Liver alterations in anorexia nervosa are not caused by insulin resistance.

BACKGROUND: Liver dysfunction has been widely reported in connection with anorexia nervosa (AN) but the pathogenesis of these alterations has never been fully understood despite reported theories about the presence of insulin resistance (IR) and non-alcoholic fatty liver disease (NAFLD). The aim of this study is to investigate if hypertransaminasemia in AN is linked to IR and NAFLD. METHODS: Anthropometric data and laboratory exams of 34 patients and 34 controls were analyzed, including alanine-aminotransferase, aspartate-aminotransferase and homeostatic model assessment of insulin resistance (HOMA-IR) index. All subjects also underwent magnetic resonance imaging (MRI), ultrasonography (US), and transient elastography (TE). RESULTS: Evidence of increased alanine aminotransferase in AN patients was confirmed in our sample together with a lower HOMA-IR index compared to controls. Positive results in US appeared in 16 patients vs none in controls (p = 0.0007); patients with liver parenchyma abnormalities in US were not different than normal-US patients in any of the studied variables. Only one patient showed non-alcoholic fatty liver disease in MRI while abnormal TE was found in four patients and never in controls. CONCLUSIONS: Liver damage suggested by increased serum liver enzymes cannot be due to liver steatosis but potentially to a different liver disease (not identified by MRI) or to an early liver fibrosis not associated with an insulin-resistant status.

Key Points for Cholelithiasis and Gallstone Ileus Prevention Following Biliointestinal Bypass.

BACKGROUND Biliointestinal bypass is a malabsorptive procedure for surgical treatment of morbid obesity. It is the evolution of jejunoileal bypass, and it is characterized by a cholecysto-jejunostomy on the proximal end of the excluded jejunum, therefore, allowing bile flow through the excluded bowel loop reducing the risk of postoperative diarrhea and malabsorption syndrome. Obesity is a well-known risk factor for cholelithiasis; moreover, bariatric surgery has been showed to increases the risk of gallstones formation. CASE REPORT A 48-years-old male (body mass index 42 kg/m²) received a laparoscopic biliointestinal bypass. Nine years later, the patient received a cholecystotomy for removal of biliary stones. No surgical procedures were performed on the cholecysto-jejunostomy. Fourteen years after the bariatric treatment, the patient underwent enterolithotomy after a diagnosis of gallstone ileus. The impacted biliary stone was documented in the excluded loop proximal to the anti-reflux valvular system. The postoperative course and 1-year follow-up were uneventful. CONCLUSIONS Few cases of gallstone ileus following biliointestinal bypass have been described in the literature. We report a new case and also propose few tips and tricks for cholelithiasis and gallstone ileus prevention after biliointestinal bypass.

Ten Years After Bariatric Surgery: Bad Quality of Life Promotes the Need of Psychological Interventions.

Background: This study aims to evaluate long-term quality of life (QoL) and primary clinical outcomes, 10 years after biliointestinal bypass (BIB) surgery. It was expected that, although BIB might show encouraging primary outcomes, long term QoL could be significantly impaired. Methods: Ninety patients were contacted for a phone interview [age 41.0 ± 10.6 (mean ± SD) years, age-range 31-65 years]. QoL (by SF-36) and the clinical situation (by ad hoc questionnaire) were collected. Data were analyzed with SPSS 22. SF-36 scores were compared with Italian normative data from general and healthy population. We also compared primary clinical outcomes and SF-36 scores between patients who reported high and low levels of satisfaction with BIB. Results: Considering SF-36 results, patients showed significant impairments in QoL compared to general and healthy populations. Sixty-five percent would repeat the BIB. All patients showed at least one chronic adverse event. It occurred a significant decrease in pre-post co-occurrence rates of diabetes (χ2 = 18.41; p < 0.001) and hypertension (χ2 = 50.27; p < 0.001). Large and significant weight loss indexes (i.e., percent excess weight loss (%EWL); body mass index) were observed between pre-post intervention. Conclusion: BIB showed promising primary clinical outcomes (i.e., hypertension, diabetes, and weight loss). However, subjects reported a significant impairment in all SF-36 domains. Ad hoc psychological interventions should be implemented to ameliorate the quality of life of these patients.

No increase in prevalence of Barrett's oesophagus in a surgical series of obese patients referred for laparoscopic gastric banding.

INTRODUCTION: Obesity is a risk factor for gastroesophageal reflux and oesophageal adenocarcinoma. However, only a few studies have examined obesity and lifestyle risk factors in relation to Barrett's oesophagus. In this prospective study we assessed the presence of oesophagitis and Barrett's oesophagus in obese patients selected for laparoscopic gastric banding. METHODS: 1049 obese patients were referred for laparoscopic gastric banding (233 males; mean age 41.0±10.7 years). oesophagogastroduodenoscopy was performed before surgery to check for upper gastrointestinal tract disorders, especially hiatal hernia, signs of inflammation and/or erosions and/or ulcers of the oesophageal mucosa, and Barrett's epithelium. RESULTS: Mean body mass index was 45.15±6.46 kg/m(2). Overall 86/1049 (8.2%) patients had endoscopic signs of oesophagitis: 84 grade A, 1 grade B and 1 grade C, according to the Los Angeles classification. Hiatal hernia was detected in 127 patients (12.1%), with a mean size of 2.1±0.7 cm (range 1-4 cm); of these, 38 (29.9%) had oesophagitis (37 grade A and 1 grade B). No patients had any visible length of columnar epithelium. CONCLUSIONS: We could not confirm a high prevalence of Barrett's oesophagus in this series of obese patients.

Subclinical hypothyroidism in a patient affected by advanced AIDS and visceral leishmaniasis.

Hypothyroidism has been shown to occur in HIV disease. Thyroid function of patients affected by AIDS and leishmaniasis is unknown. Here we report the case of an AIDS advanced patient developing hypothyroidism during leishmaniasis. The thyroid disorder might have been caused by infiltration of the gland by Leishmania. An additive impact of HIV in thyroid function impairment is suggested.