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M Hamidou

Publications and source records attributed to M Hamidou.

At least 55 records · Page 3Linked to original sources
PubMed1996

[Thrombotic microangiopathies in HIV infection: 4 cases].

Thrombotic microangiopathy (TMA) has been rarely described in HIV-infected patients. We report four cases of TMA during HIV infection and we analyse clinical, biological, etiologic, therapeutic and evolutive aspects of these four cases. Initial symptomatology is non specific and diagnosis is often delayed. Peripheric thrombopenia with haemolytic anemia and renal failure must be suggestive of the diagnosis. TMA can be present at any stage of HIV infection. Physiopathological mechanism of TMA during HIV infection remains unclear. These cases lead to suspect the role of opportunistic infections, neoplasia or HIV directly by endothelial injury or indirectly by cytokines secretion. Therapy of TMA is not different from non-HIV patients. Improvement with treatment must be obtained but long-term prognosis remains poor in account of HIV infection.

Adult↗
PubMed1996

[Hemophagocytic syndromes. A series of 23 cases].

Inappropriate macrophage activation is responsible for clinical, biological and histological features characterized by diffuse non malignant histiocytic tissue infiltration called "reactive hemophagocytic syndrome" (RHS). We report here 23 new cases. Immunodepression (10 cases), hematologic malignancies (13 cases) and infection (10 cases) are the most favorable conditions associated with RHS. In many cases, several conditions were present at time of diagnosis of RHS and increased its severity. Mechanisms of RHS remains unclear, but cytokine may play a role. Outcome is variable, but death is the most common issue (17 deaths in our series related to RHS). Corticosteroids, etoposide can improve some situations. Further study is needed to establish the role of cyclosporine A or allogenic bone marrow transplantation.

Adolescent↗
PubMed1996

[Pregnancy in primary antiphospholipid syndrome. Proposal for a common management protocol].

OBJECTIVE: Primary antiphospholipid syndrome (APS) is by definition associated with high obstetric risk. We performed a retrospective study of pregnancies in women with this syndrome in an attempt to define a common means of caring these patients. STUDY DESIGN: Women with APS followed in Internal Medicine Department and in Gynecology Department since 1989 were studied retrospectively. RESULTS: Fifteen women with primary APS had a total of 51 pregnancies, 39 (76%) of which ended in embryonic (n = 24) or fetal (n = 15) loss. Only 6/39 untreated pregnancies led to a live birth, including 2 cases of intrauterine growth retardation. Among the 12 pregnancies treated preventively for obstetric complications, 6 led to a live birth. The treatments used were dissimilar and included aspirin, corticosteroids and heparin, either alone or in association. Four of these 6 live births were obtained by aspirin alone. Gravidic toxemia was observed in one untreated patient. CONCLUSION: The obstetric prognosis for untreated APS is appalling. The benefit of heparin therapy in association with aspirin remains to be demonstrated, ideally in a protocol comparing aspirin alone with aspirin and heparin.

Adrenal Cortex Hormones↗
PubMed1995

[Clinical and bacteriological aspects of nocardiasis. 9 cases].

OBJECTIVES: Nocardial infection is usually localized in the immunocompetent patient and occurs as an opportunistic disseminated infection in about half of the cases in immunoincompetents patients. METHODS: We report a retrospective assessment of 9 cases of nocardial infection diagnosed between January 1991 and February 1994. RESULTS: Six of the patients were immunodepressed: 3 had a disseminated infection with pulmonary (n = 2), brain (n = 2), skin (n = 3) and/or ocular (n = 1) localizations. There were 3 immunocompetent patients with an isolated local infection: skin and bone mycetoma, knee joint and lung. Diagnosis was made on samples obtained invasively in 7 patients. Nocardia asteroides was isolated in 5 patients, N. farcinica in 3 and N. caviae in 1. These organisms showed in vitro sensitivity to amoxicillin-clavulanic acid 5/9, cefotaxime 5/9 (0/3 for N. farcinica), imipeneme 7/9, amikacin 8/8, minocyclin 5/8, pefloxacin 0/8 and trimethoprime-sulfamethoxazol (TMP-SMX) 3/9. Clinical outcome was favourable in all cases and was not always correlated with laboratory sensitivity. CONCLUSION: TMP-SMX remains the reference antibiotic. For one patient, only TMP-SMX (resistant in vitro) was effective; with all the other antibiotic tried (sensitive in vivo) treatment failed.

Adult↗
PubMed1994

[Neutropenia caused by acenocoumarol associated with hairy cell leukemia].

We report the case of a woman splenectomized to treat her hairy cell leukemia (at the moment in remission) 11 years before the detection of neutropenia. The neutropenia began just after the treatment of pulmonary embolism by acenocoumarol. The neutropenia disappeared quickly after substitution of acenocoumarol by fluindione. We discuss the attribution of the neutropenia to acenocoumarol and the part played by hairy cell leukemia.

Acenocoumarol↗
PubMed1993

[Bone marrow necrosis in malignant hemopathies. 7 cases].

The authors report 7 cases of bone marrow necrosis during hematological malignant diseases:3 leukemia, 4 lymphoid malignancies. The main clinical features were bone pain and fever. The bone marrow aspiration and/or biopsy allow diagnosis. The prognosis was in all cases very poor.

Bone Marrow↗
PubMed1993

Alpha 1-antitrypsin genetic polymorphism in ANCA-positive systemic vasculitis.

Alpha 1-antitrypsin (alpha 1-AT) is the major inhibitor of proteinase 3 (PR3), the main target antigen of antineutrophil cytoplasm antibodies (ANCA) in Wegener's granulomatosis. alpha 1-AT is encoded by a polymorphic gene, with over 75 alleles, defining severely, medium and non-deficient protease inhibitor (PI) phenotypes. We describe the association of severely and medium deficient PI phenotypes with anti-PR3 positive systemic vasculitis, and postulate a pathogenetic role for alpha 1-AT deficiency and the occurrence of ANCA, with specificity for PR3 in a subgroup of patients with Wegener's granulomatosis.

Adult↗