Introduction: Leptin is an important link in the regulation of body mass. An increase in fatty tissue is accompanied by increased formation of leptin, which, under physiological conditions, decreases input of energy and increases its output. A critical decrease of body mass in mental anorexia (MA) is connected with decreased leptinemia. Precise mechanisms controlling leptin level are not known. Aim: To characterize the relation of leptinemia to the indices of body mass as well as to other hormonal parameters in female patients with mental anorexia. Patients and methods: In 14 girls with MA at the beginning of the disease (mean age 15.47 ± 0.50 years), those after a partial therapeutic improvement (mean age 15.71 ± 0.53 years) and in 15 healthy girls (mean age 14.41 ± 0.52 years) the authors evaluated indices of body mass: % deviation from ideal body mass for the given age and height, body mass index (BMI), a multiple of standard deviation for the pertinent age - and the plasma level of leptin. In the patients with MA, samples of blood were taken for the determination of triiodotyronine, thyroxine, thyreotropic hormone, luteinizing hormone, follicle-stimulating hormone, estradiol, progesterone, dehydroepiandrosterone- sulfate and testosterone. Results: Anthropometric parameters and leptin levels in subjects with MA were low at the beginning of the disease and increased significantly after a partial improvement of the clinical condition, but were still lagging behind values in the control group (body mass deficit -27.12 ± 2.10% vs. -10.57 ± 3.42%, vs. 2.77 ± 2.03%, P < 0.001, P < 0.001, BMI 14.66 ± 0.57 kg/m2, vs. 18.09 ± 0.62, vs. 19.82 ± 5.63, P < 0.001, P < 0.01, and BMI SD -2.30 ± 0.2 vs. -0.87 ± 0.22 vs. -0.06 ± 0.22, P < 0.001, P < 0.001, leptin 1.70 ± 0.30 ng/ml vs. 2.91 ± 0.62 ng/ml, P < 0.001, vs. 6.06 ± 0.91 mg/ml, P < 0.05). Low mean values of triiodotyronine (1.30 ± 0,13 nmol/l) significantly increased after a partial improvement of clinical condition to 1.58 ± 0.07 (P < 0.05). A higher level of progesterone (4.80 ± 0.85 nmol/l) decreased in spite of the improvement of the disease to 2.10 ± 0.93 nmol/l (P < 0.05). The values of other observed endocrine parameters were within the limits of reference levels. After a partial improvement of the condition the LH level increased significantly (0.30 ± 0.07 vs. 5.12 ± 1.69, P < 0.01) as well as the level of FSH (1.90 ± 0.48 vs. 4.40 ± 0.35, P < 0.001), while levels of other hormonal parameters remained unchanged. The level of leptin at the beginning of the disease was not dependent on anthropometric parameters. A mutual relation was found between the levels of leptin and triiodotyronine (R = 0.52) and between leptin and luteinizing hormone (R = 0.53). After a partial improvement of body mass the level of leptin correlated with anthropometric parameters - body mass deficit (R = 0.60), BMI SD (R = 0.57) as well as with estradiol (R = 0.54). Even a higher correlation with luteinizing hormone was observed (R = 0.81). Conclusion: The results indicate a significant decrease of leptinemia in the acute stage on MA. The increase of leptin after adjustment of the clinical condition is considered to be a physiological response of leptin to increased body mass. The fact that the level of leptin correlated with that of luteinizing hormone even during the critical decrease of body mass suggests a possible role of leptin in modulation of gonadal functions.

        Key words: leptin, mental anorexia, BMI, body mass deficit, endocrine parameters