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Biomedical subjects

D Sicard

Publications and source records attributed to D Sicard.

At least 91 records · Page 5Linked to original sources
PubMed1995

[Cerebral infarction in human immunodeficiency virus infection].

Patients infected with the human immunodeficiency virus (HIV) appear to have a high risk of ischaemic cerebral events. We observed two cases of cerebral infarction in patients with acquired immune deficiency syndrome (AIDS). In the first case, a 38-year-old homosexual with no cardiovascular risk other than smoking presented with rapidly progressive hemiparesia. Brain CT-scan visualized two infarcts in the territory of the right sylvian artery and the arteriography an occlusion of the internal carotid artery. In the second, a 37-year-old homosexual, hospitalization was required for a left-sided pure sensitive epilepsy seizure. There was no cardiovascular risk other than smoking. Magnetic resonance imaging showed parietal ischaemia and thrombus in the left atrium without atrial hypertrophy was seen at transoesophageal echocardiography. In both cases, there was no evidence of endocarditis, dissection of the neck vessels or disseminated intravascular coagulation nor of associated viral or bacterial infectious complication of AIDS. Angiographic findings eliminated cerebral vascularitis. Among the perturbed haemostasis factors previously reported in HIV+ patients, we observed free proteins S deficiency (68 and 43%) and heparin cofactor II deficiency (54 and 40%). Serum albumin was 33 and 32 g/l respectively. Outcome was favourable in both cases with anticoagulant therapy. These coagulation anomalies would not appear sufficient to explain cerebral infarction. Other mechanisms including immune complexed deposition, direct HIV toxicity for endothelial cells or the effect of cytokines on smooth muscles fibres and fibroblasts are probably more important causal factors.

Acquired Immunodeficiency Syndrome↗
PubMed1995

[Cutaneous ulcerations in sarcoidosis].

We report the case of a 23 year-old Caribbean woman with sarcoidosis who developed specific skin ulcerations. Ulcerative lesions in sarcoidosis are distinctly unusual, generally multiple, painless, with preponderant location on the lower limbs. The diagnosis is difficult. The pathogenesis is discussed. The most successful therapy is hydrochloroquine with corticosteroids.

Adult↗
PubMed1995

Safety and immunogenicity of a recombinant HIV type 1 glycoprotein 160 boosted by a V3 synthetic peptide in HIV-negative volunteers.

The safety and the immunogenicity of a recombinant hybrid envelope glycoprotein MN/LAI (rgp160) followed by booster injections of a V3 (MN) linear peptide were evaluated in HIV-negative adults at low risk for HIV infection. Volunteers received either rgp160 in alum at 0, 1, and 6 months (group A), rgp160 at 0 and 1 months followed by V3 at 3 and 6 months formulated in alum (group B), or in Freund's incomplete adjuvant (FIA) (group C). Local and systemic reactions were mild to moderate and resolved within the first 72 hr after immunization. No significant biological changes (routine tests and autoantibodies) were observed. One month after the last injection in either group, neutralizing antibodies (NAs) against the HIV-1 MN isolate were detected in 4 of 5 (A), 7 of 10 (B), and 10 of 10 (C) subjects with significantly higher geometric mean titers in the latter group. Four of nine sera with the highest NA titers against MN weakly cross-neutralized the HIV-1 SF2 isolate; none had NA against the HIV-1 LAI strain or against a North American primary isolate. Specific lymphocyte T cell proliferation to rgp160 was detected in 92% of the subjects after the second injection of rgp160 and in 80% of them 12 months after the first injection. A weak and short-lived envelope-specific CD(4+)-mediated cytotoxic lymphocyte activity was detected at certain time points in few subjects. This prime-boost vaccine approach using rgp160 followed by a V3 peptide was safe in humans, and was able to elicit high levels of neutralizing antibodies and a strong and persistent T cell lymphoproliferative response to rgp160 and to V3. However, the neutralization response was restricted to the homologous HIV-1 strain and little env-specific cytotoxic activity was induced.

AIDS Vaccines↗
PubMed1995

Polymyositis associated with Ki-1 lymphoma.

We report here a case of acute polymyositis associated with a Ki-1 non-Hodgkin's lymphoma (NHL). This anaplastic large cell malignant lymphoma was a primary T-cell NHL lymphoma of the bone marrow. The malignant cells expressed the CD30 (Ki-1), CD3, and CD4 antigens, the beta chain of the interleukin 2 receptor (CD25), and the betaF1 antigen (alpha/beta T-cell receptor). Chemotherapy and high dose methylprednisolone pulse therapy were initiated. However, no clinical improvement was noticed, because the patient rapidly died of an acute respiratory distress syndrome. To our best knowledge, this represents the first case of Ki-1 lymphoma associated with Polymyositis.

Acute Disease↗
PubMed1995

Fibrin polymerization defect in HIV-infected patients--evidence for a critical role of albumin in the prolongation of thrombin and reptilase clotting times.

Thrombin clotting time (TCT) and reptilase clotting time (RCT) were found significantly prolonged in a series of 72 HIV-infected patients drawn for routine coagulation testing. Both TCT and RCT were highly significantly correlated with albumin (r = -0.64, and r = -0.73 respectively, p < 0.0001). TCT and RCT were significantly higher (p < 0.0001) in a series of 30 other HIV-infected patients selected on their albumin level below 30.0 g/l (group 1) than in 30 HIV-infected patients with albumin level above 40.0 g/l or in 30 HIV-negative controls; the two latter groups were not different. In vitro supplementation of plasma from group 1 patients with purified human albumin up to 45.0 g/l (final concentration) lead to a dramatic shortening effect on both TCT and RCT, which reached normal values. The TCT and RCT of the purified fibrinogen solutions (2.0 g/l final concentration) were not different in the three groups, and normal polymerization curves were obtained in all cases. This further ruled out the presence of any dysfibrinogenemia in the plasma from group 1 patients. Using purified proteins, highly significant correlations were demonstrated between the albumin concentration and the prolongations of both TCT and RCT, which were of the same magnitude order than those found in the patients plasma. These results suggest that hypoalbuminemia is responsible for the acquired fibrin polymerization defect reported in HIV-infected patients. The pathophysiological defect reported in HIV-infected patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗