Assessment of factors II, VII, IX, X, and protein C in hepatosplenic schistosomiasis.

Forty-four patients with schistosomiasis mansoni were divided into two groups: a group of 31 patients with hepatosplenomegaly and a group of 13 patients with advanced hepatic fibrosis and ascites. Both groups were compared to a control group of 14 healthy subjects. Screening of the extrinsic and intrinsic coagulation pathways was performed by PT (%) and aPTT. Functional assays of vitamin-K-dependent coagulation proteins: factors II, VII, IX, X, and protein C were conducted by using standard methods. A progressive reduction in PT (%) and prolongation in aPTT were detected in the diseased groups. Furthermore, all studied coagulation proteins showed a progressive reduction in their activities, which became more pronounced in the group with advanced ascites. We conclude that the significant reduction in vitamin-K-dependent coagulation proteins might add to the coagulopathy and bleeding diathesis noted in patients infected with Schistosoma mansoni.

The pathogenesis of accelerated fibrinolysis in hepatosplenic schistosomiasis.

Seventy patients with different stages of hepatosplenic schistosomiasis and 18 non-bilharzial normal controls were studied. Plasminogen, plasminogen activators (PA), tissue-type plasminogen activator (t-PA), urokinase-type plasminogen activator (u-PA), alpha 2-antiplasmin (alpha 2-AP), plasminogen activator inhibitor (PAI), fibrinogen/fibrin degradation products (FDP) and D-dimer were determined to elucidate the role of plasminogen activators and inhibitors in the pathogenesis of accelerated fibrinolysis in schistosomiasis. There was a progressive increase in the levels of PA, t-PA, u-PA, FDP and D-dimer indicating enhanced fibrinolytic activity with advancing disease. In addition, there was progressive decrease of plasminogen, alpha 2-AP and PAI levels which might be due to decreased hepatic synthesis and/or increased peripheral consumption. These findings suggest that the pathogenesis of accelerated fibrinolysis in schistosomiasis is multifactorial, but may be due to the progressive increase in the levels of plasminogen activators. In addition, the increase of FDP and D-dimer levels are evidence of secondary fibrinolysis following thrombin generation.

Study of contact activation in endemic hepatosplenomegaly.

Factors of the contact activation complex--FXII, FXI, high-molecular-weight kininogen (HMWK) and prekallikrein (PK) as well as D-dimer were measured in 68 schistosomal patients with and without co-existing chronic hepatitis B virus infection (HBV). Fifty-four cases had mixed hepatosplenic schistosomiasis and HBV infection whereas 14 were suffering from hepatosplenic (HS) schistosomiasis alone. A group of twelve age-matched, healthy individuals served as controls. All coagulation parameters were significantly reduced in both disease groups compared to the healthy controls. The decreased activity of the contact proteins could be attributed to decreased hepatic synthesis, consumption due to disseminated intravascular coagulation (DIC) and to the effect of endotoxins. In mixed schistosomiasis and HBV infections, however, the levels of the contact activation factors were not significantly different from those obtained in patients with HS alone. This apparently paradoxical finding does not, however, exclude a role for co-existing HBV infection in speeding up complications in hepatosplenic schistosomiasis.

Fibrinolysis and the bleeding tendency in patients with hepatosplenic schistosomiasis.

Fifty seven patients with schistosomiasis of the liver and spleen in both the compensated and decompensated states and 15 non-bilharzial subjects were studied. Fibrinogen, plasminogen, fibrinogen/fibrin degradation products, alpha 2-macroglobulin, antithrombin III and Cl-activator concentrations were evaluated in an attempt to assess abnormalities at various stages of the disease. The results showed a progressive decrease in fibrinogen and plasminogen concentrations; fibrin degradation products showed a progressive increase as the disease progressed. Together with a falling platelet count, these data indicate the possible occurrence of disseminated intravascular coagulation with enhanced fibrinolysis which was most pronounced in those who vomited blood. Antithrombin III concentration showed a progressive decrease in parallel with the progress of the disease, possibly due to decreased synthesis or increased consumption, or both. Cl-activator concentration showed no significant change from that in normal controls at any stage of the disease. These findings provide further evidence that disseminated intravascular coagulation and enhanced fibrinolysis in the late stages of schistosomiasis may contribute to the haemorrhagic diathesis seen in the liver and spleen.

Occupational exposure to hepatitis B virus in hospital personnel in Cairo, Egypt.

To identify hospital occupational categories at potential risk of hepatitis B virus infection, a serologic survey was conducted for hepatitis B surface antigen (HBsAg) and antibody (anti-HBs) by enzyme-linked immunosorbent assay in 765 employees at 4 hospitals in Cairo, Egypt. Overall, 3% HBsAg and 28% anti-HBs seromarkers. Combined HBsAg and anti-HBs frequencies by occupational group were: nonprofessional staff (60%), dentists (32%), graduate nurses (33%), physicians (29%), and student nurses (26%). The main risk factors for hepatitis B infection were frequency of exposure to patients' blood (for physicians, p less than 0.001) and to patients with jaundice (for dentists, p less than 0.01), and years of exposure to patients, as reflected by duration of occupation (for physicians, p less than 0.001) and by age of health care worker. Seropositivity by sex was greater for males (p less than 0.01). Physician specialties with highest risk of infection (29 to 53%) were surgery, infectious diseases, obstetrics-gynecology, and emergency medicine.