We identified five patients with a functional disorder of the vocal cords that mimicked attacks of bronchial asthma. Paroxysms of wheezing and dyspnea were refractory to standard therapy for asthma. During episodes of wheezing, the maximal expiratory and inspiratory flow-volume relationship was consistent with a variable extrathoracic obstruction. Laryngoscopy confirmed that wheezing was due to adduction of the true and false vocal cords throughout the respiratory cycle. During asymptomatic periods the maximal flow-volume relationship and laryngoscopic examination were normal. Provocation tests for bronchial asthma were negative. A variety of personality styles and psychiatric diagnoses were represented; patients were not aware of the vocal-cord dysfunction, which uniformly and dramatically responded to speech therapy and psychotherapy. This syndrome may be a form of conversion reaction.

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We conclude that GM-CSF, IL-5 and RANTES are produced in increased amounts in both allergic and non-allergic NP. Distinguishing features of non-allergic NP include fewer numbers of CD3 T lymphocytes, fewer IL-5+/CD3+ T lymphocytes and greater numbers of IL-5+ eosinophils. These differences may suggest different mechanisms of eosinophil accumulation and activation in allergic vs non-allergic NP.

Vocal cord dysfunction (VCD) is a poorly understood entity that is often misdiagnosed as asthma. We report eleven cases of VCD in which there was a temporal association between VCD onset and occupational or environmental exposure. We conducted a case-control study to determine if the characteristics of irritant-exposed VCD (IVCD) cases differed from non-exposed VCD controls. Chart review of VCD patients at the authors' institution produced 11 cases that met IVCD case criteria. Thirty-three control VCD subjects were selected by age matching. There were statistical differences between the groups in ethnicity and chest discomfort. There were no statistical differences between the groups for gender, tobacco, smoking habits, symptoms, or pulmonary function parameters. Varied irritant exposures were associated with IVCD. IVCD should be considered in patients presenting with respiratory symptoms occurring after irritant exposures.

We studied potential mechanisms of eosinophil accumulation in nonallergic chronic hyperplastic sinusitis with nasal polyposis (CHS/NP). We measured expression of endothelial vascular cell adhesion molecule-1 (VCAM-1), which mediates selective eosinophil transendothelial migration, the cytokines interleukin (IL)-1 beta, TNF-alpha and IL-13 which upregulate VCAM-1 expression, and the chemokine RANTES which mediates lymphocyte, monocyte, and eosinophil chemotaxis in chronic hyperplastic sinusitis with nasal polyposis (CHS/NP) nasal polyps (nonallergic versus allergic) and middle turbinate biopsies from normal controls. By immunohistochemical staining, the density of EG2+ eosinophils was increased in both the nonallergic and allergic CHS/NP subgroups compared to normal controls. VCAM-1 expression was significantly increased in CHS/NP subjects compared to normal controls (P = 0.0005), with the highest intensity seen in nonallergic CHS/NP. By in situ hybridization, the densities of IL-1 beta, TNF-alpha, IL-13, and RANTES mRNA+ cells were all increased in nonallergic CHS/NP compared to normal controls (P = 0.009, 0.0005, 0.0005, and 0.001, respectively). In comparison to allergic CHS/NP, nonallergic CHS/NP had a significantly higher tissue density of TNF-alpha (P = 0.04) and a lower density of IL-13 (P = 0.005) mRNA+ cells. In general, VCAM-1 expression correlated strongly in CHS/NP with the density of TNF-alpha (R = .91, P = 0.0005) but not the density of IL-1 beta, IL-13, or RANTES mRNA+ cells. We conclude that upregulation of VCAM-1 and elaboration of RANTES may contribute to the marked accumulation of eosinophils in nonallergic CHS/NP. TNF-alpha may play a critical role in VCAM-1 upregulation in this nonallergic eosinophilic disorder.

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