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Biomedical subjects

J A Saryan

Publications and source records attributed to J A Saryan.

9 recordsLinked to original sources
PubMed1998

Anaphylaxis to topical bacitracin zinc ointment.

This report describes a case of systemic anaphylaxis to bacitracin zinc ointment in a 24-year-old man who was injured in a motorcycle accident. Extensive abrasions on the patient's extremities were cleaned with Shurclens before application of viscous Xylocaine and bacitracin zinc ointment. Five minutes later, the patient exhibited symptoms of severe anaphylaxis and required the administration of epinephrine, antihistamines, intravenous fluids, and corticosteroids. Two weeks later, he underwent prick/puncture skin testing to Shurclens and bacitracin zinc ointment as well as prick/puncture, intracutaneous, and subcutaneous challenge with Xylocaine. Only the result of the prick test to bacitracin zinc ointment was positive. Although bacitracin is considered to be a safe topical antibiotic, physicians should be aware of the potential not only for delayed hypersensitivity but also for acute IgE-mediated allergic reactions and life-threatening anaphylaxis.

Administration, Cutaneous↗
PubMed1989

Failure to detect extremely high levels of serum IgE with an immunoradiometric assay.

Two patients with extreme elevations in serum IgE were found to have falsely low levels of IgE when measured by a commercial immunoradiometric assay. Dilution studies performed on serum from both patients revealed the rise and subsequent fall of the dose-response curve characteristic of the high-dose "hook" or prozone effect. Specimens with unexpectedly low levels of serum IgE obtained by either commercial immunoradiometric assay or enzyme immunoassay should be reanalyzed after dilution.

Humans↗
PubMed1983

Regulation of human immunoglobulin E synthesis in acute graft versus host disease.

Immunoglobulin (Ig) E synthesis was studied in vitro in eight patients who had received transplants of allogeneic bone marrow. Seven of these patients developed acute graft vs. host disease (GVHD) and elevated serum IgE levels, whereas the eighth did not. In vitro synthesis of IgE, but not of IgG, was elevated in cultures of lymphocytes obtained during acute GVHD (17,923 +/- 14,607 pg/10(6) cells) but not in cultures of lymphocytes obtained after resolution of the acute GVHD when the serum IgE had returned to normal (106 +/- 31 pg/10(6) cells). In contrast, lymphocytes from the patient with no acute GVHD, like normal lymphocytes, failed to synthesize IgE in vitro. The increased in vitro IgE synthesis in acute GVHD was suppressed by normal allogeneic lymphocytes and by autologous lymphocytes obtained after the resolution of the acute GVHD, but not by allogeneic lymphocytes obtained from patients undergoing acute GVHD. The deficiency in functional IgE-specific suppressor cells in acute GVHD occurred in the face of normal or increased percentages of circulating T8+ cells, which in normal subjects contain the IgE-specific suppressor cells. In two patients studied, there was evidence of activated IgE-specific, circulating helper T cells. T cells from these two patients, but not normal T cells, secreted spontaneously upon culture in vitro a factor that induced IgE, but not IgG, synthesis by normal B cells. Finally, a survey of 21 bone marrow transplant recipients revealed that acute GVHD was a necessary requirement for the development of elevated serum IgE levels in recipients of bone marrow transplants. These results suggest that acute GVHD is accompanied by an imbalance in IgE-specific immunoregulatory T cells consisting of activated helper T cells and deficient suppressor cells.

Acute Disease↗
PubMed1983

Impairment of the autologous mixed lymphocyte reaction in atopic dermatitis.

The T cell proliferative response to autologous non-T cells is termed the autologous mixed lymphocyte reaction (AMLR). Recent studies have suggested that the AMLR represents an inducer circuit for the activation of T8+ suppressor/cytotoxic effector cells. Since atopic dermatitis (AD) patients are deficient in T8+ cytolytic T cell function, we investigated the AMLR in AD. When sheep erythrocytes were used to separate T cells from non-T cells, the AMLR was found to be significantly decreased (P less than 0.001) in AD patients (n = 11; delta cpm = 1,550 +/- 393) when compared with normal control subjects (n = 13; delta cpm = 25,819 +/- 4,609). To exclude the possibility that these results were an artifact of the sheep erythrocyte separation, T cells were also separated on a fluorescence-activated cell sorter after treatment of peripheral blood lymphocytes with the OKT3 monoclonal antibody. AD T cells separated by the latter method were also found to have a significantly reduced AMLR response when compared with similarly treated normal T cells. Co-culture studies using cells from AD patients and their HLA identical siblings indicated that the defect resided at the responder T cell level rather than at the stimulator non-T cell level. Co-culture studies revealed no evidence for excessive suppressor cell activity resulting in the decreased AMLR. However, enumeration of T cells reactive with the monoclonal antibody T29, which recognizes a subset of T cells proliferating in the AMLR, demonstrated that AD patients (n = 8; % T29 = 2.5 +/- 0.7) had a significantly decreased (P less than 0.001) number of circulating T29+ T cells when compared with normal controls (n = 8; % T29 = 10.4 +/- 0.8). These studies suggest that a deficiency of T4+ T29+ cells contributes to the deficient AMLR in AD and possibly underlies the abnormalities of T8+ effector cells present in this disease.

Adolescent↗
PubMed1983

Induction of human IgE synthesis by a factor derived from T cells of patients with hyper-IgE states.

The requirements for the induction of IgE synthesis in normal B cells were studied. In contrast to peripheral blood lymphocytes (PBL) from allergic subjects, normal PBL failed to synthesize IgE spontaneously in vitro. Pokeweed mitogen (PWM) and Epstein Barr virus (EBV) failed to induce IgE synthesis in normal PBL and in tonsil lymphocytes. In the case of PWM, this failure was not overcome by prior removal of T8+ cells, which were shown previously to contain IgE-specific suppressor cells. In the case of EBV, the failure to induce IgE synthesis was not overcome by prior removal of sheep rosette-forming cells. Supernatants of T cells derived from three groups of patients with elevated serum IgE (hyper-IgE syndrome, atopic dermatitis, and acute graft-vs-host disease) induced significant IgE synthesis in cultures of normal B cells without causing an increase in IgE synthesis. In contrast, supernatants of normal T cells failed to induce IgE synthesis. Release of the IgE isotype-specific helper factor was inhibited by cycloheximide and tunicamycin, and its activity was destroyed by treatment with trypsin and neuraminidase. These results indicate that whereas classical polyclonal B cell activators (PWM, EBV) fail to induce IgE synthesis by normal B cells, IgE synthesis is readily induced by an IgE-specific helper factor released by T cells from patients with hyper-IgE states.

B-Lymphocytes↗
PubMedDate not supplied

Month of birth and sensitization to dust mites in New England.

Charts from 908 patients born in New England and seen at the Lahey Clinic because of allergic rhinitis or asthma or both were reviewed to ascertain whether or not a relationship existed between month of birth and subsequent development of allergy to house dust mites. Prick/puncture and intradermal skin tests for aeroallergens were performed on all patients. Skin tests for Dermatophagoides farinae (Df) mite were scored very positive (VP) in 451 patients (49.7%), mildly positive (MP) in 234 patients (25.7%), and negative (NEG) in 223 patients (24.6%). No discernible difference in frequency of birth could be identified for any single month for either Df-sensitive or Df-negative patients. Comparisons of 4-month periods (May through August, September through December, and January through April) failed to show a seasonal predilection for month of birth. During the 6-month period of February through July, a slight difference was observed for the overall group of 908 patients: 240 of the VP patients (53.2%), 111 of the MP patients (47.4%), and 105 of the NEG patients (47.1%) were born within this period compared with 211 VP patients (46.8%), 123 MP patients (52.6%), and 118 NEG patients (52.9%) who were born within the period of August through January. The difference among the groups was not statistically different (P = 0.20). Of the 225 children and adolescents who were either VP or MP, 125 patients (55.6%) were born within the period of February through July; of the 83 children and adolescents who were NEG, 37 patients (44.6%) were born within that same period. Although dust-mite allergic patients and, in particular, children and adolescents with asthma or rhinitis or both tended to be born within the period of February through July, no clear-cut statistically significant predilection in month of birth or season could be identified for New England-born adult or pediatric mite-allergic patients with rhinitis or asthma or both.

Adolescent↗