Majocchi's granuloma in solid organ transplant recipients.

Superficial fungal infections are fairly prevalent in transplant recipients and the incidence increases with more intense graft-conserving immunosuppressive therapy. Majocchi's granuloma is a deep folliculitis caused by dermatophytes that involves deeper layers of the dermis. Only a few case reports of the condition have been documented in transplant recipients. After an extensive review of the medical literature, 21 cases were retrieved and are summarized here, together with a new case that occurred in a recent heart transplant recipient from our institution. This report aims to provide a comprehensive analysis of Majocchi's granuloma in solid organ transplant (SOT) recipients, with special focus on potential risk factors, offending pathogens, clinical presentation, therapeutic approaches, and outcome. General observations are presented emphasizing the relevance of close clinical and dermatologic follow-up in high-risk SOT patients with specific comments regarding treatment regimens and outcomes.

Omalizumab rapidly decreases nasal allergic response and FcepsilonRI on basophils.

BACKGROUND: Omalizumab is a monoclonal anti-IgE antibody that is effective for the treatment of allergic respiratory disorders; however, its onset of action is unknown. OBJECTIVE: This study was designed to determine the onset of action of omalizumab through the use of a challenge model to determine time-dependent inhibition of ragweed-induced changes in nasal volume as well as correlate the kinetics of omalizumab-induced decreases in serum free IgE and FcepsilonRI receptors on basophils. METHODS: We conducted a 6-week, randomized, double-blind, placebo-controlled study of 24 rhinitic patients with ragweed allergy. After PD(30) ragweed nasal allergen challenge, patients received either omalizumab, approximately 0.016 mg/kg per IgE (IU/mL), or placebo at days 0 and 28 and were rechallenged with ragweed PD(30) dose biweekly. FcepsilonRI expression on blood basophils was determined by flow cytometry at baseline and 7, 14, 28, and 42 days after treatment. IgE levels were measured at baseline and on days 3, 28, and 42. RESULTS: Mean IgE levels decreased by 96% (P <.001) from baseline within 3 days in the omalizumab group. Baseline 30% ragweed-induced nasal volume response was decreased to 20.4% at 7 to 14 days (P <.001) and 12.2% at 35 to 42 days (P <.001) for the omalizumab group. There was a median decrease in basophil FcepsilonRI expression of 73% (P <.001) in the omalizumab group, with maximum inhibition occurring within 14 days of treatment. No significant changes in IgE levels, nasal allergen challenge responses, or basophil FcepsilonRI expression were observed throughout the study in the placebo group. CONCLUSIONS: Our study showed that the onset of action by omalizumab in blunting ragweed-induced nasal responses is within 2 weeks, and this response was associated with 2 putative mechanisms of action: decreased serum free IgE and decreased FcepsilonRI receptor expression on immune effector cells.

Measurement of bronchoconstriction using whole-body plethysmograph: comparison of freely moving versus restrained guinea pigs.

We have previously measured pulmonary function in guinea pigs using a double-chambered plethysmograph, however, the question remains regarding the accuracy of the double-chamber to gauge the long-term pulmonary function of late asthmatic response. This may be affected by confounding factors, such as stress on the animal and differences in size of the collar around the neck. Therefore, in this study we compared histamine-induced bronchoconstriction in the same guinea pigs using a single- versus a double-chambered body box. In the double-chambered body box, the specific airway resistance is proportional to time delay between thoracic and nasal flows and measured in cmH2O x s. Whereas, in the single-chambered body box, PenH units (Enhanced Pause) reflect "effort of breathing." This is measured as the pause between inspiration and expiration. Doubling concentrations of histamine (12.5-200 microg/ml dissolved in normal saline) were administered by DeVilbiss nebulizer for 1 min, followed by 1 min suction of residual drug in the chamber, and then the airway resistance was recorded by the computer for the following 3 min. There was a 15-min wash-out period between two doses of histamine. There was no statistically significant difference (p > 0.05) in the PC100 values for histamine between the two methods, however, it was much easier to work with the single-chambered body box in terms of handling the animal and eliminating the possible influence of collar placement on the bronchoconstriction. In conclusion, the data suggests histamine challenges produce equivalent PC100 data in both the double-chambered plethysmograph with sRAW units and single-chambered plethysmograph using the PenH units.

An in vivo model of beta-adrenoceptor desensitization.

Chronic use of beta2-agonists and increased production of inflammatory mediators during the late allergic reaction after antigen challenge results in the desensitization of beta-adrenoceptors in the airways and the accompanying rise in nonspecific airway hyperresponsiveness. In this study, we established an in vivo model of beta2-adrenoceptor desensitization in guinea pig airways by administration of IL-1beta intratracheally or chronic albuterol by inhalation. In the establishment of beta-adrenoceptor desensitization in response to both beta-agonist or inflammatory mediator, baseline pulmonary function responses were established to methacholine and isoproterenol-induced relaxation of methacholine bronchoconstriction. This was followed by the administration of IL-1beta (500 IU/d intratracheally for 2 days) or chronic albuterol (0.1 g/L by aerosol for 1 min three times a day for 10 days). After administration, the methacholine and isoproterenol-methacholine response was once again evaluated. Intratracheal administration of IL-1beta or chronic administration of albuterol significantly decreased (p < 0.05) the protective effect of isoproterenol on methacholine-induced bronchoconstriction, eliciting beta-adrenoceptor desensitization in vivo. The in vivo model will be very useful in monitoring the effect of other potential drugs on beta-adrenoceptor function in the airways.

Anti-interleukin-4 inhibits immunoglobulin E production in a murine model of atopic asthma.

Immunoglobulin E (IgE) plays an important role in allergy, acting as an initiating factor and being involved in its persistence and exacerbations. As interleukin-4 (IL-4) is critical in IgE synthesis, we propose that treatment of mice with monoclonal anti-IL-4 (11B11) prior to active sensitization with ovalbumin will inhibit IgE synthesis, therefore arresting the allergic process at an early stage. Mice treated with 11B11 and sensitized with saline or ovalbumin had significantly less serum IgE than their respective control groups which were treated with saline (p < 0.05). This study suggests that anti-IL-4 may be a prophylactic agent in asthma and allergic disease.

[Bronchial asthma. Its pattern in 2 rural areas]. / Asma bronquial. Comportamiento en 2 zonas rurales.

A survey was carried out in order to determine if bronchial asthma represents a health problem in two rural areas under the medical assistance of family doctors' offices (Argeo Martínez and Manguito del Guaso). All the case histories in the zones under study were reviewed. It was found that, in spite of the low prevalence in both areas, there is a diseased for each 28 persons, being female the most affected.