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Biomedical subjects

H Gur

Publications and source records attributed to H Gur.

69 records · Page 4Linked to original sources
PubMed1986

Acute poststreptococcal polymyalgia.

Three patients developed severe incapacitating diffuse pain and tenderness of the skeletal muscles after acute streptococcal infection. There was no evidence of concomitant arthritis, glomerulonephritis, or inflammatory muscle disease in any of the cases. All patients responded promptly to anti-inflammatory therapy. Severe myalgia should be considered an additional complication of immunologically mediated poststreptococcal response.

Acute Disease↗
PubMed1985

Primary fibroxanthosarcoma of the kidney presenting as fever of unknown origin.

Fibroxanthosarcoma is a tumor of soft tissues, mainly effecting the extremities, mediastinum and retroperitoneum. Primary fibroxanthosarcoma of the kidney is extremely rare and has been described in only 4 cases in the past. We present an additional patient, presenting with continuous spiking fever, with rapid deterioration of her condition due to widespread metastases and death within 4 months.

Female↗
PubMed1984

Transient electrocardiographic changes during two episodes of relapsing brucellosis.

Cardiac involvement in the course of acute brucellosis is rare and, when present, is usually manifested by endocarditis. Myocarditis is very infrequent and in the few reported cases, the course of the disease was fulminant. A patient with recurrent brucellosis who presented transient electrocardiographic T wave changes during two episodes of acute illness is reported. It is suggested that the patient had minor asymptomatic myocarditis in the course of recurrent brucellosis.

Acute Disease↗
PubMed1984

Disseminated mycobacterial disease caused by Mycobacterium szulgai.

Disseminated mycobacterial disease due to Mycobacterium szulgai occurred in a previously healthy young man. The clinical picture included fever, mediastinal and generalized lymphadenopathy, hemoptysis, and skin lesions but was dominated by progressive multifocal osteomyelitis. Immunological studies revealed a decrease in T-lymphocyte reaction to mitogens, but this was tested late in the course of the disease and may have been secondary. In spite of repeated surgical drainage and treatment with multiple antituberculous drugs for a period of two years, new lesions continue to appear mainly in the bones. Mycobacterium szulgai was isolated from 28 bone specimens, as well as from skin lesions and sputum. To the best of our knowledge, this is the first report of disseminated disease due to this organism.

Adolescent↗
PubMedDate not supplied

Superantigens and experimental SLE induced by idiotypic dysregulation.

OBJECTIVE: The effects of the superantigens (SAgs) Staphylococcal Enterotoxin B (SEB), Toxic Shock Syndrome Toxin-1 (TSST-1) and Mycoplasma Arthritidis Mitogen (MAM) were examined on the induction and on the course of experimental SLE-like disease. METHODS: Immunization of BALB/c mice with human anti-DNA mAb (MIV-7) carrying the pathogenic idiotype 16/6 emulsified in complete Freund's adjuvant (CFA), followed by a boost of MIV-7/PBS 3 weeks later, generated an experimental SLE via an idiotypic dysregulation. RESULTS: After immunization with MIV-7/SAg, replacing the MIV-7 boost by SAg, and then injecting SAg 7 weeks after the regular induction of the SLE-like disease, the mice failed to produce anti-hIgM and dsDNA Ab up to 6 months after the induction. The mice immunized with MIV-7/CFA and boosted with the SAg had high titers of anti-hIgM but no detectable anti-dsDNA Ab. In both experimental groups low titers of anti-CL Abs developed in 25/40 (62%) and 30/38 (79%) of the mice respectively, including the control mice immunized with non-pathogenic human IgM/SAg or PBS/SAg. The mice immunized according to the "classical" protocol showed increased titers of anti-dsDNA Ab (22%) and anti-CL Ab (28%) during 10 weeks of observation. In contrast SEB, TSST-1 and MAM induced a 29%, 1% and 17% reduction in the anti-DNA titers and a 32%, 15% and 12% reduction in the anti-CL titers, respectively. CONCLUSIONS: These data suggest that the SAg tested here cannot replace the effect of CFA in the induction of the primary humoral response. The SAgs TSST-1, SEB and MAM did not induce the SLE-like disease following idiotypic modulation. Moreover, they may have had a suppressive effect on the idiotypic network in our model. The appearance of anti-CL Abs in almost all the experimental groups including the naive mice supports the possibility that microbial SAgs can induce the production of autoantibodies by different mechanisms. The SAgs TSST-1, SEB and MAM reduced autoantibody production in the serologically established idiotypic-induced experimental SLE-like murine model. This beneficial effect may indicate new directions for research on the management of SLE.

Animals↗
PubMedDate not supplied

Rhabdomyolysis associated with clozapine treatment in a patient with decreased calcium-dependent potassium permeability of cell membranes.

A 21-year-old patient developed rhabdomyolysis during his nineteenth week of treatment with clozapine for drug-resistant schizophrenia. No risk factors for rhabdomyolysis were found, but the calcium-dependent potassium efflux, normally responsible for membrane hyperpolarization and muscle refractoriness, was severely decreased in the patient's red blood cells. Clozapine is speculated to cause rhabdomyolysis in patients with defective calcium-activated K+ channels.

Adult↗