Infections and inflammatory diseases as risk factors for venous thrombosis. A systematic review.

Inflammation and venous thrombosis are intertwined. Only in the recent 15 years clinical epidemiological studies have focussed on inflammatory or infectious diseases as risk factors for venous thrombosis. Although a few reviews and many case reports or studies on these topic has been written, a review reporting relative or absolute risks for venous thrombosis has not been published yet. We performed a systematic review using Medline, Pubmed and Embase and found 31 eligible articles. Inflammatory bowel disease, ANCA-associated vasculitis, infections in general and more specifically, human immunodeficiency virus, pneumonia and urinary tract infections are associated with an increased risk of venous thrombosis.

Imatinib mesylate in the treatment of systemic mastocytosis: a phase II trial.

BACKGROUND: Mastocytosis is characterized by the abnormal proliferation of mast cells in 1 or more organs. In most patients, a mutation is present in the gene for C-KIT, resulting in deregulation of the c-kit receptor. Imatinib mesylate is a potent inhibitor of c-kit receptor tyrosine kinase activity. Therefore, the authors evaluated the efficacy and safety of imatinib mesylate as treatment for patients with systemic mastocytosis. METHODS: Patients with systemic mastocytosis received imatinib mesylate orally at a dose of 400 mg once daily for 3 to 6 months. Low doses of prednisone were added during the first 2 weeks. Endpoints were reductions in serum tryptase, urinary N-methylhistamine excretion, skin lesions, the number of mast cells in bone marrow sections, hepatomegaly and/or splenomegaly, and symptoms. RESULTS: Of 14 patients who were included in the study, 11 patients had the D816V mutation. One patient expressed the FIP1L1-PDGFR-alpha rearrangement gene. In 2 patients, no mutation was found. In 10 patients, serum tryptase levels decreased >20%. In all patients, urinary N-methylhistamine excretion was reduced. In 8 of 13 evaluable patients, the number of mast cells in the bone marrow decreased. Skin symptoms diminished in 5 of 9 patients. Hepatosplenomegaly improved in 3 of 6 patients. Symptoms decreased in 8 of 13 patients. In all patients who had the D816V mutation, reductions in > or =2 endpoints were achieved. In the patient who expressed the FIP1L1-PDGFR-alpha rearrangement gene, a complete response was attained. In general, imatinib mesylate was tolerated well. CONCLUSIONS: Imatinib mesylate was effective in patients with systemic mastocytosis, including those who had the D816V mutation.