Treatment of upper‐extremity deep vein thrombosis

Summary. Background: Upper extremity deep vein thrombosis (DVT) can result in fatal pulmonary embolism if not treated. Patients with malignancy may be at particularly high risk. Heparin or low‐molecular‐weight heparin followed by warfarin has been used as standard treatment for lower extremity DVT. However, a paucity of studies exist reporting the efficacy and safety of these regimens in patients with upper extremity DVT. We studied the effectiveness and safety of treatment with dalteparin sodium followed by warfarin and also dalteparin sodium monotherapy for 3 months in patients with confirmed upper extremity DVT. Methods: Consecutive patients with confirmed upper extremity DVT received daily dalteparin sodium for 5–7 days followed by warfarin therapy for 3 months (phase I) or dalteparin sodium monotherapy for 3 months (phase II). The primary outcome measure was the incidence of new symptomatic venous thromboembolism during the 3‐month follow‐up period. The outcome measure of safety was the incidence of major and minor bleeding. Results: Of 631 consecutive patients screened, 74 were eligible and 67 enrolled. No patients receiving either phase I (0%; 95% CI, 0–12%) or phase II (0%; 95% CI, 0–9%) therapy had venous thromboembolism on 3‐month follow‐up. One patient (4%; 95% CI, 0–18%) receiving phase I therapy experienced major bleeding. Five patients died during the follow‐up period; none were attributed to pulmonary embolism. Conclusions: Patients with upper extremity DVT may be treated safely with either dalteparin sodium followed by warfarin or dalteparin sodium monotherapy for 3 months with a good prognosis.     

Alveolar macrophages and emphysema in surfactant protein-D-deficient mice

Abstract:   Surfactant protein-D (SP-D) is a member of the collectin family of collagenous proteins with lectin activity. SP-D is expressed in numerous tissues, primarily in type II alveolar cells in the periphery of the lung. SP-D plays an important role in host defense of the lung. To evaluate the importance of SP-D in vivo , transgenic mice lacking SP-D (SP-D-/- mice) have been generated. Lipid accumulation and airspace enlargement were observed in the lungs of SP-D-/- mice within 3 weeks after birth, and progressed with advancing age. Airspace enlargement and abnormalities in elastin fibers supported the concept that SP-D was required to inhibit destruction of the alveoli. Alveolar macrophages from SP-D-/- mice produced more H₂O₂ and matrix metalloproteinases (MMP)-2, -9, and -12 compared with wild-type mice. In vitro studies demonstrated that oxidants derived in part from NADPH oxidase enhanced NF-κB activation and MMP production in alveolar macrophages from SP-D-/- mice. A specific inhibitor of NF-κB reduced MMP production by alveolar macrophages from SP-D-/- mice. Taken together, these data demonstrated oxidant-dependent activation of NF-κB and enhanced MMP expression by alveolar macrophages from SP-D-/- mice, a process likely to mediate airspace remodeling caused by SP-D deficiency. SP-D plays a critical role in regulating alveolar macrophage activation, oxidant production, and MMP activity that may influence the pathogenesis of various pulmonary disorders.