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The endocrine system is frequently altered after a major burn trauma. Besides the endocrine response to stress characterized by hypercortisolism, several hypothalamus-hypophysis-target gland axes are rapidly perturbed within a few days. These alterations can persist in the long term and deserve an appropriate treatment. Disturbances in water clearance and glucidic metabolism are also common and need to be diagnosed and corrected to decrease morbidity in such patients. Bone and mineral metabolism is deeply compromised and requires correction of mineral abnormalities in order to improve symptoms and prevent bone loss. No large prospective and/or intervention trials are available to date to elaborate age-related, evidence-based recommendations to monitor and treat burn-related endocrine alterations.

Obesity is a multifactorial syndrome and the likelihood of success of a medical nutritional treatment (MNT) over the long term is low. As psychological and behavioural factors have an important role in both pathogenesis and the treatment of obesity, these issues were investigated in individuals with obesity who reported a long-term success or a failure in terms of weight loss following a MNT. Eighty-eight individuals of an original cohort of 251 subjects were re-evaluated 10 years after a MNT with cognitive-behavioural approach for uncomplicated obesity. Fifty-three participants were classified as failure (body weight change ≥0.5 kg) and 35 as a success (10-year body weight change

Background & aims: The role of glycemic index of the diet in glucose control and cardiovascular prevention is still not clear. The aim of this study was to determine the effects of hypocaloric diets with different glycemic indexes and glycemic loads on endothelial function and glycemic variability in nondiabetic participants at increased cardiovascular risk. Methods: Forty nondiabetic obese participants were randomly assigned to a three-month treatment with either a low glycemic index (LGI; n ¼ 19) or high glycemic index (HGI; n ¼ 21) hypocaloric diet with similar macronutrient and fiber content. Endothelial function was measured as flow-mediated dilatation (FMD) of the brachial artery before and after dieting. In addition, 48-h continuous subcutaneous glucose monitoring was done before and after dieting in a subgroup of 24 participants. Results: The amount of weight loss after dieting was similar in both groups. The glycemic index of the diet significantly influenced the FMD (P < 0.005). In particular, the change of FMD was 2.3 2.6% following the LGI diet, and 0.9 3.6% after the HGI diet (P < 0.005). The mean 48-h glycemia decreased significantly after dietary treatment (P< 0.05), but no significant effect of the glycemic index of the diet on results was observed. The glycemic index of the diet significantly influenced the 48-h glycemic variability measured as coefficient of variability (CV%; P< 0.001). The CV% decreased after the LGI diet (from 23.5 to 20.0%) and increased after the HGI diet (from 23.6 to 26.6%). The change in percentage of FMD was inversely correlated with the change in the 48-h glycemic CV% (r¼ 0.45; P < 0.05). Conclusions: Endothelial function and glycemic variability ameliorate in association with the adherence to an LGI hypocaloric diet in nondiabetic obese persons. Clinical trial registration number: ISRCTN56834511.

Purpose We evaluated the role of residual vein thrombosis (RVT) to assess the optimal duration of anticoagulants in patients with cancer who have deep vein thrombosis (DVT) of the lower limbs. Patients and Methods Patients with active cancer and a first episode of DVT treated with low molecular weight heparin (LMWH) for 6 months were eligible. Patients were managed according to RVT findings: those with RVT were randomly assigned to continue LMWH for an additional 6 months (group A1) or to discontinue it (group A2), and patients without RVT stopped LMWH (group B). The primary end point was recurrent venous thromboembolism (VTE) during the 1 year after disconinuation of LMWH, and the secondary end point was major bleeding. Analyses are from the time of random assignment. Results Between October 2005 and April 2010, 347 patients were enrolled. RVT was detected in 242 patients (69.7%); recurrence occurred in 22 of the 119 patients in group A1compared with 27 of 123 patients in group A2. The adjusted hazard ratio (HR) for group A2 versus A1 was 1.37 (95% CI, 0.7 to 2.5; P = .311). Three of the 105 patients in group B developed recurrent VTE; adjusted HR for group A1 versus B was 6.0 (95% CI, 1.7 to 21.2; P = .005). Three major bleeding events occurred in group A1, and two events each occurred in groups A2 and B. The HR for major bleeding in group A1 versus group A2 was 3.78 (95% CI, 0.77 to 18.58; P = .102). Overall, 42 patients (12.1%) died during follow-up as a result of cancer progression. Conclusion In patients with cancer with a first DVT, treated for 6 months with LMWH, absence of RVT identifies a population at low risk for recurrent thrombotic events. Continuation of LMWH in patients with RVT up to 1 year did not reduce recurrent VTE.

Treatment with bisphosphonates induces differentiation and activation of Vγ9Vδ2 T lymphocytes obtained from peripheral blood showing also an antitumoral effect in both in vitro and in vivo models. Aim of the present study was to determine in vivo the effect of BPs treatment in patients affected with osteoporosis on Vγ9Vδ2 T lymphocytes. We have studied Vγ9Vδ2 T lymphocytes expansion and differentiation from PBMC obtained from osteoporotic patients treated with one of the following bisphosphonates zoledronate, alendronate, neridronate or risedronate. We have found that zoledronic acid, followed by alendronate was the most effective on reducing CM population (100%) and increasing TEM and TEMRA γδ population. Our results indicate that in vivo treatment with BPs induces Vγ9Vδ2 cells to mature toward the effector phenotype, which may induce more antiresorptive responses.

Several evidences have shown in the last years a possible correlation between cardiovascular diseases and osteoporosis. Patients affected with osteoporosis, for example, have a higher risk of cardiovascular diseases than subjects with normal bone mass. However, the heterogeneous approaches and the different populations that have been studied so far have limited the strength of the findings. Studies conducted in animal models show that vascular calcification is a very complex mechanism that involves similar pathways described in the normal bone calcification. Proteins like BMP, osteopontin, osteoprotegerin play an important role at the bone level but are also highly expressed in the calcified vascular tissue. In particular, it seems that the OPG protect from vascular calcification and elevated levels have been found in patients with CVD. Other factors like oxidative stress, inflammation, free radicals, lipids metabolism are involved in this complex scenario. It is not a case that medications used for treating osteoporosis also inhibit the atherosclerotic process, acting on blood pressure and ventricular hypertrophy. Given the limited amount of available data, further studies are needed to elucidate the underlying mechanisms between osteoporosis and cardiovascular disease which may be important in the future also for preventive and therapeutic approaches of both conditions.

Bisphosphonates (BPs) are the most used medications for the treatment of osteoporosis and bone metastases [1]. BPs have a wide range of target cells including macrophages, osteoblasts, enterocytes, tumor and stromal cells [1]. These compounds have the ability to activate Vc9 Vd2 T lymphocytes, and their proliferation produces proinflammatory cytokines like interferon-gamma (IFN) and tumor necrosis factor (TNF) alpha; in addition, this subset displays efficient cytotoxic activity against neoplastic cells [2]. This effect was observed in both in vitro [3] and in vivo models [4]. Treatment, with zoledronic acid, of patients with prostate and breast cancer reduced effect of bone metastases and induced differentiation and activation of Vc9 Vd2 T lymphocytes obtained from peripheral blood [5]. We have already shown in vitro that treatment with BPs induces Vc9 Vd2 T lymphocytes to differentiate toward an effector/cytotoxic phenotype showing also a major content of IFN-gamma [6]. The aim of the present study was to determine in vivo the effect of BPs treatment in patients affected with osteoporosis on Vc9 Vd2 T lymphocytes.

Background Bisphosphonates (BPs) are currently the chief drugs for the prevention/treatment of osteoporosis; one of their adverse effects is the osteonecrosis of the jaw (BRONJ). The primary endpoints of this multi-center cross-sectional study are: i) an observation of the clinical features of BRONJ in 87 osteoporotic, non-cancer patients; and ii) an evaluation of their demographic variables and comorbidities. Methods 87 BRONJ patients in therapy for osteoporosis with BPs from 8 participating clinical Italian centers were consecutively identified and studied. After BRONJ diagnosis and staging, comorbidities and data relating to local and drug-related risk factors for BRONJ were collected. Results 77/87 (88.5%) patients in our sample used alendronate as a BP type; the duration of bisphosphonate therapy ranged from 2 to 200 months, and 51.7% of patients were in treatment for ≤ 38 months (median value). No comorbidities or local risk factors were observed in 17 (19.5%) patients, indicating the absence of cases belonging to BRONJ forms triggered by surgery. BRONJ localization was significantly associated with age: an increased risk of mandible localization (p = 0.002; OR = 6.36, 95%CI = [1.89; 21.54]) was observed for those over 72 yrs. At multivariate analysis, the increased risk of BRONJ in the mandible for people over 72 yrs (OR′ = 6.87, 95%CI = [2.13; 2.21]) was confirmed for a BP administration > 56 months (OR′ = 4.82, 95%CI = [2.13; 22.21]). Conclusion Our study confirms the fundamental necessity of applying protocols of prevention in order to reduce the incidence of BRONJ in osteoporotic, non-cancer patients in the presence of comorbidities and/or local risk factor as well as, less frequently, in their absence.

The association between osteoporosis and jawbones remains an argument of debate. Both osteoporosis and periodontal diseases are bone resorptive diseases; it has been hypothesized that osteoporosis could be a risk factor for the progression of periodontal disease and vice versa. Hypothetical models linking the two conditions exist: in particular, it is supposed that the osteoporosis-related bone mass density reduction may accelerate alveolar bone resorption caused by periodontitis, resulting in a facilitated periodontal bacteria invasion. Invading bacteria, in turn, may alter the normal homeostasis of bone tissue, increasing osteoclastic activity and reducing local and systemic bone density by both direct effects (release of toxins) and/or indirect mechanisms (release of inflammatory mediators). Current evidence provides conflicting results due to potential biases related to study design, samples size and endpoints. The aim of this article is to review and summarize the published literature on the associations between osteoporosis and different oral conditions such as bone loss in the jaws, periodontal diseases, and tooth loss. Further well-controlled studies are needed to better elucidate the inter-relationship between systemic and oral bone loss and to clarify whether dentists could usefully provide early warning for osteoporosis risk. Key words:Osteoporosis, periodontitis, oral bone loss, tooth loss, edentulism, bone mineral density.

Budd-Chiari syndrome may be defined as a heterogeneous group of vascular disorders characterized by obstruction of hepatic venous return to the level of hepatic venules, supra-hepatic veins, inferior vena cava or right atrium. The main cause of this syndrome is represented by myeloproliferative diseases and, in particular, by polycythemia vera. The latter may cause multiple splanchnic thrombosis, including portal vein thrombosis, particularly important for its clinical outcomes (ascites, collateral vessels genesis, etc.). We report 2 cases of a Budd-Chiari syndrome induced by polycythemia vera characterized by an abnormal clinical onset, both as regards subjects’ age (29 and 39 years old, respectively) and set of symptoms, signs and laboratory data. After a complete clinical, instrumental and genetic diagnosis, the patients were treated with combined therapy, using acetylsalicylic acid and hydroxyurea. The therapy proved successful and patients are still in follow up in our institution. Polycythemia vera should be suspected in patients affected with portal vein thrombosis and Budd-Chiari syndrome even if its clinical onset might be unusual. Every effort should be made to make a correct and early diagnosis in order to start appropriate therapy as soon as possible and to prevent patients from useless diagnostic and therapeutic treatments.

Background: The diagnosis of food hypersensitivity (FH) in adult patients with gastrointestinal symptoms, beyond the immediate IgE-mediated clinical manifestations, is very often difficult. The aims of our study were to: 1) evaluate the frequency of FH in patients with irritable bowel syndrome (IBS)-like clinical presentation; and 2) compare the diagnostic accuracy of two different methods of in vitro basophil activation tests. Methods: Three hundred and five patients (235 females, age range 18–66 years) were included and underwent a diagnostic elimination diet and successive double-blind placebo-controlled (DBPC) challenges. Two different methods of in vitro basophil activation tests (BAT) (CD63 expression after in vitro wheat or cow’s milk proteins stimulation) were evaluated: one was performed on separated leukocytes, and the other on whole blood. Results: Ninety patients of the 305 studied (29.5%) were positive to the challenges and were diagnosed as suffering from FH. BAT on separate leukocytes showed a sensitivity of 86% and a specificity of 91% in FH diagnosis. BAT on whole blood showed a sensitivity of 15%–20% and a specificity of 73% in FH diagnosis (p Conclusions: About one third of the IBS patients included in the study were suffering from FH and were cured on the elimination diet. The BAT based on CD63 detection on whole blood samples did not work in FH diagnosis and showed a significantly lower sensitivity, specificity and diagnostic accuracy than the assay based on separated leukocytes.

The gastrointestinal tract of healthy individuals is colonized by hundreds of saprophytes and mycetes, especially the Candida species, are habitual ones. Under certain conditions, the fungal flora may overgrow, resulting in lesions of the digestive mucosa which, rarely, can have a local diffusion and/or spread to the lympho-hematogenous system. Mycotic infections of the stomach can sometimes look like benign gastric ulcers. Here, we present the case report of a woman, aged 64, who presented with type II diabetes mellitus and psoriasis, on chronic treatment with cyclosporin A and with endoscopic evidence of an ulcerated, vegetating gastric lesion secondary to Candida albicans infection. Although strongly suggestive of malignancy, it completely healed after cyclosporin withdrawal and the administration of oral antifungal drugs.

SummaryBackground Lymphoid aggregates are normally found throughout the small and large intestine. Known as lymphoid nodular hyperplasia (LNH), these aggregates are observed especially in young children and are not associated with clinical symptoms being considered ‘physiological’. In children presenting with gastrointestinal symptoms the number and size of the lymphoid follicles are increased. Patients suffering from gastrointestinal symptoms (i.e. recurrent abdominal pain) should systematically undergo gastroduodenoscopy and colonoscopy. With these indications LNH, especially of the upper but also of the lower gastrointestinal tract has been diagnosed, and in some children it may reflect a food hypersensitivity (FH) condition. Aim To review the literature about the relationship between LNH and FH, particularly focusing on the diagnostic work-up for LNH related to FH. Methods We reviewed literature using Pubmed and Medline, with the search terms ‘lymphoid nodular hyperplasia’, ‘food hypersensitivity’, ‘food allergy’ and ‘food intolerance’. We overall examined 10 studies in detail, selecting articles about the prevalence of LNH in FH patients and of FH in LNH patients. Results Collected data showed a median of 49% (range 32–67%) LNH in FH patients and a median of 66% (range 42–90%) FH in LNH patients. Literature review pointed out that the most important symptom connected with LNH and/or FH was recurrent abdominal pain, followed by diarrhoea and growth retardation. Both LNH and FH are associated with an increase in lamina propria γ/δ+ T cells, but the mechanisms by which enhanced local immune responses causing gastrointestinal symptoms still remain obscure. Conclusions When assessing FH, we rely on clinical evaluation, including elimination diet and challenge tests, and endoscopic and immunohistochemical findings. Considering the possible co-existence of duodenal and ileo-colonic LNH, upper endoscopy can be recommended in children with suspected FH, especially in those presenting with additional upper abdominal symptoms (i.e. vomiting). Likewise, lower endoscopy might be additionally performed in patients with suspected FH and LNH of the duodenal bulb, also presenting with lower abdominal symptoms (i.e. recurrent abdominal pain).

We here report a very unusual presentation of ruptured thoracic aortic aneurysm. In a 50-year-old patient, almost asymptomatic and in stable clinical conditions, the chest radiograph and computed tomography scan revealed a right-sided rupture of a previously undiagnosed thoracic aortic aneurysm. The patient was treated successfully with an emergency surgical procedure.