Effect of maternal immunotherapy on immediate skin test reactivity, specific rye I IgG and IgE antibody, and total IgE of the children.

The effect of specific immunotherapy during pregnancy was studied in 14 children, 3 to 12 years after delivery. Fourteen additional children from the same allergic mothers, in whom immunotherapy was not given during the pregnancy, served as controls. The immediate skin test response to grass allergens of the children of mothers given immunotherapy. Levels of rye I IgG and total IgE were lower in the sera of children born to mothers who received immunotherapy (not statistically significant) than their control cohorts. Paired cord blood and maternal blood samples drawn at delivery showed similar levels of rye I IgG, indicating that blocking antibody freely crosses the placenta. This evidence indicates that immunotherapy during pregnancy may have an inhibitory effect on immediate skin reactivity to grass allergens in some of the offspring. Whether tolerance to other allergens can be induced in children by maternal immunotherapy remains to be determined.

Double-blind comparison of itraconazole with griseofulvin in the treatment of tinea corporis and tinea cruris.

Seventy-eight patients with tinea corporis or tinea cruris participated in a double-blind study with either 100 mg itraconazole or 500 mg ultramicronized griseofulvin for 15 consecutive days. Clinical outcome was significantly in favor of itraconazole at completion of treatment (72% response rate vs. 51%) and at the follow-up visit (91% response vs. 64%). The most important difference between both treatments was the mycologic outcome, for which itraconazole showed a cure rate of 87% compared to 57% for griseofulvin 2 weeks after completion of therapy. It is suggested that 100 mg of itraconazole orally once daily is significantly more effective than 500 mg of griseofulvin once daily for 15 days in the treatment of glabrous skin infections. Both drugs were well tolerated.

Activated complement in inflamed aqueous humor.

Activated complement is an important mediator of inflammation. Radioimmunoassay was used to measure levels of C3a, an activated fragment of C3, in aqueous humor. Additionally, immunoelectrophoresis was performed on aqueous humor to detect Factor B and its conversion product, Bb, as well as C3c, a breakdown product of C3. All six samples of normal aqueous humor had no detectable C3a, C3c, or Factor B. All eight samples of aqueous humor from patients with anterior uveitis had measurable levels of C3a. Factor B and C3c were detected in 3/7 samples of inflamed aqueous humor. Factor B was converted fully to Bb in two of these three samples, suggesting alternative pathway activation of complement. Activated complement fragments are present in the aqueous humor of eyes with anterior uveitis and may help mediate the inflammatory process.

Effects of particulate beta-1,3 glucan on human, rat, and guinea pig complement activity.

Particulate glucan, a beta-1,3-linked polyglucose derived from Saccharomyces cerevisiae, has been demonstrated to have a wide range of immunopotentiating effects. Glucan administration is associated with the modification of a variety of experimentally induced infectious disease states as well as the inhibition of growth of implantable and spontaneous tumors. The present study was designed to evaluate the effect of glucan upon activation of the complement system in rats and guinea pigs. Additional studies were performed to determine the in vitro activating effect of glucan and zymosan on complement activity of human serum. Glucan activated both the classical pathway of normal human sera and the alternate pathways in C2hu-deficient sera in vitro releasing anaphylatoxins such as C3a. The intravenous injection of glucan activated the alternate pathway of guinea pig plasma. The influence of glucan on complement depletion induced by cobra venom factor (CVF) was also ascertained. Complement activation by glucan may contribute, in part, to the enhanced resistance of the host against tumor growth as well as infectious episodes.

Anaphylaxis after sesame seed ingestion.

Four patients with histories of systemic anaphylaxis or angioedema and urticaria after ingestion of sesame seed or sesame oil-containing products were studied for anti-sesame seed extract IgE by the radioallergosorbent test (RAST). Three of four were found to be positive. RAST inhibition after density-gradient ultracentrifugation of sesame seed extract indicates that the most active allergens appear to have molecular weights between 8,000 to 62,000 daltons.

Identification of allergens in dog dander extract. I. Clinical and immunological aspects of allergenicity activity.

Allergenic activity of mixed dog dander extract was compared with dog serum albumin by skin testing, RAST testing and RAST inhibition. Whereas albumin is a potent allergen, additional lower molecular weight allergens determined by sucrose density gradient centrifugation and immunoelectrophoresis were found. Identification of the most potent allergens and standardization of extract used for testing and treatment is a necessary prerequisite in understanding dog dander hypersensitivity.

Quantitative requirements for C3 to induce Forssman systemic shock and cutaneous hemorrhagic vasculitis in guinea pigs.

The requirements of complement (C) to induce systemic and cutaneous Forssman reactions were studied in inbred DHC-BA and Hartley strain guinea pigs. After intravenous injection of Forssman antibody, fatal systemic shock was associated with a marked drop in CH50, C4, and C3 and a lesser decrease in C5 hemolytic activity. Platelet counts and leukocyte counts dropped as well. With the use of the purified low molecular weight factor from cobra venom (CVF) to deplete C3, guinea pigs with less than 1% intravascular C3 were protected from lethal shock. Approximately 1% to 3% C3 activity is required for Forssman cutaneous vasculitis. These results confirm earlier studies that classical complement pathway activation occurs in Forssman shock and demonstrate the exquisite biologic efficiency of C3 in provoking the shock syndrome.