Objective-To test the hypothesis that smoking increases the risk of sensitisation by occupational allergens.Design-Historical prospective cohort study.
IntroductionAbout 5-10% of the population has asthma, and a recent report from the Tucson longitudinal study suggests that IgE dependent allergic mechanisms are important in asthma at all ages.' Little is known about the aetiology of asthma and that of related allergic conditions, such as hay fever, but studies of asthma induced by occupation are likely to be informative because occupational exposures are important "natural experiments." Smoking seems to promote the development of asthma and of specific IgE antibody in occupational settings.2-4 These studies, including our previous study of workers exposed to tetrachlorophthalic anhydride,! were cross sectional and possibly subject to survivor bias. We now report a longitudinal study in the platinum refining industry of the development of respiratory symptoms and of responses to platinum salts on skin prick testing in relation to smoking habit and atopic state.Charged halogenated platinum salts stimulate an IgE response", and cause allergic asthma. They are intermediates in the process of refining platinum, a corrosion resistant metal used as a catalyst and in jewellery. 9 In the past workers in refineries had a high
This is a prospective, open-label, proof-of-concept study of tofacitinib, a Janus kinase inhibitor, as a steroid sparing therapy in corticosteroid-dependent pulmonary sarcoidosis. 5 patients with corticosteroid-dependent pulmonary sarcoidosis were treated with tofacitinib 5 mg twice daily. The primary endpoint was a ≥50% reduction in corticosteroids at week 16 with no worsening in pulmonary function or respiratory symptoms. 60% of patients (3/5) met the primary endpoint. One patient was lost to follow up prior to steroid taper, and another was withdrawn due to worsening of known neurosarcoidosis. The three patients who met the primary endpoint each tapered to ≤5 mg/day prednisone, respiratory symptoms improved, and spirometry remained stable. In this proof-of-concept study, the addition of a JAK-inhibitor allowed 60% of patients with pulmonary sarcoidosis to successfully taper corticosteroids. JAK-inhibitors are a promising therapy for pulmonary sarcoidosis, which require further investigation in randomized trials.
This is a prospective, open-label, proof-of-concept study of tofacitinib, a Janus kinase inhibitor, as a steroid sparing therapy in corticosteroid-dependent pulmonary sarcoidosis. 5 patients with corticosteroid-dependent pulmonary sarcoidosis were treated with tofacitinib 5 mg twice daily. The primary endpoint was a ≥50% reduction in corticosteroids at week 16 with no worsening in pulmonary function or respiratory symptoms. 60% of patients (3/5) met the primary endpoint. One patient was lost to follow up prior to steroid taper, and another was withdrawn due to worsening of known neurosarcoidosis. The three patients who met the primary endpoint each tapered to ≤5 mg/day prednisone, respiratory symptoms improved, and spirometry remained stable. In this proof-of-concept study, the addition of a JAK-inhibitor allowed 60% of patients with pulmonary sarcoidosis to successfully taper corticosteroids. JAK-inhibitors are a promising therapy for pulmonary sarcoidosis, which require further investigation in randomized trials.Trial Registration: clinicaltrials.gov NCT03793439; registered Jan 4, 2019
The management of acute submassive pulmonary embolism is undertaken on an individualized basis because of the wide spectrum of clinical presentations. In this report we review the literature and discuss the evidence behind the management of cases of acute pulmonary embolism complicated by hypoxemia from a patent foramen ovale. In a case of acute pulmonary embolism complicated by refractory hypoxemia from an intracardiac shunt, adjunctive therapies in addition to anticoagulation and thrombolysis must be considered.
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