Nasal eosinophilia in allergic and nonallergic rhinitis: usefulness of the nasal smear in the diagnosis of allergic rhinitis.

Diagnostic nasal cytology has been advocated for use in distinguishing allergic from nonallergic rhinitis. We sought to determine prospectively the frequency of nasal eosinophilia (NE) in 100 patients in whom having allergic rhinitis (AR), nonallergic rhinitis, and other atopic conditions not involving the respiratory tract have been diagnosed. A nasal smear was obtained from consenting adults using the Rhino-Probe curette. Patients taking local or systemic corticosteroids, those with chronic rhinitis associated with aspirin sensitivity, and those with sinusitis were excluded. All cytograms were coded and read by a single "blinded" investigator. NE was considered significant if greater than 20% of sampled cells were eosinophils. Twenty-six of 61 (43%) patients with AR had NE. No NE was detected in the control population or in the skin test negative group of patients in whom having nonallergic rhinitis was diagnosed. One of 16 patients with allergic disease not involving the respiratory tract exhibited NE; this patient had atopic dermatitis with peripheral eosinophilia. No cases of eosinophilic nonallergic rhinitis were detected. There was no significant correlation of symptoms or the number of positive skin tests with NE. These data suggest that the nasal smear for eosinophils is an insensitive but specific test for the diagnosis of allergic rhinitis, when patients with nasal polyposis and aspirin sensitivity and/or negative skin tests are excluded.

Aortic insufficiency and mitral regurgitation in patients with systemic lupus erythematosus and the antiphospholipid syndrome.

PURPOSE, PATIENTS, AND METHODS: Heart disease has not been well characterized in patients with systemic lupus erythematosus (SLE) and the antiphospholipid syndrome. During a prospective study of cerebrovascular disease in autoimmune disease and SLE, 11 lupus patients were identified with an antiphospholipid syndrome characterized by significant cardiac valvular disease in addition to cerebral infarction, deep vein thromboses, and thrombocytopenia. Patients were reviewed for criteria for systemic lupus and underwent echocardiographic studies and measurements of anticardiolipin antibodies, VDRL, and the lupus anticoagulant. RESULTS: Eight of the 11 patients had aortic insufficiency, two of whom had associated mitral regurgitation. Three patients had mitral regurgitation alone. Microscopic analysis of a surgically excised aortic valve indicated typical Libman-Sacks verrucous endocarditis. Infective endocarditis was ruled out in all patients. CONCLUSION: This report expands previous descriptions of antiphospholipid syndromes by describing a subset of lupus patients with significant aortic and mitral valvulitis in addition to circulating antiphospholipid antibodies, thrombocytopenia, and recurrent thromboses.

Dysregulation of arachidonic acid release and metabolism by atopic mononuclear cells.

We studied the ability of monocytes to metabolize [3H]arachidonic acid (AA) provided exogenously by activated T cells, and the extent to which dexamethasone suppressed eicosanoid production by normal and atopic cells. [3H]AA metabolites were identified using a reverse-phase high pressure liquid chromatography system (HPLC). Unstimulated and PHA-stimulated T cells from normal and atopic subjects exhibited a similar uptake and time-dependent release of radiolabel, 90% of which was identified as free AA. The addition of autologous normal and atopic monocytes to these cultures enhanced the release of radiolabel, even in the absence of stimulation with mitogen. Atopic T cell/monocyte cultures released significantly (P = 0.046) more radiolabel than normal cells when stimulated with PHA. Furthermore, the monocytes from both normal and atopic subjects metabolized T cell derived [3H]AA into cyclo-oxygenase (CO) and lipoxygenase (LO) products. Under unstimulated conditions, atopic cells produced significantly (P = 0.04) less CO products than normal cells. In contrast, under PHA and calcium ionophore-stimulated conditions, the atopic cells produced significantly (P = 0.048) more prostaglandins than normal donor cells. Furthermore, although the total release of radioactivity was comparable in both groups, significantly less (P = 0.02) free AA remained in ionophore-stimulated culture supernatants from atopic cells. In order to study the regulation of AA release by normal and atopic T cells, dexamethasone (1 microM) was added to T cell cultures. Dexamethasone inhibited the release of [3H]AA from normal T cells to a significantly (P = 0.003) greater extent than it did to atopic cells.(ABSTRACT TRUNCATED AT 250 WORDS)