Protamine allergy as a complication of insulin hypersensitivity: A case report.

BACKGROUND: Although most patients receiving insulin produce insulin-specific IgE, significant allergic symptoms develop in very few of them. Patients receiving neutral protamine Hagedorn (NPH) insulin are at increased risk for the development of protamine hypersensitivity. The case of a 19-year-old woman with insulin-dependent diabetes and regular and NPH insulin hypersensitivity is presented. OBJECTIVE: The purpose of this study was to determine whether desensitization to NPH insulin, as well as standard insulin desensitization, could control allergic symptoms in a patient allergic to both NPH and regular insulin. METHODS: The patient required insulin desensitization for severe urticaria, angioedema, and occasional wheezing resulting from her insulin dose. She underwent a standard protocol for insulin desensitization twice in a 2-month period, with persistence in her symptoms. She was found to have high protamine-specific, as well as insulin-specific, IgE levels, and because of her poor response to regular insulin desensitization, she was desensitized to both regular and NPH insulin. RESULTS: Dual desensitization resulted in marked improvement in her symptoms. The patient had recurrence of urticaria and angioedema a year and a half later, at which point the NPH was stopped and she was desensitized to regular insulin. She continued to receive regular insulin 4 times per day over the following 3 years with only occasional hives. CONCLUSION: Patients with insulin allergy may not have complete resolution of their symptoms after standard desensitization, particularly those patients with concomitant protamine allergy. These patients may require protamine/NPH desensitization, an alternative insulin preparation, or both.

Cat antigen in homes with and without cats may induce allergic symptoms.

Although Fel d 1, the major cat allergen, has been found in settled dust samples from homes both with and without cats, the clinical relevance of this allergen has never been studied. In this study we measured airborne concentrations of Fel d 1 in homes both with and without cats and then attempted to relate these levels to those obtained in our experimental cat challenge model to assess their clinical significance. In baseline samples we found measurable levels of airborne Fel d 1 in all 37 homes with cats (range, 1.8 to 578 ng/m3; median, 45.9 ng/m3) and in 10 of the 40 homes without cats (for detectable samples: range, 2.8 to 88.5 ng/m3; median, 17 ng/m3). Fel d 1 was present in the settled dust of 38 of 40 homes without cats (range, 39 to 3750 ng/gm; median, 258 ng/gm), although these levels were only weakly predictive of airborne levels. Repeat samples obtained weekly from 12 homes without cats yielded measurable airborne levels. Fel d 1 in at least one of the four samples from all homes. When compared with challenges performed in our cat room facility at low levels of airborne Fel d 1 (<500 ng/m3), these home levels are within the range capable of causing upper and lower respiratory symptoms in subjects allergic to cats. We therefore conclude that the low level cat exposure that occurs in many homes without cats is capable of inducing symptoms in some patients who are sensitive to cats. The assessment of cat exposure should not be based solely on the presence or absence of a cat in the home.

Dexamethasone inhibits the antigen-induced contractile activity and release of inflammatory mediators in isolated guinea pig lung tissue.

Treatment for 24 h in vitro with dexamethasone inhibited the antigen-induced contractile response in guinea pig tracheal rings and parenchymal strips without inhibiting the contractile response of the tissues to either methacholine or histamine, respectively. Antigen-induced histamine release was inhibited by approximately 50% in both tissues by prior treatment with dexamethasone. Dexamethasone treatment also inhibited the release of immunoreactive sulfidopeptide leukotriene from parenchymal strips. In tracheal rings, dexamethasone treatment reduced spontaneous release of all cyclooxygenase metabolites (PGE2, PGF2 alpha, TXB2, PGD2, and 6-k-PGF1 alpha were tested), with the exception of PGD2, and also inhibited the antigen-induced release of all cyclooxygenase metabolites studied. Dexamethasone-treatment did not inhibit the spontaneous release of cyclooxygenase metabolites in the guinea pig lung strips, and only modestly inhibited the antigen-induced release of PGE2, PGF2 alpha, and PGD2. The results suggest that the inhibition of contractile response of guinea pig lung strips and airway tissue to antigen by dexamethasone is the result of a reduced release of inflammatory mediators. The inhibition by dexamethasone of antigen-induced release of mast cell mediators from guinea pig lung parenchyma contrasts with results previously obtained with human parenchymal lung tissue.