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K Juvin

Publications and source records attributed to K Juvin.

6 recordsLinked to original sources
PubMed2004

[Late presentation of a traumatic pulmonary arteriovenous malformation].

INTRODUCTION: Pulmonary arteriovenous malformations (PAVM) are rare, and most often of congenital origin. Among secondary causes of PAVM, trauma is exceptional. CASE REPORT: We describe here one such case, discovered very late over twenty years after a thoracic perforing wound. Recent vascular imaging techniques (angio-CT scanning and -RMI) have largely contributed to their diagnosis, but direct pulmonary arteriography remains the reference technique preoperatively when surgery is required. In all cases, treatment is as conservative as possible, and embolization of small sized PAVM, even multiple, by coils has become the standard procedure. However, surgery is required when the PAVM is large and/or proximal, particularly when its feeding vessel is complex. Itwas the case of our patient, who has been cured by a lobectomy. CONCLUSIONS: PAVM are rare but should be sytematically searche for in case of hypoxemia along with a pulmonary nodule.

Arteriovenous Fistula↗
PubMed2000

An uncommon etiology of isolated pleural effusion. The ovarian hyperstimulation syndrome.

We report three cases of pleural effusion in the context of ovarian stimulation for in vitro fertilization. The ovarian hyperstimulation syndrome usually causes pleural effusion and ascites. When the latter is lacking, an isolated pleural effusion in a pregnant patient can be mistaken for pulmonary embolism. Early recognition of the condition should allow for an appropriate diagnostic and therapeutic management. Except for some rare but life-threatening complications, such as major hypovolemia or respiratory distress syndrome, the spontaneous outcome is usually favorable. The pathogenesis of this condition may involve an increase of capillary permeability due to the release of vasoactive mediators.

Adult↗
PubMed1997

Role of bronchoalveolar lavage in predicting survival of patients with human immunodeficiency virus infection.

In this multicenter study, we investigated the prognostic factors that influence the risk of death in patients with human immunodeficiency virus (HIV) infection. Clinical and laboratory indices obtained from 161 HIV-seropositive patients who underwent a detailed morphologic and immunophenotypic evaluation of bronchoalveolar lavage (BAL) and peripheral blood cell populations were retrospectively analyzed. In 155 patients, death occurred within the 48-mo follow-up (mean follow-up: 14.8 mo; range: 1 to 48 mo). In the univariate analysis, the patient's age (> 30 yr), HIV disease status, HIV transmission category, number of opportunistic pathogens isolated from the BAL, percentage of BAL neutrophils, and low number of BAL CD4 T cells were predictive of increased mortality. In contrast, the presence of an alveolitis or an increase in the numbers of alveolar macrophages and CD3 T cells was associated with a decreased mortality. In the multivariate analysis, significant independent predictors were age, risk factor for HIV, and presence of an alveolitis. Furthermore, patients with a low number of BAL CD4 T cells had a particularly poor prognosis while the CD4 T-cell count in the peripheral blood (< 50 cells/mm3 in the majority of our patients) had a negligible effect on predicting survival. Our findings suggest the clinical utility of BAL analysis in patients infected with HIV.

AIDS-Related Opportunistic Infections↗
PubMed1996

Heparin-induced thrombocytopenia with thrombotic complications during prophylactic treatment with low-molecular-weight heparin.

Heparin-induced thrombocytopenia is very uncommon with low-molecular-weight heparin, especially when given for prophylaxis of venous thromboembolism. In two of the four published cases, with thrombotic complications, thrombocytopenia may have been related to cross-reactivity between unfractionated heparin and low-molecular-weight heparin. We report one patient who received low-molecular-weight heparin for prophylaxis against venous thromboembolism without any previous injection of unfractionated heparin, and experienced thrombocytopenia with thrombotic complications. Heparin-induced thrombocytopenia was confirmed by several laboratory assays. This observation emphasizes the need for platelet count monitoring during low-molecular-weight heparin therapy.

Aged↗