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Biomedical subjects

T Papo

Publications and source records attributed to T Papo.

At least 91 records · Page 5Linked to original sources
PubMed1994

[Pancreatitis in systemic lupus erythematosus. Review of the literature apropos of 5 cases].

We report five cases of pancreatitis in systemic lupus erythematosus. Three patients died. The cause of death was directly related to pancreatitis in two cases. Several causes of pancreatitis may be suspected: vasculitis, thrombosis when associated to antiphospholipid syndrome, biliary calculi, infection, metabolic abnormalities or adverse effects of therapy. About seventy cases of pancreatitis have been reported in systemic lupus erythematosus in the literature Pancreatitis was the inaugural sign of lupus in six cases. In 12 cases, besides lupus, no other cause of pancreatitis was found. However, pancreatic vasculitis or thrombosis was rarely demonstrated even in post-mortem examinations. The role of corticosteroids in pancreatitis in lupus is controversial since the evolution of pancreatitis in lupus is generally good with corticosteroids. We think that diagnosis of pancreatitis in lupus should not implicate discontinuation or decrease of corticosteroids dosage, unless their responsibility is absolutely demonstrated.

Acute Disease↗
PubMed1994

[Are antineutrophil cytoplasmic antibodies pathogenic?].

ANCA mainly recognize proteinase 3 (cytoplasmic fluorescence) in Wegener's granulomatosis and myeloperoxidase (perinuclear fluorescence) in other types of vasculitis. A causative role of ANCA seems not obvious because: a) active generalized Wegener's granulomatosis may exist with no detectable ANCA, b) ANCA titres don't reliably parallel clinical activity and c) of the increasing diversity of clinical situations where ANCA are described. Nevertheless, some lines of evidence point to a pathogenetic role of ANCA, especially in vascular lesions genesis: a) ANCA may prevent inactivation of antigenic proteases by antiproteases, b) translocation at the outer membrane of intracellular antigens make them accessible to ANCA, c) activation of polymorphonuclear leucocytes and increase of their aggregation and cytotoxicity to endothelial cells are specifically induced by ANCA, d) proteinase 3 and myeloperoxidase may adhere to the endothelial cell membrane and then be recognized by ANCA, e) a specific T-lymphocyte response to ANCA antigens could be elicited in Wegener's granulomatosis and f) an in vivo model of ANCA-related glomerulonephritis has recently been established.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed1994

Multiple subungual splinter hemorrhages in the antiphospholipid syndrome: a report of five cases and review of the literature.

Multiple subungual splinter hemorrhages have been initially described as an important sign of subacute endocarditis. Secondly, they were reported in various other conditions, especially in isolated cases of primary antiphospholipid syndrome. We report five patients with multiple fingernail subungual splinter hemorrhages occurring in the course of antiphospholipid syndrome. Antiphospholipid syndrome was secondary to systemic lupus erythematosus in two, to Fasciola hepatica infection in one and was considered as primary in two. In all patients multiple subungual splinter hemorrhages occurred concomitantly with thrombotic events of diverse arterial sites. The mechanism of subungual splinter hemorrhages is most probably thrombotic.

Adult↗
PubMed1994

T lymphocyte subsets in primary antiphospholipid syndrome.

OBJECTIVE: To study T, natural killer (NK) and B blood cell subsets in primary antiphospholipid syndrome (APS). METHODS: We studied 10 patients with primary APS and 12 healthy subjects. Blood lymphocytes counts, proportions of B cells (CD19+), total CD5 and CD5 B cells, NK cells (CD16+CD56+), T cells (CD3+), CD4+ helper (naive CD4+CD45RA+, memory CD4+CD45RO+ and CD4+CD29+, activated CD4+CD25+), CD8 (immunoregulatory CD8+CD57+, activated CD8+HLA-DR+) T cell subsets were measured by flow cytometry analysis. RESULTS: In the primary APS group, we observed a lower total lymphocyte count (p = 0.009), an expansion of naive CD4 cells (p = 0.025), a lower proportion of memory CD4 cells (p = 0.04) and an increased ratio of naive/memory CD4 cells (p = 0.015). CONCLUSION: Blood T cells phenotypes in primary APS differ markedly from healthy controls, indicating that immunologic abnormalities in primary APS might extend beyond autoantibody production.

Adult↗
PubMed1994

[Treatment of pulmonary vasculitis].

Pulmonary vasculitides require major therapeutic regimens which, though symptomatic, are often effective. Corticosteroids have greatly changed the prognosis of most of these vasculitides, particularly polyarteritis nodosa and the Churg and Strauss syndrome. Cyclophosphamide must be added for Wegener's granulomatosis although the route of administration is still under discussion. Plasma exchanges are rarely indicated. Other treatments for Wegener's granulomatosis including combined trimethoprim-sulfamethoxazole in limited forms and methotrexate in sub-acute systemic forms are currently under study. A better understanding of the underlying mechanisms, including the role of antineutrophil cytoplasmic antibodies, and especially the identification of the causative factors will lead to an aetiologic treatment still unknown today.

Adrenal Cortex Hormones↗
PubMed1993

[Intra-alveolar hemorrhage in Wegener's granulomatosis. Retrospective study of 9 cases].

Among 66 patients with Wegener's granulomatosis, 9 had an intra-alveolar haemorrhage which revealed the disease. The diagnosis was based on dyspnoea (n = 9), haemoptysis (n = 9) and anaemia (n = 9) with a mean haemoglobin level of 8 +/- 1 g/dl. Radiology showed bilateral alveolar infiltrates (n = 9), and numerous siderophages were found either in the alveolar lavage fluid (n = 7/7) or in sputum (n = 2). In every case, the alveolar haemorrhage was accompanied by a rapidly progressive extracapillary glomerulonephritis and by lesions of the upper airways which preceded it by several months or years. All patients received corticosteroids combined, in 8 cases, with cyclophosphamide. The respiratory disease improved rapidly, in contrast with the renal disease which became worse (n = 5). Two patients died in the acute phase of the vasculitis: one of acute renal failure, the other of infectious shock.

Adolescent↗
PubMed1993

[Antiphospholipid syndrome. A new cause of bilateral hemorrhage of the adrenal glands. 4 cases].

Four cases of adrenal insufficiency due to bilateral adrenal haemorrhage in patients with antiphospholipid syndrome are reported. The 1st patient had repeated episodes of thrombosis on a background of altered general condition; he was examined by computed tomography (CT) which showed enlarged and presumably tumoral adrenal glands; adrenal insufficiency was present and improved under hormone replacement therapy; the thrombotic episodes were attributed to the antiphospholipid antibodies; after a 5-year follow-up the antiphospholipid syndrome remained alone, and further examinations showed progressive adrenal atrophy. The 2nd patient had systemic lupus erythematosus with thrombocytopenia; because of abdominal pain CT was performed, showing bilateral adrenal enlargement; treatment with intravenous pulses of cyclophosphamide and high-dose immunoglobulins combined with corticosteroids failed, and splenectomy was performed disclosing an old adrenal haematoma which was evacuated. The 3rd patient had bilateral and asymmetrical adrenal hypertrophy at CT; subsequently, systemic lupus erythematosus was diagnosed with anti-prothrombinase and anticardiolipin accounting for the initial findings; follow-up examinations showed the formation of pseudocysts in the adrenals; following myocardial infarction the patient died of cerebral haemorrhage, and autopsy confirmed the presence of old, bilateral adrenal haematomas. The 4th patient had recurrent vein thrombosis associated with distal ischaemia, which prompted CT in search of a neoplasia; this examination revealed 2 large adrenal haematomas while anticardiolipin antibodies were found. In patients with antiphospholipid syndrome any functional or morphological abnormality of the adrenals should prompt a search for bilateral adrenal haemorrhage. Conversely, in all cases of adrenal insufficiency a search for antiphospholipid antibodies should be part of all aetiological investigations, and this search should be carried out prior to withdrawing corticosteroids in cases of systemic lupus erythematosus with antiphospholipid antibodies.

Adrenal Gland Diseases↗
PubMed1993

[Long-term prognosis of arterial lesions of Behçet's disease].

We analyzed the charts of 25 patients with arterial lesion in Behçet's disease with mean follow-up 76 months. We conclude that prognosis is poor. Corticosteroids and surgery if possible is needed, anti-aggregant or anticoagulants and prosthetic rather than venous graft are suitable. This therapy does not exclude the risk of relapse. Immunosuppressive drugs in addition to corticosteroids seem to be more efficient than corticosteroids alone but the therapeutic modalities need to be define.

Adult↗
PubMed1993

Disseminated histoplasmosis with glomerulonephritis mimicking Wegener's granulomatosis.

Renal complications of disseminated histoplasmosis include chronic recurrent abcesses of the interstitium and urogenital tract. To our knowledge, glomerulonephritis has never been reported in histoplasmosis. We describe a case of proven histoplasmosis presenting with oral granulomatous ulceration and segmental glomerulonephritis that mimicked Wegener's granulomatosis (WG). All symptoms and renal parameters remitted under itraconazole treatment alone. In conclusion, glomerulonephritis may complicate the course of chronic disseminated histoplasmosis. Since it can masquerade as WG, systematic tissue staining for intracellular microorganisms should be done when WG is suspected.

Diagnosis, Differential↗