Biomedical subjects
Publications and source records attributed to M Karmochkine.
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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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The antiphospholipid syndrome (APS) is usually defined by the association of a clinical manifestation (venous or arterial thrombosis or miscarriage) with the presence of antiphospholipid antibodies (lupus anticoagulant and/or anticardiolipin antibodies). It frequently occurs in the course of systemic lupus erythematosus but is also encountered as a "primary" disease. APS is responsible for diverse respiratory manifestations. Pulmonary embolism is common. The site of the causal venous thrombosis is frequently unusual. Pulmonary hypertension may be a consequence of repeated embolism or may belong to the primary idiopathic variety. Pulmonary manifestations may also result from left-sided heart failure due to mitral or aortic valve abnormalities, myocardial infarction or a specific myocardiopathy. APS is probably involved in the occurrence of some cases of adult respiratory distress syndrome. Long term secondary prevention of recurrent thrombosis is a central point in the management of APS.
In order to determine the characteristics and the course of diseases treated with long-term plasmapheresis (e.g., more than 25 plasma exchanges), we retrospectively studied 850 patients who underwent plasmapheresis. Long-term plasma exchange was prescribed to 38 patients who failed to respond to conventional therapy; cryoglobulinemias, peripheral neuropathies and monoclonal gammopathies were their most frequent underlying diseases. Improvement was noted in 65.8% cases. Only minor side effects were observed and the risk/benefit ratio for such therapy was excellent.
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Antiphosphatidylethanolamine antibodies (aPEA) were investigated in a population of 78 systemic lupus erythematosus (SLE) patients, by means of an enzyme-linked immunosorbent assay method. These antibodies are specifically directed against phosphatidylethanolamine, one of the zwitterionic phospholipids present in cell membranes. Antiphosphatidylethanolamine antibodies were found in 13 patients (16.6%). They were generally associated with lupus anticoagulant (two patients), antiphospholipid antibodies directed against anionic phospholipids (six patients), or both (four patients). In only one case, aPEA were the sole detectable antiphospholipid antibodies. Thrombosis, recurrent fetal loss, valvular disease or neurological involvement was present in most (11 of 13) of the patients with aPEA. It seems valuable to carry on further searches for these antibodies in SLE, since patients with aPEA are at higher risk of thrombosis and/or recurrent fetal losses than are patients with antiphospholipid antibodies (anticardiolipin, anti-anionic phospholipid and/or lupus anticoagulant) other than aPEA. Moreover, since aPEA can be the sole detectable antiphospholipid antibodies, they should be investigated in SLE with thrombosis when neither lupus anticoagulant nor anticardiolipin antibodies can be demonstrated.
In membranes, phosphatidylethanolamine (PE) is usually in a lamellar phase, but it can also adopt a hexagonal II phase (HexII PE), which has been demonstrated to be immunogenic in mice and has recently been used in a new clotting assay to detect lupus anticoagulant (LA). A population of 58 patients susceptible of having LA or antiphospholipid antibodies (aPLA), was screened for reactivity to HexII PE using the new clotting assay and for the presence of anti-PE antibodies (aPEA) using ELISA. The patients could be classified as follows: 26 systemic lupus erythematosus, 14 primary antiphospholipid syndromes and 18 miscellaneous non autoimmune disorders. HexII PE reactivity was detected in 22 patients. It was significantly more often associated with LA-positivity (20/29) than with LA-negativity (2/29), (p < 0.0001). However, 9 patients with LA had negative HexII PE assays. Anti-PE antibodies were detected by ELISA in only 12% of the cases. No correlation was observed between the distribution of aPEA and that of HexII PE reactivity. Interestingly, 2 LA- and aPLA-negative patients exhibited HexII PE reactivity. The absence of identity between the distribution of HexII PE reactivity and that of either LA or aPEA indicates that this new assay has its own specificity. It might detect antibodies to the immunogenic hexagonal PE and may therefore have a broader scope than that proposed initially. Although in the studied populations, no significant relationship could be found between HexII PE positivity and clinical complications (thrombosis and/or recurrent fetal losses), it might be associated with other complications of the antiphospholipid syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
OBJECTIVES: An open clinical study was conducted in the haematological department of an intensive care unit to investigate cure of staphylococcal septicaemia in neutropenic central venous catheter carriers without removal of the line. METHODS: Thirteen neutropenic patients with a central venous catheter were investigated. These patients were under treatment for haematological malignancies and had at least 2 blood cultures positive for Staphylococcus aureus or coagulase-negative staphylococcus. Antibiotherapy including vancomycin was given through the catheter. Each case was re-evaluated on day 3 of treatment. The catheter was removed if blood cultures remained positive or if clinical signs of bloodstream infection persisted or worsened. RESULTS: Clinical recovery was obtained in ten patients and bacterial eradication in twelve. Three patients died from septic shock: two deaths were not related to staphylococcal septicaemia; one death was due to a staphylococcal septic shock which occurred within a few hours of admission, despite of prompt removal of the central venous catheter. CONCLUSIONS: With appropriate antibiotherapy, leaving the central venous catheter in place would appear possible in cases of staphylococcal septicaemia. Response to treatment, however, must be carefully monitored.
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A 65-year-old woman with refractory anemia with excess of blasts received sequential courses of granulocyte-macrophage colony-stimulating factor therapy (GM-CSF) and low-dose cytosine arabinoside. Each course of GM-CSF induced a rapid and tremendous increase in leukocyte count as well as in spleen size, 111indium chloride scanning suggested a myeloid metaplasia of the spleen. This observation suggests that in some patients the granulopoietic response to the myeloid growth factor stimulation may be predominant in the spleen.
Four cases of plasma cell type Castleman's disease (CD) are described. Two patients had localized forms (one mediastinal and the other mesenteric) and presented systemic manifestations associated with hypergammaglobulinemia and severe anemia. In both cases, the lesions were revealed by computerized tomography scans and cures were obtained by the complete surgical removal of the masses, which led to the rapid disappearance of the systemic manifestations. The other 2 patients had the multicentric form of CD and presented more extensive clinical and biological symptoms. One of these developed severe peripheral neuropathy and endocrine anomalies during the late phase of his disease, which led us to discuss the relationship between multicentric CD and the POEMS (polyneuropathy, organomegaly, endocrinopathy, M-protein, skin change) syndrome first described in Japan. Three of our patients presented with hypochromic microcytic anemia too severe to be explained by an inflammatory syndrome alone, and was likely due to several mechanisms. The etiology of CD remains unknown. The histological characteristics of angiofollicular lymph node hyperplasia are among the most important criteria for the diagnosis of localized and multicentric forms of CD, which can easily be made on a lymph node biopsy. However, it must be noted that this lesion can also be observed (but only rarely) in HIV (human immunodeficiency virus) - infected patients. The localized form is always considered to be benign, but, to date, there is no formal argument definitively supporting the malignancy of the multicentric one, in spite of its clinical similarity to a lymphoproliferative syndrome.
Since 1970, the types of glomerulopathy encountered in patients with cirrhosis of the liver have been accurately determined. In alcoholic cirrhosis IgA glomerulonephritis is frequent, usually non-proliferative and latent, sometimes membranoproliferative. Defective elimination of circulating immune complexes made up of bacterial or food antigens and IgA antibodies is thought to play a part in the pathogenesis of this type of glomerulonephritis. Extramembranous or membranoproliferative glomerulonephritis, occasionally containing the viral antigen, may complicate post-hepatitis cirrhosis, in which case an antiviral treatment might be effective against the renal disease.