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Letters to the Editor |
Döbelnsgatan 32 F 752 37 Uppsala Sweden
Dear Sir:
In their paper on the nutritional status of patients with newly diagnosed celiac disease, Kemppainen et al (1) wrongly state that no systematic studies have been carried out on the association of nutritional status with the severity of mucosal villous atrophy. They also state that the association between biochemical measurements and the grade of villous atrophy has not been reported previously.
In 1976 I published data on serum and urinary zinc concentrations, serum copper concentrations, albumin, orosomucoid, haptoglobin, cobalamin, folate, fecal fat, and bone marrow hemosiderin together with findings from intestinal mucosal biopsies in 13 patients (2). Patients with total and subtotal villous atrophy had low serum zinc concentrations in relation to serum albumin values and also low urinary zinc excretion, indicating profound zinc deficiency. Orosomucoid concentrations were within the normal range, indicating no inflammatory reaction. In 4 patients, serum copper concentrations were below the normal range.
In a later study, fasting serum zinc concentrations were abnormally low in 16 of 17 patients with celiac disease and various degrees of villous atrophy (3). A standard oral zinc citrate and folic acid absorption test showed significantly lower uptake in patients than in control subjects. Two patients who had only slight villous changes and 5 who had previously received folate treatment had the highest concentrations, one of which overlapped with the control range. There was also a good positive correlation between peak concentrations of zinc and folate in serum (r = 0.64). From this study we concluded that abnormally low serum zinc concentrations are an early and common finding in celiac disease and that folic acid treatment increases the ability to absorb folic acid and zinc despite villous atrophy.
Next followed a study of 174 adults with proven or suspected proximal gastrointestinal disease in whom biopsies were performed (4). Of the 90 women and 84 men, 85 had celiac disease, 24 had celiac disease and dermatitis herpetiformis, and 22 had probable celiac disease but were not consuming gluten-free diets. The biochemical findings were grouped according to biopsy findings, inflammation, and partial, subtotal, or total villous atrophy. Serum zinc concentrations were abnormally low (<11 µmol/L) in 92% of patients with total villous atrophy (
± SD: 7.5 ± 2.3 µmol/L), in 80% with subtotal atrophy (9.1 ± 2.3 µmol/L), in 60% with partial atrophy (10.8 ± 1.7 µmol/L), and in 63% with inflammatory duodenal mucosal changes (11.6 ± 2.0 µmol/L). The same stepwise patterns, but in fewer patients, were found for D-xylose uptake, fecal lipids, serum folate, blood hemoglobin, serum iron, transferrin saturation, serum albumin, serum copper, and serum cobalamin. Serum selenium and manganese were analyzed in a few patients and concentrations were low, indicating deficiency. One conclusion was that the more pronounced the mucosal lesion, as judged from duodenal biopsy specimens, the lower the circulating concentrations of zinc, copper, and iron. The same holds true for serum zinc and albumin concentrations (5).
Kemppainen et al (1) quote data from Bodé and Gudmand-Höyer's (6) study but omit the important findings that 49% of the celiac patients had abnormally low plasma folate concentrations, 32% had low concentrations of coagulation factors, 43% had low serum calcium concentrations, 13% had low plasma magnesium concentrations, and 31% had low serum zinc concentrations. It is important to recognize such defects in calcium, magnesium, zinc (7), and vitamin K metabolism when discussing defects in skeletal growth and bone mineralization, which now are so commonly diagnosed in celiac disease and which are reversible in children consuming gluten-free diets (7, 8).
Furthermore, the number of patients reported in Figure 1 for serum zinc is not consistent with the number given in the text (1); more important is that the authors seem to have used inadequate methods to analyze their serum zinc samples. The figures they report for patients with subtotal and total villous atrophy ( ± SD: 13 ± 2 and 12 ± 2 µmol/L) differ markedly from earlier data in the literature and are even slightly higher than the mean serum zinc concentrations reported in 1416 Finns from the general population (12.7 µmol/L for men and 11.7 µmol/L for women) when equipment free from zinc was used (9). Last, the final sentence in the abstract (1) is invalid and ought to be corrected.
REFERENCES
Department of Clinical Nutrition University of Kuopio PO Box 1627 70211 Kuopio Finland
Department of Pathology and Forensic Medicine University of Kuopio Kuopio Finland
Unit of Gastroenterology Department of Medicine Kuopio University Hospital KuopioFinland
Dear Sir:
We thank Jameson for his interest in and comments on our paper published in the Journal (1). By our statement that no systematic follow-up studies have been carried out on the association of nutritional status (nutrient intake and anthropometric and biochemical measurements) with the severity of mucosal villous atrophy in patients with newly diagnosed celiac disease (1), we wanted to indicate that the association between villous atrophy and nutritional status has been studied with only a few components of nutritional status. Jameson (2) published a study in which several biochemical indexes of nutritional status were associated with the severity of mucosal villous atrophy. He found lower circulating zinc concentrations in patients with more pronounced mucosal lesions as judged from duodenal biopsy specimens. In our study, serum zinc concentrations were low in 19 of 37 patients at the time their disease was diagnosed. After 1 y of follow-up, 10 patients with partial villous atrophy had low serum zinc values. Follow-up studies indicate that a gluten-free diet can improve villous atrophy and abnormal biochemical measurements (1, 3, 4). Bodé and Gudmand-Höyer (5) found a low percentage of anemia (22%) and other hematologic signs of severe malabsorption in a series of consecutively studied, uniformly diagnosed patients with celiac disease. Their findings agree with the results of our study (1). In their study, 31% of patients had low zinc values at diagnosis, whereas in our study 50% of patients did. Unfortunately, the number of patients in our study was too low to draw any conclusion regarding the association of villous atrophy and zinc.
Jameson pointed out that our patients had mean zinc values that were higher than the mean serum zinc concentrations reported in 1416 Finns from the general population (6). However, in the latter study, zinc concentrations were lower than observed in many other reports (7, 8). Plasma zinc concentrations have been downplayed as a measure of zinc status because they respond to metabolic conditions unrelated to zinc status and because they are insensitive to changes in dietary zinc. Furthermore, whole-body zinc content is conserved during zinc deficiency (9). The method we used to measure serum zinc concentrations (atomic absorption spectrophotometry) was the same as that used by Björkstén et al (6). More accurate measurements of zinc status might be obtained by plasma metallothionein concentrations (9) or stable-isotope methods (10). However, the latter test is not easily performed in a clinical situation. We investigated the nutritional status of celiac disease patients by using several indexes. Because serum zinc is not a good indicator of zinc status, we did not pay major notice to zinc values. In fact, weight loss before diagnosis and severe villous atrophy in celiac disease patients are more reliable indicators of abnormalities in biochemical measurements and poor nutritional status (1). Therefore, our major finding was that patients with total mucosal villous atrophy at diagnosis had low erythrocyte folate and serum ferritin values but no other major abnormalities in nutritional status.
REFERENCES
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  M. J Gibney The dietary pyramid Am. J. Clinical Nutrition, October 1, 1999; 70(4): 576 - 576. [Full Text]
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