Abstract. ghrelin increases hunger sensation and food intake in various patients with appetite loss. anorexia nervosa (an) begins with psychological stress-induced anorexia and some patients cannot increase their food intake partly because of malnutrition-induced gastrointestinal dysfunction. the effects of ghrelin on appetite, food intake and nutritional parameters in anorexia nervosa (an) patients were examined. Five female restricting-type an patients (age: 14-35 y; body mass index: 10.2-14.6 kg/m 2 ) had persistently complained of gastrointestinal symptoms and failed to increase body weight. they were hospitalized for 26 days (6 days' pre-treatment, 14 days' ghrelin-treatment, and 6 days' post-treatment) and received an intravenous infusion of 3 µg/kg ghrelin twice a day. ghrelin infusion improved epigastric discomfort or constipation in 4 patients, whose hunger scores evaluated by visual analogue scale questionnaires also increased significantly after ghrelin infusion. daily energy intake during ghrelin infusion increased by 12-36 % compared with the pre-treatment period. Serum levels of total protein and triglyceride as nutritional parameters significantly increased after ghrelin treatment. there were no serious adverse effects including psychological symptoms. we found that ghrelin decreases gastrointestinal symptoms and increases hunger sensation and daily energy intake without serious adverse events in an patients. although the present study had major limitations of the lack of a randomized, placebo-controlled group, nonblindness of the investigators and the small number of patients recruited, it would contribute to further investigations for therapeutic potential of ghrelin in an patients.

Octanoylated ghrelin (1-28) (intact ghrelin) is rapidly and easily degraded to desoctanoyl forms or smaller fragments (degraded ghrelin). Plasma levels of intact and degraded ghrelin were examined in 30 patients with anorexia nervosa (AN) (body mass index, 8.81-22.4 kg/m(2)) and 16 age-matched healthy women using several assay methods. Plasma levels of ghrelin measured using immunocomplex transfer-enzyme immunoassay, which specifically detects intact ghrelin, were lower in AN than controls. Plasma ghrelin levels in AN measured using the active ghrelin ELISA kit, which is advertised as specifically detecting intact ghrelin, did not differ significantly from controls. Plasma levels of desoctanoyl ghrelin using the desacyl-ghrelin ELISA kit, N-terminus ghrelin using the ghrelin active RIA kit, and C-terminus ghrelin using the ghrelin total RIA kit were significantly higher in AN than controls, and displayed significant negative correlations with body mass index. Plasma levels of ghrelin determined using immunocomplex transfer-enzyme immunoassay or active ghrelin ELISA during iv glucose infusion were suppressed in both AN and controls, whereas plasma levels of degraded ghrelin levels were not significantly decreased in AN. Plasma levels of intact ghrelin are therefore not higher in AN than controls, whereas degraded forms of ghrelin are elevated in AN. Rapid suppression of plasma intact ghrelin, but not degraded ghrelin, occurs in AN in response to glucose infusion. The profiles of intact and degraded forms of ghrelin in plasma of AN patients differ from those of healthy women.

Serum levels of cholesterol, CETP, and apolipoproteins decreased after weight gain, indicating that cholesterol metabolism is accelerated in patients with AN with normal serum levels of FFA.

Ampulla cardiomyopathy is named after the echocardiographic abnormalities occurring in this condition, characterized by extensive akinesis (ballooning ) of the apical region with hypercontraction of the basal segment of the ventricle. We describe 3 young female anorexia nervosa patients showing evidence of this cardiac complication after hypoglycemia. One case was complicated by echocardiographically confirmed ampulla cardiomyopathy while the other 2 patients showed increases in myocardial enzymes and transient electrocardiographic abnormalities consistent with this complication. The precipitating event for all three patients was hypoglycemic coma, and this is the first case report in which this factor lead to the complication of ampulla cardiomyopathy in anorexia nervosa patients.

Abstract. Osteoporosis is one of the major complications in anorexia nervosa (AN) patients. Receptor activator of nuclear factor κB ligand (RANKL) and osteoprotegerin (OPG) have been identified as important regulators of bone turnover. The objective of this study was to clarify the role of RANK-RANKL-OPG system, and their relationship with other regulators for bone metabolism in AN patients. We investigated serum levels of RANKL, OPG, and bone turnover markers of 26 Japanese young female AN patients and 7 age-matched healthy women. We measured serum levels of estradiol (E2), insulin like growth factor-I (IGF-I) and triiodothyronin (T3) from the same samples and studied their relationship with RANKL or OPG. Mean serum levels of E2, IGF-I, T3 and leptin in AN patients were significantly lower than those of controls (p<0.05). Serum levels of OPG in AN patients were significantly higher than those in controls and negatively correlated with body mass index (BMI), E2, IGF-I or leptin. Serum levels of free RANKL could not be detected except for only one healthy control in both groups. These results suggest that serum OPG levels may be increased by a compensatory mechanism for malnutrition and estrogen deficiency which induces an increase in bone resorption. FIFTY percent of new AN outpatients show a decrease in lumbar bone mineral density (BMD) [1][2][3][4][5][6]. We have previously reported that the mechanism of osteoporosis in AN patients is both decreased bone formation and increased bone resorption due to decreased serum levels of insulin like growth factor-I (IGF-I) and estradiol (E2) [4,5]. Receptor activator of nuclear factor κB ligand (RANKL) and osteoprotegerin (OPG) have been identified as important regulators of bone turnover [7][8][9]. RANKL is essential for osteoclast differentiation via its receptor located on the surface of osteoclast precursor cells. OPG is a soluble decoy receptor which inhibits osteoclast differentiation through its binding to RANKL. Estrogen negatively regulates osteoclast differentiation and proliferation via RANK-RANKL system, and increases osteoclast apoptosis. Estrogen also inhibits osteocyte apoptosis, maintains osteocyte viability, and stimulates osteoblast-like cells to produce OPG [10][11][12][13]. It is reported that serum levels of RANKL and OPG increased in postmenopausal women [14,15]. AN is accompanied with amenorrhea and demonstrates low serum levels of E2. Serum levels of OPG In AN patients have been already reported [16,17], but the results are controversial. The objective of this study is to clarify the role of RANK-RANKL-OPG system and their relationship with other regulators for bone metabolism in AN patients.

A 50-year-old Japanese manwith Grave's disease had been taking propylthiouracil (PTU) for 10 years prior to the diagnosis of pneumonia. He noticed dyspnea on exertion and had a dry cough for at least 2 years and then

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