Immunoglobulins and aminotransferases were followed in 66 haemophilia patients and 13 von Willebrand patients over a six-year period. The results were correlated to HIV serology and lymphocyte subsets. Elevated IgG levels were found in 29/53 patients with haemophilia A, 2/13 with haemophilia B and in 0/13 with von Willebrand's disease. Elevated IgA and IgM levels were seen in 20% and 27% of the patients respectively, with a distribution similar to the elevated IgG levels, except that elevated IgA and IgM levels were also seen in 4/13 patients with von Willebrand's disease. Patients with HIV antibodies had significantly higher immunoglobulin levels than seronegative patients, and this elevation occurred in connection with seroconversion in the majority of the former. The IgG levels could not be correlated to the T4 cell count, but there has been a trend to less clinical symptoms related to HIV infection among those with stable IgG levels during the past few years. No correlation was found between elevated IgG levels and the aminotransferase levels, nor was any correlation found with the amount of blood coagulation factor concentrate given to the patients. The elevation of immunoglobulins observed in our haemophiliacs is multifactorial, but HIV infection is maybe the most important mechanism. The longitudinal IgG pattern may contribute to the prediction of the clinical outcome of this infection.

Adolescent↗

PubMedDate not supplied

Low levels of coagulation inhibitors in patients with Clostridium difficile infection.

To investigate levels of coagulation inhibitors in sera from patients with Clostridium difficile-associated diarrhoea and colitis, commercially available antigen assays were used for immunochemical determination of antithrombin III, protein C and free protein S. Sera from patients with Clostridium difficile-associated diarrhoea and colitis showed significantly lowered levels of all measured inhibitors as compared to controls (Student's t test). Protein C (mean +/- SD): 0.70 +/- 0.30 vs. 1.28 +/- 0.23, t = 6.61, p less than 0.001; antithrombin: 0.70 +/- 0.21 vs. 0.90 +/- 0.17, t = 3.12, p less than 0.01; free protein S: 0.27 +/- 0.06 vs. 0.37 +/- 0.08, t = 3.7, p less than 0.001. Infection with C. difficile may lead to loss of coagulation inhibitors and constitutes a risk for thromboembolic complications.

Aged↗

PubMedDate not supplied

The role of coagulation and inflammation after angioplasty in patients with peripheral arterial disease.

PURPOSE: Restenosis remains a frequent complication after angioplasty in peripheral arterial disease. Inflammation plays a critical role in the vascular response to injury. Effective medical treatment to improve patency after angioplasty is still elusive. The aims of this prospective clinical study were to investigate changes in blood coagulation and inflammatory markers after angioplasty and their significance for restenosis. METHODS: Thirty-four patients with peripheral arterial disease underwent angioplasty of the iliac and superficial femoral arteries. Ten patients undergoing diagnostic angiography were included in the study as controls. Plasma levels of tissue factor, prothrombin fragment 1 + 2, D-dimer, P-selectin, C-reactive protein (CRP), and fibrinogen were analyzed before and after angioplasty. Patients were followed up with angiography after 6 months to assess restenosis. RESULTS: CRP was elevated the day after angioplasty (6.6 mg/l, p = 0.0001) and tended to peak after 1 week (11 mg/l, p = 0.09). There was a significant increase of D-dimer and P-selectin 1-4 hr after angioplasty (0.4 mg/l, p = 0.001 and 68 ng/ml, p = 0.05, respectively). None of the biochemical markers was a statistically significant predictor of restenosis. CONCLUSION: We have observed a much more prolonged inflammatory response than previously noted, but only minor changes in coagulation activity after angioplasty. The biochemical markers, before and after angioplasty, were not related to restenosis. Further studies are needed to delineate the molecular mechanisms behind these observations and their involvement in thrombosis and restenosis. If these pathways are further defined, improved treatment strategies, including antithrombotic treatments and statins, could be tailored to modulate postprocedural inflammation.

Aged↗

PubMedDate not supplied

Effect of venous occlusion and DDAVP injection on platelet aggregation and platelet cyclic AMP.

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Arginine Vasopressin↗