Serum biomarkers are similar in Churg-Strauss syndrome and hypereosinophilic syndrome.

RATIONALE: Churg-Strauss syndrome (CSS) and hypereosinophilic syndrome (HES) overlap considerably in clinical presentation. A reliable means of distinguishing between these groups of patients is needed, especially in the setting of glucocorticoid therapy. METHODS: A retrospective chart review of 276 adult subjects referred for evaluation of eosinophilia > 1500/µl was performed, and subjects with a documented secondary cause of eosinophilia or a PDGFR -positive myeloproliferative neoplasm were excluded. The remaining subjects were assessed for the presence of American College of Rheumatology (ACR) criteria. Laboratory and clinical parameters were compared between subjects with biopsy-proven vasculitis (CSS; n = 8), ≥4 ACR criteria (probable CSS; n = 21), HES with asthma and/or sinusitis without other CSS-defining criteria (HESwAS; n = 20), HES without asthma or sinusitis (HES; n = 18), and normal controls (n = 8). Serum biomarkers reported to be associated with CSS were measured using standard techniques. RESULTS: There were no differences between the subjects with definite or probable CSS or HES with respect to age, gender, or maintenance steroid dose. Serum CCL17, IL-8, and eotaxin levels were significantly increased in eosinophilic subjects as compared to normal controls, but were similar between the eosinophilic groups. Serum CCL17 correlated with eosinophil count (P < 0.0001, r = 0.73), but not with prednisone dose. CONCLUSIONS: In patients with a history of asthma and sinusitis, distinguishing between ANCA-negative CSS and PDGFR-negative HES is difficult because of significant overlap in clinical presentation and biomarker profiles.

Mutagens and modulator of mutagenesis in fried ground beef.

It is now well documented that bacterial mutagens form in proteinaceous foods during cooking at moderate temperatures. Three heterocyclic amine mutagens have been identified by Sugimura and coworkers in fish and beef cooked under moderate heating conditions (T. Sugimura and S. Sato, Cancer Res. (Suppl.), 43: 2415s-2421s, 1983). The distribution of these known mutagens in commercial bacteriological-medium grade and food-grade beef extract, and in fried ground beef, is discussed. Of the known mutagens, we have been able to confirm only that 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline is present in fried ground beef. Deficiencies in currently used mutagen extraction procedures are addressed. It is likely that there are many mutagens in fried ground beef that are yet to be identified. Fried ground beef (and raw beef) also contains an activity which modulates bacterial mutagenesis apparently by interacting with rat liver microsomes which are added to metabolically activate promutagens. The modulator activity has been partially purified and either inhibits, enhances, or has no effect on promutagen activation depending on the promutagen under study and the pretreatment of the rat from which the microsomal fraction was obtained.