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Allen Kaplan

Publications and source records attributed to Allen Kaplan.

4 recordsLinked to original sources
PubMed2006

Pleural fluid and peripheral eosinophilia from hemothorax: hypothesis of the pathogenesis of EPE in hemothorax and pneumothorax.

Blood and air in the pleural space are the most common conditions associated with an eosinophilic pleural effusion. The recruitment of eosinophils is dependent upon stimulation by cytokines, specifically interleukin (IL)-3, IL-5, granulocyte-monocyte cell stimulating factor (GM-CSF), and RANTES (regulated upon activation, normal t-cell expressed and secreted), that cause eosinophil proliferation in the bone marrow, movement into the circulation, and adhesion and migration across endothelial barriers into tissues. There are several possible mechanisms that can explain eosinophilic pleural effusions. We report a case of an eosinophilic pleural effusion after spontaneous hemothorax that illustrates the course of pleural fluid and blood eosinophilia in following hemothorax and describe the different pathophysiology of eosinophil trafficking in the pleural space and serum following hemothorax and pneumothorax.

Adult↗
PubMed2005

Incidence and characteristics of angioedema associated with enalapril.

BACKGROUND: Angioedema is a rare but potentially serious adverse event of angiotensin-converting enzyme inhibitor therapy. However, no prospective, controlled studies have reported on its incidence and clinical characteristics. METHODS: We studied the occurrence of angioedema in a randomized, double-blind, controlled trial of 12 557 persons with hypertension treated with enalapril maleate, 5 to 40 mg/d, using a prospective ascertainment and adjudication of angioedema by an expert committee. RESULTS: Angioedema occurred in 86 (0.68%) of the subjects. Stepwise logistic regression identified black race (odds ratio [OR], 2.88; 95% confidence interval [CI], 1.72-4.82), history of drug rash (OR, 3.78; 95% CI, 1.80-7.92), age greater than 65 years (OR, 1.60; 95% CI, 1.02-2.53), and seasonal allergies (OR, 1.79; 95% CI, 1.06-3.00) as independent risk factors for angioedema. The incidence of angioedema was higher after initiation of therapy (3.6/1000 patients per month) and declined to 0.4/1000 patients per month. Treatment was not given in 44 (51%) of the cases; antihistamines were administered in 35 (41%); corticosteroids, in 20 (23%); and epinephrine, in 1 (1%). Two patients were hospitalized but none had airway compromise. CONCLUSIONS: Enalapril-related angioedema is uncommon. Although it is most likely to occur early after initiation of therapy, it may occur at any time. It is more likely to occur in black patients, those older than 65 years, and those with a history of drug rash or seasonal allergies. Fatal angioedema or angioedema requiring airway protection did not occur in this study.

Adult↗
PubMed2004

Eucalyptus as a specific irritant causing vocal cord dysfunction.

BACKGROUND: Vocal cord dysfunction (VCD) is a well-recognized clinical entity that frequently mimics asthma and is characterized by inappropriate adduction of the vocal cords during inspiration. The pathogenesis of VCD has not yet been defined. The only previous report suggested that respiratory irritants may trigger paradoxical motion of the vocal cords. OBJECTIVE: To report the case of a 46-year-old woman with VCD precipitated by eucalyptus exposure. METHODS: A masked flexible fiberoptic nasolaryngoscopy was performed to confirm whether VCD occurred with eucalyptus and not with other known respiratory irritants. The patient underwent inhalation challenges consisting of water, ammonia, pine oil, and a combination of eucalyptus (dried leaves) and ammonia. Two independent observers before patient challenge could not identify eucalyptus. RESULTS: Vocal cord dysfunction occurred within minutes of exposure to eucalyptus. This is the first report to prospectively document that a specific irritant, eucalyptus, can precipitate VCD. Negative skin prick test results, total IgE level, and negative IgE eucalyptus-specific antibodies support a nonimmunologic mechanism. CONCLUSIONS: A new pathogenic mechanism for this clinical entity is supported by our observations. Furthermore, a nonimmunologic mechanism in which respiratory irritants may induce VCD is suspected. Future studies to elucidate this mechanism need to be performed in individuals with irritant-specific VCD.

Alveolitis, Extrinsic Allergic↗