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Biomedical subjects

J J Lasserre

Publications and source records attributed to J J Lasserre.

At least 19 recordsLinked to original sources

Laboratory tests of iron status: correlation or common sense?

We demonstrate that simple correlation between the various tests of iron status is not sufficient for examining their value in diagnosing iron deficiency (ID). Three degrees of ID are recognized: Iron depletion (ID grade I) is defined by decreased total body iron and normal iron support to erythropoiesis, as diagnosed by decreased storage iron, decreased ferritin, normal sideroblast count, normal zinc protoporphyrin (ZPP), and transferrin saturation >15%. When the iron supply to erythropoiesis becomes insufficient, as diagnosed by transferrin saturation < or = 15%, increased ZPP, and decreased sideroblast count, iron-deficient erythropoiesis (ID grade II) occurs. When finally hemoglobin is below its normal range, iron-deficiency anemia (ID grade III) results. The various tests for ID cannot be compared without taking into account the severity of the deficiency. Depending on the grade of ID examined, the correlation of markers seen in our patients' data varied considerably. We conclude that a "best" marker of ID does not exist. However, the different tests efficiently complement each other by detecting different stages and individually show the clinical extent of ID. Ferritin reflects the iron stores. ZPP indicates whether the ID in a given patient is clinically relevant or not. Finally, the extent of a clinically relevant ID can be assessed by the measured ZPP, hemoglobin concentration, and red cell indices.

Anemia, Iron-Deficiency↗

Central role of zinc protoporphyrin in staging iron deficiency.

In iron deficiency, zinc protoporphyrin (ZPP) is produced instead of heme, and the ZPP concentration in erythrocytes is increased (normal < or = 40 mumol/mol heme). We investigated the relevance of ZPP for staging iron deficiency. ZPP was determined by hematofluorometry in samples from 103 patients. Nineteen patients with iron depletion showed decreased serum ferritin (12.1 +/- 4.4 micrograms/L) with normal ZPP and hemoglobin (Hb). Twelve patients with iron-deficient erythropoiesis had decreased ferritin (10.4 +/- 2.4 micrograms/L), increased ZPP (72 +/- 9 mumol/mol heme), and normal Hb concentrations. In 72 patients with iron-deficiency anemia, ferritin was < 12 micrograms/L. In mild anemia (Hb between 100 and 120 g/L, and normal erythrocyte indices), ZPP was 100 +/- 16 mumol/mol heme. In severe anemia (Hb < 100 g/L, decreased erythrocyte indices), ZPP values were significantly higher (265 +/- 109 mumol/mol heme). We conclude that measurements of ZPP, ferritin, and Hb can reliably be combined to classify the degree of iron deficiency.

Anemia, Hypochromic↗

Zinc protoporphyrin in anemia of chronic disorders.

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.

Anemia↗

Washing erythrocytes to remove interferents in measurements of zinc protoporphyrin by front-face hematofluorometry.

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.

Blood Donors↗

Effect of low-protein diet on renal function: are there definite conclusions from adult studies?

Low-protein diets have been used for roughly a century in order to alleviate uraemic symptoms and to delay progression of chronic renal failure (CRF). Currently a number of different low-protein diets are used, supplying either 0.6 g protein/kg body weight or 0.3-0.4 g supplemented with amino-acids or keto-acids. Single centre trials have attempted to demonstrate the efficacy of these diets in slowing down the progression of CRF. The results from these trials are, however, sometimes inconclusive, showing either a high efficiency of the low-protein diet or no efficiency at all. Conclusive data from multicentre trials, however, are not yet available. A crucial point in analysing the efficacy of low-protein diets is the degree of compliance with the protein restriction. Today, the data available indicate that sometimes only a poor degree of compliance is achieved both in single and in multicentre trials.

Dietary Proteins↗

A low-protein diet protects uremic rats against the negative sequelae of metabolic acidosis.

Metabolic acidosis is a common finding in uremia. The metabolic consequences, however, are poorly understood. Thus, the aim of our study was to assess the effect of chronic metabolic acidosis in 5/6-nephrectomized male Sprague-Dawley rats given a normal (18%; n = 19) and a low-protein diet (8%; n = 23). Each of these groups was sequentially given CaCO3 and CaCl2 in the drinking water for a fortnight each. The animals were randomly assigned to start either with CaCO3 or CaCl2 (random cross-over design). The blood pH decreased significantly in both CaCl2 groups (18% protein: CaCO3 7.18 vs. CaCl2 7.11; 8% protein: CaCO3 7.26 vs. CaCl2 7.09) as did standardized base excess (18% protein: CaCO3-5.9 vs. CaCl2-9.7; 8% protein: CaCO3-3.6 vs. CaCl2-12.6). Food intake declined during acidosis in both groups, but more in the 18% protein group. The same occurred with body weight (g) in the 18% group, which decreased dramatically (8% protein: CaCO3 389 vs. CaCl2 390; 18% protein: CaCO3 413 vs. CaCl2 366). The change in body weight was reflected in the urinary urea excretion (mg/24 h/g food) (8% protein: CaCO3 0.9 vs. CaCl2 1.0; 18% protein: CaCO3 2.2 vs. CaCl2 30.8). There was a significant increase in proteinuria (mg/24 h) in the 8% group (CaCO3 10 vs. CaCl2 15), while in the 18% group no real change occurred (CaCO3 24 vs. CaCl2 18). Factoring the proteinuria for food intake, however, also resulted in a tendency towards an increased proteinuria in the 18% group.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Renal Tubular↗