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Other Original Articles: Denis Franchimont, Sandrine Roland, Thierry Gustot, Eric Quertinmont, Youssef Toubouti, Marie-Christine Gervy, Jacques Deviere, and Andre Van Gossum Impact of Infliximab on Serum Leptin Levels in Patients with Crohn’s Disease J Clin Endocrinol Metab 2005; 90: 3510-3516 [Abstract] [Full text] [PDF]

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Serum leptin levels in Crohn’s disease.

ESMERALDA CAPRISTO, Noemi Malandrino, Sara Farnetti, Geltrude Mingrone, Giovanni Gasbarrini   (25 October 2005)

Serum leptin levels in Crohn’s disease. 25 October 2005
ESMERALDA CAPRISTO, Catholic University, Insitute of Internal Medicine CATHOLIC UNIVERSITY, INSTITUTE OF INTERNAL MEDICINE, Noemi Malandrino, Sara Farnetti, Geltrude Mingrone, Giovanni Gasbarrini Send letter to journal: Re: Serum leptin levels in Crohn’s disease. e.capristo{at}rm.unicatt.it ESMERALDA CAPRISTO, et al.	We read with great interest the article by Franchimont et al., who reported an increase in serum leptin levels in Crohn's disease (CD) patients after 4-wk treatment with the anti-tumor necrosis factor (TNF)-alpha chimeric monoclonal antibody, infliximab, independent of body fat stores (1). They concluded that the rise in leptin levels represented biological evidence of a correction of energy imbalance in CD patients. We point out that malnutrition could easily occur in CD patients who showed unusual nutritional and metabolic characteristics, including reduced fat mass, enhanced utilization of lipids as a fuel substrate and increased diet-induced thermogenesis, compared to both healthy subjects and patient with ulcerative colitis (2,3) Thus, the maintenance of energy balance in CD is an extremely complicated process, involving central, peripheral and environmental signals, in addition to genetic determinants. The authors reported an increase in body weight after treatment with infliximab, although no variation in fat mass content was found. This suggests that CD patients had increased their fat-free mass, and in particular, the muscle mass content, which is definitely not likely to take place in these patients. This may have been a misperception because the patients’ body composition was evaluated by bioimpedance analysis (BIA), a simple technique based on body water content, which can create a bias in fat mass determination. It would have been more accurate to use the dual-energy X-ray absorptiometry, which is considered the gold standard for fat mass measurement (4). Furthermore, no data on energy intake or physical activity level were provided, and both of these factors are crucial in energy balance assessment. A great challenge in studying nutritional features in CD is the identification of a homogeneous group of patients with comparable types of disease, localization, previous intestinal resection and other treatments (3). In their study, approximately half of patients had disease strictly localized to the colon, while the 55% had ileal involvement. In Table I, it is not clear what the gender distribution was in the infliximab treated group, which is important because leptin levels are strongly influenced by gender. Preliminary reports by our group showed reduced circulating leptin level in CD patients in comparison with both control subjects and patients affected by ulcerative colitis, and that serum leptin level highly correlated with body fat stores (5). No correlations between serum leptin level and inflammatory activity, energy requirements, body composition, and glucose metabolism were found (6). We hypothesized that, as already reported in other diseases characterized by malabsorption, plasma leptin concentration did not seem to mediate the nutritional and metabolic alterations found in CD (2,3,5). Since poor nutritional status can independently increase morbidity and mortality (2,3), study of the mediators responsible for energy balance in CD is highly relevant role, not only in the attempt to better understand the pathophysiology of malnutrition, but also to investigate the potential role of therapy directed at these substances in clinical practice. These studies may also have relevance to the emerging role of the gut in energy balance regulation in humans (6). References 1. Franchimont D, Roland S, Gustot T, Quertinmont E, Toubouti Y, Gervy M-C, Deviere J, Van Gossum A. 2005 Impact of infliximab on serum leptin levels in patients with Crohn's disease. J Clin Endocrinol Metab 90:3510-3516 2. Capristo E, Addolorato G, Mingrone G, Greco AV, Gasbarrini G. 1998 Effect of disease localization on the anthropometric and metabolic features of Crohn's disease. Am J Gastroenterol 93:2411-2419 3. Capristo E, Addolorato G, Mingrone G, Greco AV, Gasbarrini G. 1999. Nutritional status and energy metabolism in Crohn disease. Am J Clin Nutr 69:339-341 4. Pietrobelli A, Formica C, Wang Z, Heymsfield S.B. 1996 Dual-energy X-ray absorptiometry body composition model: review of physical concepts. Am J Physiol 271:E941-951 5. Capristo E, Farnetti S, Addolorato G, Leggio L, De Lorenzi L, Abenavoli L, D'Angelo Di Paola ME, Mingrone G, Greco AV, Gasbarrini G. 2004 Relationship between circulating leptin, inflammatory activity and insulin sensitivity in patients with Crohn's disease. Dig Liv Dis 36:S213 6. Badman MK, Flier JS. The gut and energy balance; visceral allies in the obesity wars. 2005 Science 307:1909-1914