Evaluation of different therapeutic approaches for spontaneous bacterial peritonitis.

BACKGROUND AND STUDY AIMS: Spontaneous bacterial peritonitis (SBP) is a significant cause of mortality in cirrhosis. Reducing toxic burden of infected ascitic fluid through paracentesis needs further studies as adjunctive therapy of SBP. We aimed to evaluate different therapies for SBP. PATIENTS AND METHODS: Thirty-six cirrhotic ascitic patients with SBP were examined and classified according to treatment modality (5-7 days) into: Group A received cefotaxime, group B received cefotaxime and albumin 1.5 g/kg body weight within 6h of SBP being diagnosed and 1g/kg body weight on day 3, group C received cefotaxime and paracentesis with volume dependent albumin infusion. Control group of 12 cirrhotic ascitic patients free from SBP were included. Routine laboratory tests, ascitic fluid analysis for leucocytes and culture were done, inflammatory mediators such as nitric oxide and tumour necrosis factor alpha were measured in serum and ascitic fluid. Duplex-Doppler assessment of portal flow volume and renal resistive index, Echocardiography to measure end diastolic and end systolic volumes, stroke volume and cardiac output were done. Tests were carried out before and after therapy. RESULTS: Treatment response was assessed by, cardiac haemodynamics, portal and renal flow and NO and TNF. All studied parameters; laboratory, cardiac, Doppler exhibited a significant improvement in group B in contrast to the other groups as demonstrated by post therapy reduction of (blood and ascitic fluid WBCs & PNLS, serum and ascitic NO & TNF and renal resistive index), elevation of (serum albumin and portal flow volume) and improvement of cardiac haemodynamic. CONCLUSION: Treatment of spontaneous bacterial peritonitis by cefotaxime and body weight based albumin infusion gave most favourable results compared to other regimens. Postulation of removing toxic burden through paracentesis has not been confirmed.

Protein C levels in beta-thalassemia major patients in the east Nile delta of Egypt.

BACKGROUND AND OBJECTIVES: Thalassemic patients have an increased risk for thromboembolic complications. To determine if this might be due to a deficiency in protein C, we investigated the status of the protein C anticoagulant pathway in thalassemia major patients and its relationship to the hypercoagulable state. PATIENTS AND METHODS: Fifty patients with beta-thalassemia major (30 non-splenectomized and 20 splenectomized) and 20 healthy children as a control group were tested for levels of serum ferritin, liver enzymes, serum albumin, fibrinogen, protein C and protein S, thrombin antithrombin complex (TAT) and D-dimer. RESULTS: Thalassemic patients had lower levels of protein C and S and higher levels of D-dimer and TAT than the control group. These findings were more obvious in splenectomized patients and in those with infrequent blood transfusion. CONCLUSIONS: Protein C plays a major role in the hypercoagulable state in thalassemic patients. These findings raise the issue as to whether it would be cost-beneficial to recommend prophylactic antithrombotic therapy in high-risk thalassemic patients. A wider prospective study is necessary to delineate under which circumstances therapy might be needed, and at what level of protein C deficiency to start prophylactic antithrombotic therapy.

Impact of CD4+CD25high regulatory T-cells and FoxP3 expression in the peripheral blood of patients with systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by various immunological abnormalities. Regulatory T cells (Tregs) CD4+CD25+ play an important role in maintaining tolerance to self-antigens controlling occurrence of autoimmune diseases. It has been shown that the transcription factor forkhead box P3 (FoxP3) is specifically expressed on CD4+CD25+T cells. FoxP3 has been described as the master control gene for the development and function of Tregs. A decrease in the number of CD4+CD25highFoxP3+ regulatory T cells can play a key role in the loss of tolerance to self antigens. The study was designed to assess expression levels of FoxP3 in peripheral CD4+CD25+ regulatory T cells in patients with SLE and to evaluate the level of some cytokines that are implicated in the extent of the disease activity. The study was carried out on 30 SLE patients, they were 27 females and 3 males, 10 age and sex matched healthy volunteers were studied as a control group. They were divided into two groups: group I: had active disease (12 patients) and group II: had inactive disease (18 patients) according to Systemic Lupus Erythematosus Disease Activity Index. All individual were subjected to CBC, ESR, s.creatinine, RF, CRP, C3, ANA, anti ds-DNA and flowcytometeric assay of CD4+CD25+ (Tregs) and FoxP3 for patients and controls. Quantitative determination of serum interleukin 10 (IL-10) and transforming growth factor-beta1 (TGF-beta1) concentrations in serum samples by ELISA technique. The results revealed a significant decrease of CD4+CD25high cells in peripheral blood in active lupus patients when compared with patients with inactive lupus and those in healthy controls. Intriguingly, the percentage level of FoxP3 on CD4+CD25high cells was significantly decreased in SLE patients with active disease (2.9 +/- 1.05) when compared with those with inactive SLE (3.5 +/- 0.8) and control groups (4.7 +/- 1.2) (P < 0.05). As regard cytokines levels; the level of IL-10 was significantly increased in patients with active and inactive disease (158.8 +/- 50.8, 82.8 +/- 14.08 respectively) when compared with the control group (P < 0.001). While, the level of TGF-beta1 was significantly decreased in patients with active and inactive disease (22.5 +/- 7.03, 29.07 +/- 10.14 respectively), when compared with the control group (P < 0.05). Our data revealed impaired production of Tregs in SLE patients, which may play a reciprocal role with some cytokines to affect the activity of the disease. Tregs cells should be the target to determine the clinical effectiveness of novel therapy to modulate Tregs in vivo besides the conventional treatments.