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Hematofluorometric determination of zinc protoporphyrin (ZPP) is a screening method for the assessment of iron deficiency (ID). Chronic disorders are frequently accompanied by anemias of unclear origin, most probably caused by an impairment of iron metabolism. We investigated the relevance of ZPP for the detection of derangements of iron metabolism in anemias of chronic disorders (ACD). In 19 patients with ACD caused by chronic inflammatory non-neoplastic diseases, ZPP was determined and correlated with ferritin, transferrin saturation, and hemoglobin (Hb). Marrow sideroblast counts and semiquantitative grading of the marrow hemosiderin were performed in all patients to exclude ID and to show the decreased iron bioavailability. In all ACD patients who exhibited the typical laboratory findings of disturbed iron metabolism, such as hypoferremia, decreased transferrin saturation, decreased bone marrow sideroblasts, and increased marrow hemosiderin, strongly elevated ZPP levels were found (131 +/- 23 mumol/mol heme). ZPP returned to normal after successful treatment of the underlying disease. This is shown in three patients with polymyalgia rheumatica. We conclude that the fluorometric determination of ZPP allows detection and quantification of derangements of iron metabolism associated with chronic inflammatory disorders. By recording the derangements quantitatively, ZPP allows monitoring of therapy of chronic inflammatory diseases.

Zinc protoporphyrin (ZPP) is determined by hematofluorometry of whole blood to detect iron deficiency in blood donors. In hospitalized patients, ZPP did not correlate with established markers of iron status. We performed 4500 ZPP measurements with the Aviv front-face hematofluorometer in samples from 475 patients and measured ferritin, transferrin saturation, hemoglobin, and erythrocyte indices. We found that the fluorometric determination is affected by substances dissolved in plasma but that this interference can be eliminated by using washed erythrocytes. In validation tests the within-day variation was < 3.5%; the day-to-day variation was < 6.8%. In 130 healthy persons without iron deficiency, ZPP was < or = 40 mumol/mol heme, which we consider a normal value. Mean ZPP in 46 iron-deficient patients was 256 (SD 105) mumol/mol heme (correlation with ferritin: -0.73; with hemoglobin: -0.85; P < 0.001). When washed erythrocytes are used, the hematofluorometric determination of ZPP is sensitive and specific for detecting iron deficiency in otherwise healthy individuals and hospitalized patients.

In the present study we tested the hypothesis that the natriuretic and pressor effects of intracerebroventricularly (icv) injected hypertonic saline involve a central angiotensinergic pathway. All experiments were performed in conscious Wistar rats. Bolus injections of hypertonic saline (0.19, 0.23, 0.30, and 0.60 M icv; injection volume 5 microliters) induced a concentration-dependent increase of renal sodium excretion without affecting urinary flow. The increase in renal sodium excretion after the two highest saline concentrations was accompanied by significant increases in mean arterial blood pressure (MAP). Pretreatment with the angiotensin (ANG) AT1 receptor antagonist, losartan (5 micrograms icv), reduced the natriuretic effect of 0.23 and 0.30 M saline but did not affect the natriuresis induced by 0.60 M saline. The increase in MAP after 0.30 and 0.60 M saline icv was markedly attenuated by intracerebroventricular pretreatment with losartan. Our results demonstrate the involvement of a central angiotensinergic mechanism in the natriuretic and pressor responses to hypertonic saline. In addition to the ANG II-mediated natriuresis, an additional natriuretic mechanism, independent of ANG II and associated with the saline-induced pressor effect, seems to be recruited with increasing concentrations of saline in the cerebrospinal fluid.

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Gastroenterologists and (to a somewhat lesser extent) referring physician appear to be following the current guidelines for Hp treatment. As expected, two thirds of referring physicians consider NUD to be absolute or relative indication for Hp eradication. Check-up examinations are apparently being performed less frequently than recommended.

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