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Biomedical subjects

W Sheremata

Publications and source records attributed to W Sheremata.

At least 19 recordsLinked to original sources
PubMed1997

Cutaneous reactions to recombinant human interferon beta-1b: the clinical and histologic spectrum.

BACKGROUND: Recombinant human interferon beta-1b has been recently approved for the treatment of multiple sclerosis. A significant proportion of patients treated with this medication experienced cutaneous reactions. OBJECTIVE: We describe the clinical and histologic features of cutaneous reactions to recombinant human interferon beta-1b. METHODS: Consecutive patients with cutaneous reactions to recombinant interferon beta-1b were evaluated clinically and by biopsy. RESULTS: Clinical lesions varied from subtle uninflamed sclerotic dermal plaques to erythematous plaques to cutaneous ulcers at injection sites. The nonsclerotic lesions were frequently painful. The firm plaques showed fibrosis histologically, whereas nonsclerotic inflammatory lesions demonstrated a consistent pattern of vascular thrombosis. Hematologic evaluation demonstrated platelet activation in most patients with inflammatory lesions, a feature also noted before interferon treatment in some patients. CONCLUSION: Therapy with recombinant interferon beta-1b is associated with a spectrum of cutaneous reactions and vascular thrombosis.

Adjuvants, Immunologic↗
PubMed1995

Clinical spectrum of HTLV-I in south Florida.

A total of 113 patients with infection due to human T-cell leukemia virus type 1 (HTLV-I) were evaluated at the University of Miami from January 1988 to March 1993. Forty patients were identified with adult T-cell leukemia/lymphoma (ATLL) and 63 with HTLV-I-associated myelopathy (HAM). Three had concomitant ATLL and HAM. Two HAM patients co-infected with human immunodeficiency virus type 1 (HIV-I) developed clonal lymphoproliferative disease during the study period. Patients with ATLL have a poor prognosis; multiple chemotherapy regimens including high-dose cytotoxic agents have been utilized with a small impact on survival. Most of our patients are currently treated with experimental regimens. Rheumatologic or autoimmune illnesses were identified, mostly in HAM patients, and a small number developed immunodeficiencies in the absence of other definable etiologic factors. Most of the patients were immigrants from areas of endemicity in the Caribbean basin, although many Americans were also recognized. HTLV-I/II infection was diagnosed serologically and typed as HTLV-I by polymerase chain reaction (PCR) or a modified Western blot when a DNA sample was not available. In 24 of 40 patients with ATLL, Southern blot hybridization performed on DNA extracted from peripheral blood lymphocytes or tumor tissue demonstrated clonal HTLV-I integration. In South Florida, ATLL and HAM are now seen frequently. Since HTLV-I infection is associated with a 4% lifetime risk of developing ATLL and an additional 0.25% lifetime risk for developing HAM, a large pool of asymptomatically infected individuals must exist here.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Efficacy and safety of tizanidine in the treatment of spasticity in patients with spinal cord injury. North American Tizanidine Study Group.

Tizanidine, an imidazoline that acts as an agonist at alpha 2-adrenergic receptors, has been shown to be effective in reducing spasticity caused by MS. This multicenter study (14 sites) assessed the efficacy and safety of oral tizanidine in patients who had spinal cord injury of > 12 months' duration. Of the 124 patients admitted to the study, 78 completed it. Tizanidine was titrated to an optimized dosage in each patient to a maximum of 36 mg/d. Muscle tone, assessed by Ashworth score, was significantly reduced (p = 0.0001) by tizanidine treatment in comparison with placebo. Video motion analysis of the pendulum test showed improvement in the tizanidine-treated patients vs placebo (p = 0.04) and showed a significant correlation with the Ashworth score (p < 0.001). No significant alterations in muscle strength or vital signs were noted in either treatment group. The most common adverse events during tizanidine treatment were somnolence, xerostomia, and fatigue. It was concluded that, overall, tizanidine is effective in reducing spasticity in patients with spinal cord injury.

Activities of Daily Living↗
PubMed1993

Spastic ataxia associated with human T-cell lymphotropic virus type II infection.

Human T-cell lymphotropic virus type one (HTLV-1) is associated with tropical spastic paraparesis or HTLV-I--associated myelopathy. We report 2 women with a spastic ataxic illness similar to HTLV-I--associated myelopathy infected solely with HTLV-II. Identification of HTLV-II infection was made serologically, by polymerase chain reaction, and by viral culture (in 1 woman). One woman, treated with 200 mg of danazol orally, three times daily, had pronounced improvement in ambulation, nocturnal spasticity, and nighttime urinary frequency. It appears that infection with HTLV-II may cause an illness similar to HTLV-I--associated myelopathy, but distinguished by the presence of ataxia.

Antibodies, Monoclonal↗
PubMed1992

Relapsing and remitting human immunodeficiency virus-associated leukoencephalomyelopathy.

We describe a 33-year-old homosexual man with a steroid-responsive, remitting and relapsing leukoencephalopathy associated with recent human immunodeficiency virus type 1 (HIV-1) seroconversion. Biopsy of a parieto-occipital lesion revealed demyelination and astrogliosis with focal necrosis. Detailed investigations demonstrated no pathogens in the brain other than HIV-1. This patient illustrates that a neurological disorder clinically indistinguishable from multiple sclerosis may be the presenting manifestation of HIV-1 infection and may occur in the absence of clinically significant immunosuppression.

AIDS Dementia Complex↗
PubMed1992

Atypical Creutzfeldt-Jakob disease in an American family with an insert mutation in the PRNP amyloid precursor gene.

An American family of English origin with an unusually early onset and long-duration form of Creutzfeldt-Jakob disease (CJD) had a heterozygous insert mutation in the region of repeating octapeptide coding sequences between codons 51 and 91 of the PRNP gene on chromosome 20. Affected members were 23 to 35 years old at the onset of illnesses that lasted from 4 to 13 years, yet experimental transmission of disease from the proband (11-year duration) produced a typically brief incubation period and duration of illness in each of three inoculated primates. Also, the PrP amyloid protein that accumulates in CJD brain was only barely detectable in extracted brain tissue from one case with massive spongiform change and was undetectable in another case with no spongiform change, perhaps because of epitope shielding by a configurational change in the protein induced by the mutation. Analysis of this and other families with similar inserts suggests that such mutations in the PRNP gene not only predispose to CJD, but also modify its phenotypic expression.

Adult↗
PubMed1990

Multiple sclerosis sibling pairs: clustered onset and familial predisposition.

We evaluated 48 relapsing-remitting multiple sclerosis (R/R MS) sibling pairs derived from 44 families for age and date of onset of MS symptoms, clinical course, and family history of MS. Age- and sex-matched R/R MS clinic patients provided a statistical comparison group. The age of onset tended to cluster within multiplex families. The initial symptom of MS occurred within 5 years of age in 30/48 sibling pairs compared with 16/48 controls. A positive family history of MS (other than siblings) was present in 43% of the multiplex families compared with 20% among simplex controls. In 1st-, 2nd-, and 3rd-degree relatives who had lived into the age at risk, 22/1,134 family members of multiplex sibling pairs had probable or definite MS compared with 10/1,215 control family members. Age of onset clustering in siblings concordant for R/R MS and an increased risk of MS in other family members suggest that factors influencing disease onset may be in part inherited in these kindreds.

Adult↗
PubMed1987

HTLV-I infection of cerebrospinal fluid T cells from patients with chronic neurologic disease.

Antibodies reacting with HTLV-I, the etiologic agent of acute T cell leukemia/lymphoma and a transforming agent for T4-positive lymphocytes in vitro, have recently been described in sera of patients with chronic neurologic disease in the absence of lymphoproliferative disorders. The largest number of such cases was described in Japan and in the Caribbean and parts of South America. We report here two cases of patients with chronic neurologic disease whose cerebrospinal fluid (CSF)-derived T cells contain HTLV-I specific RNA sequences and antigens and are expressing retroviral particles. Only one of these patients has demonstrable antibody to HTLV-I in serum or CSF.

Adult↗
PubMed1980

Experimental embolic stroke in the guinea pig (Cuvis cobaya).

Because of the demonstrated suitability of the guinea pig (Cuvis cobaya) for a large variety of laboratory investigations, we sought to develop a stroke model in this animal. Many ingenious stroke models in other animals exist; some depend on anomalous anatomy, others utilize methods of intracranial or extracranial vascular occlusion and yet others combine ischemia and anoxic damage (1-14). As one proposed application for this work was to study immune responses following experimental stroke, survival of several days after cerebral infarction was a requirement. Three to five days elapse before detection of a hymoral and cellular immune response is possible. The guinea pig is especially suited to immunological studies because of the enormous amount of accumulated data on the immunology of this animal. However, the guinea pig has proved relatively invulnerable to existing small animal techniques. Moreover the unacceptably short postoperative survival associated with the use of existing techniques necessitated the development of a new procedure. We have successfully pursued the development of an embolic stroke procedure applicable to this animal.

Animals↗
PubMed1978

Subacute sclerosing panencephalitis and multiple sclerosis: in vitro measles immunity and sensitization to myelin basic protein.

Three children with subacute sclerosing panencephalitis (SSPE), 12 patients with multiple sclerosis (MS) and 12 healthy persons were studied by the macrophage migration inhibition factor (MIF) assay with measles and rubella antigens and with myelin basic protein. For the SSPE patients the mean migration indexes +/- standard deviation were 44.1 +/- 10.9 for measles antigen, 38.7 +/- 12.3 for rubella antigen and 49.8 +/- 25.7 for myelin basic protein; for the MS patients the indexes were 103.0 +/- 10.6, 93.8 +/- 15.0 and 89.3 +/- 19.9; and for the healthy subjects the indexes were 68.8 +/- 22.6, 77.7 +/- 31.3 and 100.1 +/- 6.5. The results of this study showed increased cellular immunity to measles and rubella in SSPE patients as compared with healthy persons, and absence of immunity to measles in MS patients. Patients with MS showed hypersensitivity to myelin basic protein during clinical exacerbations that was not associated with changes in immunity to measles, whereas all SSPE patients showed a significant response regardless to stage of illness.

Adolescent↗
PubMed1978

Cellular and humoral responses to myelin basic protein in multiple sclerosis: a dichotomy.

The macrophage migration inhibition factor (MIF) assay and a counterimmunodiffusion assay were utilized to measure immune responses to human myelin basic protein in 75 patients with multiple sclerosis (MS) and in 120 control subjects. Eight out of ten MS patients in acute exacerbation and one out of seventeen convalescent, but none of chronically ill MS patients gave positive results in the MIF test. Forty-six percent of the patients with negative MIF assays but only 22% of those with positive assays had positive antibody results. In the counterimmunodiffusion assay, myelin basic protein antibody was demonstrated in almost 2/3 of patients during convalescence but it was not present in those whose illness had been stable for 6 months or longer. While no correlation with the stage or duration of the illness was present in other disorders, in MS an inverse correlation with clinical activity and in vitro evidence of cellular sensitization to encephalitogenic basic protein was apparent.

Autoantibodies↗
PubMed1978

Sensitization to myelin basic protein in attacks of multiple sclerosis. A preliminary report.

Recent attempts to detect the presence of antibody to encephalitogenic basic protein in multiple sclerosis have generally been unsuccessful. The utilization of a new system of double immunodiffusion in detecting such antibody in EAE serum prompted us to apply this method in the search of such antibody MS sera. In our preliminary investigation of 67 sera, antibody was detectable in MS sera, but it was most often found during convalescence rather than an acute exacerbation of illness. Antibody was also found in several myasthenic patients, and occasionally in subjects with other neurological disease.

Antibodies↗
PubMed1977

Direct leukocyte migration inhibition by myelin basic protein in exacerbations of multiple sclerosis.

Studies in 13 normal subjects, 9 patients with multiple sclerosis (MS) within 3 weeks of exacerbation and 16 others 1 to 6 months after onset were carried out for evidence of cell-mediated hypersensitivity to myelin basic protein. Ten patients with stroke and 10 with Guillain-Barré syndrome were studied as additional controls. Peripheral leukocytes obtained by leukapheresis were packed into capillary tubes and allowed to migrate out onto glass in the presence or absence of myelin basic protein. Cells of patients within 3 weeks of an MS episode gave a mean migration index of 68 +/- 9%, and those 1 to 6 months after onset, 93 +/- 21%. For the entire MS group the mean index was 88 +/- 20%, for those with Guillain-Barré, 103 +/- 7%; and for the stroke patients, 107 +/- 11%. Results for the acutely ill MS patients were significant (P less than 0.005). The data are similar to those obtained using the migration inhibition factor assay but show that sensitized lymphocytes also elaborate a second mediator during acute exacerbations of illness. These observations strengthen evidence that sensitization to this potent encephalitogen occurs simultaneously with exacerbations of clinical illness.

Acute Disease↗