Summary Background Gastrointestinal angiodysplasias (GIADs) may be the cause of recurrent bleeding, despite endoscopic treatment. Aim To evaluate the effect of long‐acting somatostatin analogues on blood transfusion requirements, in patients with refractory bleeding due to GIADs. Methods Consecutive patients with recurrent bleeding from GIADs were enrolled. They received somatostatin analogue treatment for at least 6 months. The efficacy was evaluated in terms of blood transfusions, frequency of bleeding episodes and haemoglobin level during 6 months of treatment (Period During) compared to a 6‐months' period before treatment (Period Before). Results Fifteen patients were enrolled from 2007 to 2010. The median duration of somatostatin analogue treatment was 12 months (range: 6–36). The number of transfusions significantly decreased in Period During compared with Period Before [median number: 2 (0–14) vs. 10 (6–24); P < 0.001]. The percentage of patients who experienced a bleeding event was lower during somatostatin analogues treatment (20% vs. 73%; P = 0.01). The mean haemoglobin level was significantly higher when somatostatin analogues were offered [median: 10 g/dL (9–13) vs. 7 (5–8.5); P < 0.001]. None of the patients discontinued treatment due to side effects. Conclusions Long‐acting somatostatin analogues treatment decreased transfusion needs in patients with refractory bleeding from gastrointestinal angiodysplasias. Bleeding episodes were limited and haemoglobin improved during treatment. Long‐acting somatostatin analogues may represent an option for the management of patients with chronic bleeding due to gastrointestinal angiodysplasias.

Symptomatic oesophageal involvement affected 5·4% of patients with MMP. Dermatologists and gastroenterologists should be aware of these mucocutaneous diseases and their oesophageal involvement, as it could lead to earlier diagnosis and better care. Oesophageal dilatation could be a therapeutic option for symptomatic stricture not relieved by optimized systemic therapy alone.

Wasting can occur at an early stage of HIV infection. Both reduced energy intake and increased resting energy expenditure (REE) have been considered as factors in wasting with predominant lean body mass loss, suggesting disturbances of protein metabolism. Our aim was to study protein-energy metabolism in relation to body composition and oral energy intake in asymptomatic patients with HIV infection but receiving no active antiretroviral therapy. Stable-weight asymptomatic male patients (n = 8) at stage A of HIV infection with a detectable viral load were compared with 9 healthy control men. Protein metabolism was studied in the postabsorptive state using a primed constant infusion of l-[1-(13)C]leucine and l-[2-(15)N]glutamine. REE was studied by indirect calorimetry, body composition by bioelectrical impedance, and energy intake by dietary records. BMI and lean body mass did not differ between patients and controls. In HIV-infected subjects, energy intake, protein breakdown, protein synthesis, and REE were 57% (P < 0.05), 18% (P < 0.05), 22% (P < 0.05) and 14% (P < 0.05) greater than in controls, respectively. REE and protein breakdown were correlated (r = 0.73, P < 0.05). The hormonal profile was normal in HIV-infected subjects with the exception of low urinary C-peptide and plasma reverse triiodothyronine. Plasma interleukin-6 and tumor necrosis factor-alpha were greater than in controls, but energy intake was 1.53 times the REE in the HIV-infected men. Thus, at the asymptomatic stage of HIV infection, increased protein turnover contributes to the increase in the REE. Moderate hyperphagia, which occurred despite increased levels of cytokines, in conjunction with increased protein synthesis maintains a normal body composition, without significant loss of lean body mass.