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Biomedical subjects

A Schattner

Publications and source records attributed to A Schattner.

At least 127 records · Page 7Linked to original sources
PubMed1989

Ameboma presenting as acute urinary retention.

A patient with several weeks of diarrhea developed for the first time severe urinary frequency and urgency and was admitted with acute urinary retention. Imaging techniques showed a large mass compressing the posterior wall of the bladder adjacent to the rectosigmoid colon, leading to a bilateral dilatation of the ureters. Cystoscopy and biopsy of the affected part of the bladder showed no tumor but a nonspecific acute inflammation. After identification of trophozoites of Entamoeba histolytica in the stool and confirmation by colonoscopy, barium enema, and serology of acute amebic colitis, the patient was treated with metronidazole. Urinary symptoms immediately resolved with a complete disappearance of the mass and a later cure of the colitis. This is a first report of severe urinary symptomatology dominating the clinical picture in amebic colitis, due to compression of the urinary bladder by an ameboma.

Adult↗
PubMed1988

Tumor necrosis factor in middle ear effusions.

The presence of tumor necrosis factor (TNF) was determined in middle ear effusions from 27 ears of children with chronic otitis media with effusion. Cytotoxic activity was assessed by quantitation of target (HeLa) cell death after incubation with the aspirate. Moderate cytotoxic activity was found in 17 of 27 samples (mean cell death of 53% and 32% at 1:2 and 1:4 dilutions, respectively). In ten (37%) of the middle ear effusion aspirates no cytotoxic activity was detected. To confirm that cytotoxicity was due to TNF, 13 of the samples with cytotoxic activity were incubated with a monoclonal anti-TNF antibody and retested. Cytotoxicity was blocked by the anti-TNF antibodies in all cases. Tumor necrosis factor, derived most probably from macrophages or mast cells in the middle ear, may mediate various pathologic processes associated with otitis media, such as generation of mucoid effusion, fibroblast proliferation, and bone resorption.

Child↗
PubMed1988

Interferons and autoimmunity.

Autoimmunity can be accelerated in several genetically prone murine models and can even be induced in normal mice by treatment with interferon (IFN) or IFN-inducers. Several cases of IFN-induced autoimmune disease in humans also have been observed; however, more striking is the fact that some of the clinical manifestations in autoimmune diseases and many of the immunological aberrations can be mediated or enhanced by IFN. The finding of high levels of circulating IFN in many patients may be highly significant in that respect, and the characterization of the predominant type of IFN as an unusual acid-labile IFN-alpha may indicate an infectious etiologic agent in autoimmunity, since this peculiar IFN was mostly associated with viral infections in vivo or in vitro. The induction of MHC class II antigens on previously HLA-DR or Ia negative cells appears to be caused primarily by IFN-gamma and may have a central role in the pathogenesis of autoimmunity in susceptible individuals. Such aberrant HLA-DR expression on nonlymphoid cells can be detected early in the disease in the target organs of many varied autoimmune conditions and may trigger a cascade of self-directed, uncontrolled immune response in conjunction with other factors.

Animals↗
PubMed1988

Lymphokines in autoimmunity--roles of interferons in systemic lupus erythematosus and other autoimmune disorders.

All healthy subjects have the capacity to produce autoantibodies markedly similar to those seen in autoimmune disease. This capacity may be activated by viruses, through the release of IFN or other mechanisms. Autoimmune disease can be induced or enhanced by interferons in mice and in humans. Circulating IFNs are very frequent in patients with autoimmune diseases and may participate in the mediation of several clinical and immunologic manifestations. IFN-induced aberrant HLA-DR expression is common on epithelial cells of target organs of many autoimmune diseases; it may present autoantigen to T-cells and initiate a cycle of self-perpetuating autoimmunity. Interaction of IFN with other lymphokines (TNF, interleukin 1, etc.) may contribute to disease development. Further understanding of the role of lymphokines in autoimmunity may provide the basis for specific therapy in the future.

Animals↗
PubMed1988

Severe reversible interstitial pneumonitis induced by low dose methotrexate: report of a case and review of the literature.

A patient treated with 7.5 mg methotrexate/week (MTX) for rheumatoid arthritis (total dose 300 mg) developed high fever, dry cough and progressive dyspnea and hypoxemia due to a severe interstitial pneumonitis. MTX was discontinued and an infectious etiology was ruled out by cultures, serology and lung biopsy. Corticosteroids administered intravenously in high dose led to a dramatic improvement and a complete amelioration of all symptoms and signs. Pulmonary toxicity is a rare adverse effect of low dose MTX therapy and a review of the literature reveals 6 additional cases. Since MTX induced pneumonitis is a potentially fatal, yet completely reversible, disease, attention should be paid to even mild early respiratory symptoms in patients treated with low dose MTX and patient monitoring should include pulmonary function tests.

Adrenal Cortex Hormones↗
PubMed1987

Interferons: cytokines in autoimmunity.

The presence of circulating interferons in the blood of patients with autoimmune diseases and the acquired immune deficiency syndrome (AIDS) raises the question of their possible pathogenetic or defence functions. Interferons control levels of HLA class I and II antigens on cells and can activate or inhibit immune killer cell activities. Tumour necrosis factors (TNF) and interleukin 1 induce a new autocrine species of interferon known as IFN-beta-2 whose gene has been cloned, sequenced and expressed. This IFN mediates the increase in HLA expression caused by TNF as well as the antiviral activity of this cytotoxin.

Autoimmune Diseases↗
PubMed1987

Anti-platelet and anti-DNA IgM in Waldenström macroglobulinemia and ITP.

We describe a monoclonal IgM that was purified from the serum of a patient with Waldenström macroglobulinemia and thrombocytopenia. The binding and idiotypic characteristics of the patient's macroglobulin were similar to those of a human monoclonal IgM secreted by a hybridoma established from peripheral blood lymphocytes of a patient with systemic lupus erythematosus and immune thrombocytopenia. In the absence of other causes for thrombocytopenia in this patient, our results suggest an autoimmune mechanism for destruction of platelets by the monoclonal IgM. This is the first report of a Waldenström macroglobulinemia with anti-platelet activity of monoclonal IgM. Although the study involves a single patient, the results suggest that there may be a common origin for autoantibodies in autoimmune diseases and monoclonal immunoglobulins having autoantibody activity in monoclonal gammopathies.

Aged↗
PubMed1987

Anti-DNA antibody idiotypes in primary biliary cirrhosis.

A significant increase in 16/6 Id--a major cross-reactive idiotype of anti-DNA antibodies (Ab) derived from a patient with systemic lupus erythematosus (SLE) and hitherto identified in SLE patients and their relatives, was found in 16/17 patients with primary biliary cirrhosis (PBC). The increased serum level of Ab with the 16/6 idiotype (16/6 Id) in PBC patients (median 50 ng/ml) was not found in 6/7 of the patients' spouses nor among 27/28 healthy controls or most patients with other types of cirrhosis. The quantity of 16/6 Id was not correlated to either the stage of disease or the presence of antimitochondrial, antinuclear, or anti-dsDNA antibodies. However, 16/6 Id could be shown to be associated with anti-ssDNA antibodies. The high frequency of the lupus-derived 16/6 Id in PBC may accompany the polyclonal B-cell activation seen in that disease. Of 14 healthy first-degree relatives of the PBC patients, 4 (29%) also had elevated serum 16/6 Id (20-25 ng/ml) and the cluster of 3 of them in a single family may indicate a genetic predisposition to develop PBC.

Adult↗