Pulmonary alveolar proteinosis and disseminated Mycobacterium avium infection.
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Biomedical subjects
Publications and source records attributed to L J Couderc.
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Cytomegalovirus (CMV) is often suspected as the causal agent in lung disease occurring in various immunodepressive states: AIDS, organ transplantation, bone marrow graft. The mechanisms involved in these three situations is however quite different. The role played by the cytopathogenic effect of the virus and the immune reaction of the host vary considerably depending on the underlying immunodepression. Thus, the criteria allowing to distinguish between CMV infection (presence of the virus or anti-CMV antibodies, no clinical signs) and CMV disease (generalized or organ specific disease resulting from the pathogenic effect of CMV replication) lack precision. The aim of this review of the literature is to assess the implicated immunovirology mechanism and thus the diagnostic (and thus therapeutic) criteria of CMV lung diseases. There is a graduation scale from AIDS, to organ transplantation and bone marrow allograft in the degree of immune reaction implicated in the lung disease and thus the need and timing of antiviral treatment. In AIDS, an interstitial pneumonia, associated with an isolation of CMV (whatever the sample origin, blood, bronchoalveolar lavage or the isolation technique) does not usually implicate treatment. Treatment may be indicated in rare cases (advanced stage immunodepression, high virus titre, endothelial involvement) or in cases in which the infection is also located in other organs. For organ transplantation, observation of CMV in blood or lavage samples in a patient with clinical or radiological signs would justify treatment. For lung transplantation, more so than for any other organ, treatment should be started early whenever respiratory signs are associated with evidence of CMV infection. Finally, in bone marrow allografts, the high rate of failure when pneumonitis has become patent implicates starting treatment immediately upon diagnosis of CMV infection. The strategy proposed here is based on a certain rationale but can be open to discussion. Controlled clinical trials are required to determine the most rigorous and coherent attitude. Finally, within the framework of the diseases examined here, search for lung disease caused by cytomegalovirus should not mask other organ localizations in, for example, the retina, the digestive tract.
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OBJECTIVES: We analyzed the clinical and biological characteristics as well as the clinical course and outcome observed in 20 patients with antiphospholipid antibodies and clinical signs including thrombosis or repeated spontaneous abortion to better identify the recently described antiphospholipid syndrome. METHODS: We retrospectively studied all patients observed in our unit from 1981 to 1992 who fulfilled the following inclusion criteria: a) at least one episode of arterial or venous thrombosis and/or repeated spontaneous abortions, b) positive for antiphospholipid antibodies. RESULTS: Twenty patients were included, 3 with systemic lupus erythematosus (according to the American Rheumatism Association criteria). Arterial or venous thrombosis occurred in 9 and 16 respectively, including exceptional cases of cerebral phlebitis and thrombosis of dermal capillaries. High blood pressure was recorded in 8. Only 1 or 2 types of antiphospholipid antibodies were found in most patients. Anticardiolipin, a circulating anticoagulant and a false-positive Bordet-Wassermann reaction were found together in only 3 out of 16. In addition, the antibody level varied independently from the thrombotic events. There was no case with a clinical course from primary antiphospholipid syndrome to systemic erythromatosus lupus. The effect to treatment on occurrence of new thrombotic events was studied. Three patients suffered one or more haemorrhagic events during antivitamin K treatment. CONCLUSION: It is difficult to establish a differentiation between primary antiphospholipid syndrome, systemic lupus erythematosus and lupus-like syndromes, and precise methods of identifying antiphospholipid antibodies should be further developed.
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A patient developed an interstitial pneumonitis while receiving chlorambucil for a chronic lymphocytic leukemia (cumulative dose, 8,340 mg). Withdrawal of drug treatment was followed by rapid improvement in the clinical condition. Bronchoalveolar lavage showed a T-lymphocytic alveolitis, whereas blood lymphocytes were predominantly of the B phenotype. The T-lymphocytic alveolitis persisted 6 weeks after drug therapy cessation with a predominant CD8+ phenotype, as observed in some hypersensitivity pneumonitis induced by drugs.
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