We investigated whether serum titers of interleukin 10 (IL-10), a cytokine known to shift lymphocyte responses towards humoral immunity, reflect disease activity in systemic lupus erythematosus (SLE). Sera from 72 SLE patients, 25 RA patients and 30 healthy controls were tested for IL-10 by ELISA. Low titers of IL-10 were detected in the serum of 37.5% of SLE patients and in 24% of RA patients but in only 3% of healthy controls. Interestingly, serum IL-10 titers in SLE patients were positively correlated with the SLE Disease Activity Index (SLEDAI) and with anti-DNA antibody titers, but negatively with complement fraction C3 levels. These results indicate that serum IL-10 values reflect SLE disease activity and suggest that overexpression of IL-10 might play a pathogenic role in severe lupus disease.

Plasma adiponectin levels are increased in anorexia nervosa. This may, at least in part, be due to the lack of negative feedback exerted by fat mass on adiponectin production and/or to enhanced insulin sensitivity. We speculate that hyperadiponectinaemia could, in turn, contribute to maintain a state of enhanced insulin sensitivity and possibly exacerbate haematological and infectious complications of anorexia nervosa.

We measured lumbar spine, hip (total and sub-regions) and total body bone mineral densities (BMDs) by dual-energy X-ray absorptiometry (DXA) in 47 premenopausal female patients suffering from systemic lupus erythematosus (SLE). As compared to health controls, SLE patients had lower BMDs at all trabecular and cortical sites. Comparison of BMDs between patients ever and never treated with glucocorticoids indicated that patients who had ever received glucocorticoids had a significantly lower lumbar spine BMD compared to those who never did. Moreover, bone loss in patients ever treated with glucocorticoids was commensurate with their cumulated oral glucocorticoid intake. Interestingly, patients never treated with glucocorticoids had a lower hip BMD compared to controls, thereby suggesting that the disease per se might induce some bone loss. Taken together, SLE patients suffer from a significant trabecular and cortical bone loss indicative of an increased risk of future fracture.

Leptin is a protein encoded by the ob gene that is expressed in adipocytes and regulates eating behavior via neuroendocrine mechanisms. Plasma leptin levels have been shown to correlate with weight and body fat in normal, obese and anorexic subjects. In the last of these populations, the dynamic profile of plasma leptin levels during short-term refeeding has never been assessed. We thus investigated basal plasma leptin levels in 29 female patients with anorexia nervosa (AN) (age 21.9 Ϯ 1.4 years, body mass index (BMI) 15.2 Ϯ 0.3 kg/m 2 ) and in 80 normal female controls (age 21.2 Ϯ 0.2 years, BMI 20.3 Ϯ 0.3 kg/m 2 , mean Ϯ S.E.M.). Basal plasma leptin levels in AN were decreased by 77% compared with controls (2.5 Ϯ 0.2 vs 11.1 Ϯ 0.7 ng/ml, P < 0.0001). In both AN subjects and controls, plasma leptin levels correlated significantly with BMI (r 2 ¼ 0.448, P < 0.0001 and r 2 ¼ 0.339, P < 0.0001 respectively). Five AN patients (four female, one male, age 22.0 Ϯ 4.7 years, BMI 14.2 Ϯ 0.4 kg/m 2 , body fat 4.3 Ϯ 0.9 kg or 11.0 Ϯ 1.9% of body weight, basal metabolic rate (BMR) 958 Ϯ 122 kcal/day) were studied during a 3-day refeeding period and compared with eight control subjects (two male, six female, age 25.7 Ϯ 1.2 years, BMI 21.3 Ϯ 0.8 kg/m 2 , body fat 15.1 Ϯ 0.9 kg or 24.6 Ϯ 1.7%, BMR 1455 Ϯ 78 kcal/day) submitted to 36-h fasting. The amount of calories administered was based on BMR þ 20% (carbohydrate 60%, protein 17%, fat 23%). In contrast to the rise in leptin levels that occurred during refeeding after a prolonged fast period in normal subjects, plasma leptin levels remained low and unchanged throughout the 3 days of renutrition in AN patients. The circadian rhythm of leptin was also completely abolished. This contrasted with the preserved circadian variations of cortisol, whose mean levels were increased. In conclusion, we confirmed that plasma leptin levels are low in AN and correlate with body weight. We further demonstrated that plasma leptin levels do not respond to short-term refeeding in anorexic patients in whom circadian variations are not restored, which suggests that the acute regulation of leptin by positive changes in energy balance is not preserved under a critical threshold of body fat. [415][416][417][418][419][420] European Journal of Endocrinology 138

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