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Biomedical subjects

B Godeau

Publications and source records attributed to B Godeau.

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

Rabies encephalitis in a patient with AIDS: a clinicopathological study.

A 46-year-old man was bitten by a dog in Mali; anti-rabies vaccination was incomplete. Three months later he was admitted to hospital with fever and diarrhea. Human immunodeficiency virus (HIV) serology was positive and CD4 count was 70/mm3. His status worsened rapidly with confusion hydrophobia and hypersialorrhea. Despite anti-rabies serotherapy and vaccination, he died suddenly 12 days after admission. Immunofluorescence on cerebral tissue samples established rabies encephalitis. Neuropathology showed mild encephalitis with occasional Babès nodules and rare perivascular mononuclear cuffs. Intraneuronal Negri inclusion bodies were remarkably diffuse and abundant. They were clearly demonstrated by immunocytochemistry and electron microscopy. Apoptotic neurons were identified in the brain stem and hippocampus in the vicinity of inflammatory foci. In contrast, apoptosis could not be demonstrated in non-inflammatory areas, even where Negri bodies were numerous. There was no associated HIV encephalitis or opportunistic infection. The occurrence of rabies encephalitis in AIDS represents a random association, but is probably not exceptional as rabies is endemic in many countries and the AIDS epidemic is spreading worldwide. In this case, although the incubation duration and clinical presentation were comparable to those in classical rabies the T-cell-mediated immunosuppression may account for the weak inflammatory reaction and unusually abundant viral multiplication. This observation confirms that all those at risk for rabies, particularly immunocompromised patients, should receive complete anti-rabies treatment including vaccines and specific immunoglobulins, as soon as possible after infection.

Acquired Immunodeficiency Syndrome↗
PubMed1996

[Treatment of autoimmune thrombopenic purpura in adults].

Autoimmune thrombocytopenic purpura (AITP) is a common hematological problem. Steroids are the usual first-line treatment but give long-term remission in less than 20% of adults. High doses of human intravenous immunoglobulin G (IVIg) can increase the platelet count in 70 to 80% of patients, but the treatment is expensive and the platelet response usually only transient. Seventy to 80% of the adults have the chronic form of AITP (ie, disease duration of more than 6 months) that only improves on specific treatment. Splenoctomy is the treatment of choice when thrombocytopenia is severe and/or associated with life threatening bleeding, as it cures 60-80% of patients. The best treatment for patients with severe chronic AITP in whom splenectomy is ineffective or contra-indicated is a difficult challenge. In this situation, spontaneous remission is rare and 5% of patients will die from hemmorrhage. However, the treatments so far proposed in refractory chronic AITP (danazol, vinca alcaloids, azathioprine, cyclophosphamide, dapsone, etc) are inconsistently and transiently effective. The aim of the treatments in AITP are thus different in the acute and chronic forms of the disease. In the acute phase, the treatment should quickly increase the platelet count, even if the effect in transient, and aggressive treatments (ie, splenectomy, immunosuppressive drugs) must be avoided since spontaneous remission is possible. On the contrary, splenectomy is the treatment of choice for chronic AITP since it obtains complete persistent recovery in nearly 80% of patients. In the case of unsuccessfullness, treatments should then be administered with the aim to maintain a "safe" platelet count (> 20 to 30 x 10(9)/L).

Acute Disease↗
PubMed1996

Fusidic acid induced acute immunologic thrombocytopenia.

Fusidic acid is used in hospitals as second-line therapy for multidrug-resistant staphylococcal infections. We report the first fully documented case of fusidic acid induced thrombocytopenia, in a 48-year-old patient. The thrombocytopenia was abrupt and severe but resolved spontaneously 7 d after drug withdrawal. The thrombocytopenia transiently relapsed 6 d later, when fusidic acid was reintroduced. Haemorrhagic signs were observed, but no severe bleeding occurred. Platelet transfusions failed to increase the platelet count. We detected an IgG platelet antibody in the patient's serum, that specifically recognized platelet glycoprotein IIb/IIIa only in the presence of fusidic acid. Fusidic acid induced thrombocytopenia should be considered as a possible cause for the thrombocytopenia frequently seen in the intensive care setting.

Acute Disease↗
PubMed1996

Treatment of chronic autoimmune thrombocytopenic purpura with monoclonal anti-D.

BACKGROUND: The platelet count increases transiently after treatment with polyclonal anti-D in about 50 percent of D+ patients with autoimmune thrombocytopenic purpura (AITP). The effect is usually attributed to macrophage Fc-receptor blockade by antibody-coated red cells. As polyclonal anti-D is in limited supply, prospective testing was performed on a monoclonal anti-D (MoAb D) in such patients. STUDY DESIGN AND METHODS: Seven D+ patients with chronic AITP received MoAb D intravenously at doses of 47 to 95 microg per kg of body weight. Response was assessed by studying platelet count increment. Hemolysis and red cell-bound MoAb D were measured before and after MoAb D administration. RESULTS: MoAb D red cell binding was demonstrated in all patients at a ratio higher than that observed in AITP patients successfully treated with polyclonal anti-D. However, little or no platelet count increment was observed in six patients, while a transient response was observed in only one (platelet count 97 x 10(9)/L before MoAb D infusion and 163 x 10(9)/L 4 days later). Furthermore, because five patients showed signs of hemolysis and two became anemic, higher doses of MoAb D should be used only with caution in patients with AITP. CONCLUSION: The MoAb D used in this study cannot be proposed as an alternative treatment for patients with AITP.

Antibodies, Monoclonal↗
PubMed1996

Acute arterial obliteration: a new feature of the POEMS syndrome?

The POEMS (polyneuropathy, organomegaly, endocrinopathy, monoclonal gammapathy, and skin changes) syndrome is a rare variant of plasma cell dyscrasia with multisystemic manifestations. We present 4 cases with arterial symptoms typical of acute arterial obliteration (AAO) and review 9 similar cases in the literature. The clinical course of AAO was unusual and particularly severe when affecting the lower limbs; recurrent events required amputations. As demonstrated by angiographic and histologic studies, thrombotic and atheromatous lesions were the main pathologic features of AAO. Atherosclerotic risk factors were absent or moderate in 3 of our cases, and no cause of thrombosis other than the POEMS syndrome was found. A high production of cytokines was found in all cases, with elevated serum levels of interleukin-1 beta (9/9 samples), interleukin-6 (7/9 samples), and tumor necrosis factor-alpha (6/9 samples). We suggest that arterial manifestations should be added to the spectrum of manifestations of the POEMS syndrome. Cytokines may mediate the POEMS syndrome-associated AAO, as previously proposed for the other systemic manifestations of this disorder.

Acute Disease↗
PubMed1996

Bronchoalveolar lavage in adult sickle cell patients with acute chest syndrome: value for diagnostic assessment of fat embolism.

Fat embolism of necrotic bone marrow could be a frequent cause of acute chest syndrome (ACS) in sickle cell syndromes (SC), as suggested by postmortem findings. To check this hypothesis in living patients, we evaluated the presence of fatty macrophages recovered by bronchoalveolar lavage (BAL) in ACS. We investigated 20 consecutive cases of ACS by BAL, and identification of alveolar cells containing fat droplets was performed using oil red O (ORO), a specific neutral fat stain. The specificity of the method was determined on control groups, including eight SC patients without acute chest syndrome and 15 non-SC patients. A cut-off of > 5% of alveolar macrophages containing fat droplets was determined from the control groups to assess the diagnosis of fat embolism. In 12 ACS episodes, BAL exhibited > 5% of fatty macrophages, ranging from 10% to 100% (median value 46.5%). In 11 cases, fat embolism was associated with proven (n = 8) or probable (n = 3) bone marrow infraction, which mostly predated ACS. Eight ACS episodes were associated with a low percentage (< or = 5%) of fatty alveolar macrophages and could be related to a cause other than fat embolism in six episodes, such as sepsis, in-situ thrombosis, or rib infarcts generating hypoventilation. This study supports the diagnostic yield of BAL for fat embolism, which can be incriminated in 60% of cases of ACS in this adult population.

Adolescent↗
PubMed1996

Prolonged remission of SLE-associated polyradiculoneuropathy after a single course of intravenous immunoglobulin.

Polyradiculoneuropathy is a rare and potentially severe complication of systemic lupus erythematosus (SLE). Treatment is not codified and response to corticosteroid is inconstant. We report the case of a patient with severe SLE-associated polyradiculoneuropathy and autoimmune thrombocytopenia. Dramatic neurologic improvement and correction of thrombocytopenia were observed after a single course of high-dose intravenous immunoglobulin infusions (IVIg, 2g/kg body weight). Our case suggests that IVIg may be effective in the treatment of this unusual condition.

Aged↗
PubMed1995

High-dose methylprednisolone is an alternative treatment for adults with autoimmune thrombocytopenic purpura refractory to intravenous immunoglobulins and oral corticosteroids.

Eight patients with severe chronic autoimmune thrombocytopenic purpura (AITP) refractory to high-dose intravenous immunoglobulin (IVIgG) and/or oral prednisone were treated with one to three infusions of high-dose methylprednisolone (HDMP) (15 mg/kg/day). The mean platelet count before treatment was 12 +/- 10 x 10(9)/L. HDMP therapy led to a safe platelet count (> 50 x 10(9)/L) after 2-5 days in five patients, and a minimal platelet increase (34 x 10(9)/L) able to stop bleeding in a sixth patient. The effect of HDMP was, however, transient in four of five responders. No side effects were observed, even in the four patients older than 70 years. HDMP thus appears to be a good alternative in emergency situations or prior to surgery for patients with AITP refractory to conventional therapy.

Administration, Oral↗
PubMed1995

Posttransfusion purpura-like syndrome associated with CD36 (Naka) isoimmunization.

BACKGROUND: CD36 deficiency, which could lead to CD36 isoimmunization, has been reported in the Japanese population. CD36 isoantibody has been involved in platelet transfusion refractoriness. CASE REPORT: A 50-year-old woman originally from Corsica developed severe acute thrombocytopenia after massive transfusion. She was found to be CD36 deficient, and platelet immunoassays revealed a CD36 (Naka) platelet isoantibody. Although the involvement of another mechanism could not be entirely ruled out, the thrombocytopenia was attributed to posttransfusion purpura-like syndrome. The antibody was also involved in platelet transfusion refractoriness. CD36 deficiency was present in two members of the patient's family as well. Flow cytometry studies demonstrated the absence of CD36 expression on the surface of blood monocytes and cultured erythroblasts and megakaryocytes from one of the two CD36-deficient family members studied, but, in the absence of previous immunization, these CD36-deficient patients were not isoimmunized. In contrast, CD36 deficiency was not found in a population of 808 healthy blood donors in the Paris, France, area. CONCLUSION: CD36 isoantibody might be involved in some cases of posttransfusion purpura and platelet transfusion refractoriness. These findings also confirm the extremely low frequency of CD36 deficiency among whites.

Blood Platelets↗