Ambophyllin, an office-dispensed tablet for asthma, contains triamcinolone.
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Biomedical subjects
Publications and source records attributed to M W Yocum.
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A case of common variable immunodeficiency, a relatively rare disorder, is presented. This case was complicated by the presence of an anti-IgA antibody in the patient's serum and a history of a possible anaphylactic reaction to a prior intravenous infusion of gamma-globulin. Common variable immunodeficiency is actually a heterogeneous group of demonstrable immunoglobulin deficiencies that have in common low levels of most immunoglobulin isotypes, the inability to form antibodies to antigen, an absence of gross defects in cell-mediated immunity, and the presence of recurrent bacterial infections. The history of immunoglobulin deficiency and its treatment is reviewed. Although the primary therapy for common variable immunodeficiency is gamma-globulin replacement, ancillary measures such as early treatment of infections with antibiotics are also important. Intravenous gamma-globulin replacement therapy is preferred to intramuscular replacement therapy in these patients because intramuscular doses must be limited in volume to minimize local pain and take 2 to 14 days to achieve maximal blood levels, during which time in situ degradation of up to 50% of the administered dose can occur. Five intravenous gamma-globulin preparations are currently available in the United States. The potential adverse effects of intravenous gamma-globulin infusion and the precautions currently taken to ensure safety during administration of this product are discussed.
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Intravenous pretesting with radiocontrast media (RCM) was performed in 204 RCM-sensitive patients considered for repeat contrast radiography. Group 1 had vague histories of prior anaphylactoid reaction and negative pretests, and 2 of 41 (4.9%) had reactions upon contrast radiography. Groups 2 to 5 had definite histories of prior anaphylactoid reaction. Group 2 had the radiographic study cancelled: 18 of 21 (85.7%) had positive pretests. Group 3 had positive pretests and underwent contrast radiography, and 9 of 15 (60%) had reactions despite premedication. Group 4 (no premedication) and group 5 (diphenhydramine premedication) had negative pretests, but 11 of 53 (20.7%) and 3 of 71 (4.2%), respectively, developed reactions (p less than 0.001). The reaction frequency in group 3 (posivie pretest) of 12 of 18 (66.7%) was greater than that in groups 4 and 5 (negative pretest) combined (14 of 124 (11.3%), p less than 0.001). Intravenous pretesting identified a high-risk group and diphenhydramine premedication decreased the frequency of reaction in patients sensitive to radiocontrast media.
Anaphylactoid reactions to protamine sulfate have been attributed to its capacity for nonimmunologic mast cell degranulation and/or complement consumption. In the current study, evidence is presented for the occurrence of an immunologic anaphylactic reaction mediated by a complement-dependent IgG skin-sensitizing antibody. A retrospective study of blood component donors given protamine for heparin neutralization revealed that prior exposure to protamine is associated with increased risk of adverse reaction to the drug.
Three weeks after a massive inhalation of mold present on infected oats, a farmer's wife had extrinsic allergic alveolitis. Aspergillus fumigatus was cultured from the moldy oats and from deep bronchial washings obtained at fiberoptic bronchoscopy. Spores and hyphae characteristic of Aspergillus species were demonstrated within granulomas in the pulmonary tissue obtained by transbrochial biopsy. Serum precipitins, delayed (48 hour) cutaneous hypersensitivity and in vitro lymphocyte transformation to A. fumigatus were demonstrated. The findings in this case suggest that a type IV immunologic response and subsequent (lymphocyte-mediated) tissue inflammation may underlie the pathogenesis of this and other forms of hypersensitivity pneumonitis.
Two adult men with recurrent pyoderma due to Staphylococcus aureus and a selective deficiency of immunoglobulin M (IgM) antibody synthesis are described. An analysis of each patient's polymorphonuclear leukocyte chemotaxis, phagocytosis and killing of Staph. aureus, serum opsonizaiton of Staph. aureus, and serum and lymphocyte-mediated responses to antigenic stimulation was performed. Family studies revealed a possible autosomal dominant inheritance pattern with heterogenetic expression of various dysgammaglobulinemic states in each patient's first degree relatives. In vivo studies of delayed hypersensitivity and in vitro studies of polymorphonuclear leukocyte and lymphocyte function were normal. A defect in IgM, but not in IgG (immunoglobulin G), antibody synthesis to a number of antigens, and a mild decrease in serum opsonic activity to Staph. aureus correctable by heat inactivated normal human serum were found in each patient. In these patients, the recurrent staphulococcal pyoderma prompted an investigation of host defense mechanisms and revealed low to absent IgM levels and a defect in IgM antibody synthesis.
Parameters of cell-mediated immunity (CMI) were studied in 17 allergic rhinitis patients selected for markedly elevated total serum IgE levels (greater than 300 IU/ml) and 14 normal controls. Mean serum IgE levels were 1,421 IU/ml and 101 IU/ml in the allergic and control groups, respectively (p less than 0.001). There were no significant differences between the allergic patients and the normal controls in delayed cutaneous hypersensitivity, in mitogen and antigen lymphocyte transformation in heterologous or autologous plasma, or in percentage of sheep erythrocyte rosettes. The allergic patient group had a significantly higher percentage of sheep erythrocyte-antibody-complement rosettes (p less than 0.05). Markedly elevated total serum IgE levels in allergic rhinitis patients were not associated with any detectable impairment of CMI.
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A pair of monozygotic twins discordant for systemic lupus erythematosus(SLE) were studied and no differences noted in their immune respose to tetanus toxoid, keyhole lympet hemocyanin, DNCB, delayed sensitivity, or antibody titers to viruses. Both were noted to have biologically false positive serology at an early age, but only one twon developed SLE. The clinically unaffected twin underwent castration at an early age, suggesting that ovarian hormones may play an important role in the development of SLE.