05), and ameliorated the LPS-induced deterioration in lung mechanics (decreased lung dynamic compliance (p < .05); increased peak airway pressure (p < .05)). Xanthine treatment, however, failed to significantly improve arterial PO2 and did not affect peripheral leukopenia. The results of this study suggest a potential therapeutic role for HWA 138 and A 80,2715 in attenuating endotoxin-induced acute lung injury.

Sensitive detection of the activation state of blood coagulation in porcine DIC models by a new fibrin immunoassay.

Elevated levels of soluble fibrin in plasma indicate that thrombin converts fibrinogen to fibrin without sufficient inhibitory control. Therefore, measurement of soluble fibrin (SF) in plasma may be considered as a laboratory test for intravascular coagulation. We have demonstrated that a new immunoassay for detection of SF in human plasma (Lill et al., Blood Coag Fibrinol 1993; 4: 97-102), based on a fibrin specific monoclonal antibody, also detects porcine SF with high sensitivity. Thrombin-dependent generation of SF in porcine plasma in vitro resulted in increased reactivity of the assay system, which was time and dose dependent. Dextran sulphate (DXS) and bacterial lipopolysaccharide (LPS) were used as stimuli in in vivo experiments in pigs. Plasma levels of SF increased steadily after intravenous administration of DXS (5 mg/kg for 1 h) to 38 +/- 7.8 micrograms/ml (mean +/- SEM) at 2 h, whereas LPS (2 micrograms/kg/h for 6 h) markedly increased plasma SF levels to over 120 micrograms/ml (at 6 h) after a lag phase of 2 h. In conclusion, this new immunoassay for human fibrin allows specific and sensitive detection of soluble fibrin in porcine plasma.

Development of a chromogenic substrate assay for the determination of hirudin in plasma.

Hirudin is a potent and specific thrombin inhibitor. Since recombinant hirudin is being considered for anticoagulant and antithrombotic therapy we developed a fast and sensitive chromogenic substrate assay for its determination in plasma. The plasma samples (20 microliters) were incubated with 1 ml reagent mixture (0.2 M Tris buffer, 0.025 M NaCl, pH 8.1, containing 0.833 M urea, 0.7 trypsin inhibitor U/ml aprotinin, 100 ng/ml Polybrene and 0.31 NIH U/ml bovine thrombin) for 1 min. Thereafter 100 microliters Chromozym TH (Tos-Gly-Pro-Arg-pNA, 1.9 mM) was added. The change in absorbance/min (delta A/min) was recorded at 405 nm. delta A/min was linear for at least 3 min. The calibration curve was linear at least up to 800 ng hirudin/ml plasma. Intra-assay and inter-assay coefficients of variation were 2.8-3.1% and 5.3-5.8% respectively. The influence of progressive thrombin inhibitors can be neglected because of the short incubation time. Plasma samples can be assayed directly if aprotinin, polybrene and urea are added to the reagent mixture.