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Biomedical subjects

L Swiader

Publications and source records attributed to L Swiader.

At least 55 records · Page 3Linked to original sources

Acute transverse myelitis and primary urticarial vasculitis.

We report the case of a 56-year-old man with severe normocomplementaemic primary urticarial vasculitis for 16 years. Nine and 11 years after the onset of the symptoms, he developed two severe neurological complications, seizure and transverse myelitis, that must be attributed to the vasculitis. Transverse myelitis has been reported in other systemic diseases, particularly lupus erythematosus, but this is the first case of transverse myelitis complicating urticarial vasculitis.

Acute Disease↗

[Pseudo-Glanzmann thrombasthenia in the course of autoimmune thrombocytopenic purpura].

INTRODUCTION: Auto-immune thrombocytopenic purpura is associated with platelet anti-glycoprotein antibodies, particularly with anti-GPIIb/IIIa complex. Persistence of these antibodies sometimes leads to acquired auto-immune thrombopathy. EXEGESIS: We report the case of a woman treated by splenectomy for auto-immune thrombocytopenic purpura, who developed 5 years later an ecchymotic syndrome despite normal platelet count. High bleeding time and platelet aggregation defect in vitro were evidenced. Following the initial thrombocytopenia, anti-glycoproteins GPIIb/IIIa with lupus anticoagulant and benign monoclonal gammapathy were noticed. Platelet controls showed that hypoaggregant activity was secondary to the persistence of anti-GPIIb/IIa antibodies. CONCLUSION: This acquired auto-immune thrombopathy simulating Glanzmann's thrombasthenia was secondary to the persistence of platelet anti-glycoproteins GPIIb/IIIa.

Aged↗

[Diagnostic approach to hypereosinophilia].

Blood hypereosinophilia is a common finding in medical practice requiring further investigation. There are a wide range of potential causes including atopic disorder, drug allergy, parasitic infection, certain forms of immune deficiency, inflammatory process, hemopathy, and malignant disease. Diagnosis of persistent hypereosinophilia not associated with parasitic infection is one of the major diagnostic dilemmas in medicine. If through investigation fails to achieve diagnosis, idiopathic hypereosinophilia may be suspected including the possibility of essential hypereosinophilic syndrome or Chusid syndrome. The primary determination for diagnosis of hypereosinophilia involves the presence or absence of parasitic infection. If parasitic infection is ruled out, it is often difficult to distinguish benign, self-limiting forms from severe forms requiring careful surveillance and subsequent treatment. From a pathophysiological standpoint, one may ask if some eosinophilic conditions are not due to deregulation of immunologic mechanisms that normally protect the organism against parasitic infection.

Diagnosis, Differential↗

[Occlusion of the central retinal vein after vaccination against viral hepatitis B with recombinant vaccines. 4 cases].

OBJECTIVES: Hepatitis B vaccination has been proven to be effective and well-tolerated. Certain neurological, ocular or systemic complications have, however, been reported to be induced by the vaccine. Clinicians should be aware of exceptional ocular complications. CLINICAL REPORT: Four patients under 50 years of age developed occlusion of the central vein of the retina after vaccination with recombinant hepatitis B vaccine. None of the classical causes of occlusion of the central vein of the retina could be evidenced. DISCUSSION: Several pathophysiological hypotheses have been proposed to explain these ocular manifestations after vaccination: role of immunocomplexes, antigenic cross-reactions, role of immediate hypersensitivity, simulation of a pathogenic lymphocyte repertoire. None of these hypotheses is entirely satisfactory. It is important however to emphasize the need for a complete general evaluation, including an ophthalmological examination in the presence of unexplained ocular manifestations following hepatitis B vaccination.

Adult↗

Crohn's disease and gastrocnemius vasculitis: two new cases.

We report two cases of gastrocnemius muscle vasculitis revealing Crohn's disease. Gastrocnemius muscle biopsy evidenced a necrotizing vasculitis resembling panarteritis nodosa in one case; a nonnecrotizing vasculitis was found in the other case. Neither of the patients had systemic vasculitic involvement, and the muscle disease resembled calf muscle-located panarteritis nodosa. Our literature review shows five cases of calf-located myalgia occurring during Crohn's disease characterized by heterogenous histopathological findings including vasculitic and myositic lesions. Thus, faced with calf-located myalgia with vasculitis or myositis, a search for Crohn's disease is probably necessary to determine precisely the frequency and the etiopathogenic mechanisms of this association.

Adult↗

Cutaneous panniculitis and relapsing polychondritis: two cases.

We report 2 uncommon cases of skin panniculitis (Pa) occurring during the course of relapsing polychondritis (RP). Skin histological findings were characterized by septal and lobular involvement associated with vasculitis. Chondritis and Pa lesions both regressed with steroid therapy and showed parallel clinical courses. To our knowledge, this type of cutaneous involvement has never been reported in RP.

Adult↗

[Anetoderma during antiphospholipid syndrome. 3 cases].

INTRODUCTION: Anetoderma is a skin disease of unknown etiology sometimes encountered in patients with a lupus syndrome. We report a clinical and pathology analysis of 3 selected cases of anetoderma associated with systemic lupus erythematosus and/or antiphospholipid syndrome. CASE REPORTS: Three patients had skin lesions typical of anetoderma. Antiphospholipid antibodies were present in all three (anticardiolipin in 3, circulating lupus anticoagulants in 3, anti-beta 2GP1 in 2). One patient with systemic lupus erythematosus had signs of antiphospholipid syndrome, the two others had primary antiphospholipid syndrome. DISCUSSION: The analysis of our cases and a review of the literature suggest that anetoderma is a disease which develops in the immunological environment of lupus, and is apparently more related to the presence of antiphospholipids than lupus itself. Thus anetoderma could be another cutaneous sign of the antiphospholipid syndrome.

Adult↗