This guideline presents recommendations for the step-wise management of patients with overt upper gastrointestinal bleeding. Hemodynamic status is first assessed, and resuscitation initiated as needed. Patients are risk-stratified based on features such as hemodynamic status, comorbidities, age, and laboratory tests. Pre-endoscopic erythromycin is considered to increase diagnostic yield at first endoscopy. Pre-endoscopic proton pump inhibitor (PPI) may be considered to decrease the need for endoscopic therapy but does not improve clinical outcomes. Upper endoscopy is generally performed within 24h. The endoscopic features of ulcers direct further management. Patients with active bleeding or non-bleeding visible vessels receive endoscopic therapy (e.g., bipolar electrocoagulation, heater probe, sclerosant, clips) and those with an adherent clot may receive endoscopic therapy; these patients then receive intravenous PPI with a bolus followed by continuous infusion. Patients with flat spots or clean-based ulcers do not require endoscopic therapy or intensive PPI therapy. Recurrent bleeding after endoscopic therapy is treated with a second endoscopic treatment; if bleeding persists or recurs, treatment with surgery or interventional radiology is undertaken. Prevention of recurrent bleeding is based on the etiology of the bleeding ulcer. H. pylori is eradicated and after cure is documented anti-ulcer therapy is generally not given. Nonsteroidal anti-inflammatory drugs (NSAIDs) are stopped; if they must be resumed low-dose COX-2-selective NSAID plus PPI is used. Patients with established cardiovascular disease who require aspirin should start PPI and generally re-institute aspirin soon after bleeding ceases (within 7 days and ideally 1-3 days). Patients with idiopathic ulcers receive long-term anti-ulcer therapy.

Tuberculous pleurisy can result in pleural fibrosis, calcification and thickening. To prevent these complications, corticosteroids are frequently used in addition to antituberculous drugs; however, new therapeutic regimens can control the disease and minimise the sequelae, and there is no convincing evidence of the benefit of the use of corticosteroids as adjuvant therapy. Patients received isoniazid 5 mg/kg and rifampicin 10 mg/kg daily for six months. Additionally, they were randomly assigned to a double blind treatment with either prednisone (1 mg/kg/day for 15 days and then tapering off) or placebo during the first month of treatment. Different clinical, radiological, and functional parameters were evaluated to assess the effect of corticosteroids. Fifty seven patients received prednisone and 60 placebo. At the end of the treatment the clinical outcome, the rate of reabsorption of the pleural fluid, the pleural sequelae, as well as lung capacity were similar in both groups. Corticosteroids do not influence the clinical outcome or the development of long term pleural sequelae in tuberculous pleurisy.

Liver hydatid cyst is a disease of zoonosis caused by Echinococcus granulosus or less frequently by Echinococcus multilocularis and Echinococcus oligarthrus. The primary carriers are canines, while human beings are secondary hosts. Early diagnosis is important for cysts not to become complicated and for the treatment not to get difficult. The most effective treatment of uncomplicated hydatid cyst is to reduce the dead space of the cavity and to discharge the fluid as much as possible. However, if the cysts get complex, there is no standard treatment management defined other than offered management options by authors. In complex conditions, the treatment is determined according to the stage of the cyst and the relation of the cyst with biliary ducts or surrounding organs. In this chapter, the treatment regimens of liver hydatid disease mainly based on interventions and surgical operations are going to take a part.

Thyroid dysfunction and diabetes mellitus are closely linked. Several studies have documented the increased prevalence of thyroid disorders in patients with diabetes mellitus and vice versa. This review critically discusses the different underlying mechanisms linking type 1 and 2 diabetes and thyroid dysfunction to demonstrate that the association of these two common disorders is unlikely a simple coincidence. We assess the current state of knowledge on the central and peripheral control of thyroid hormone on food intake and glucose and lipid metabolism in target tissues (such as liver, white and brown adipose tissue, pancreatic β cells, and skeletal muscle) to explain the mechanism linking overt and subclinical hypothyroidism to type 2 diabetes and metabolic syndrome. We also elucidate the common susceptibility genes and the pathogenetic mechanisms contributing to the autoimmune mechanism involved in the onset of type 1 diabetes mellitus and autoimmune thyroid disorders. An untreated thyroid dysfunction can impair the metabolic control of diabetic patients, and this association can have important repercussions on the outcome of both of these disorders. Therefore, we offer recommendations for the diagnosis, management, and screening of thyroid disorders in patients with diabetes mellitus, including the treatment of diabetic patients planning a pregnancy. We also discuss the major causes of failure to achieve an optimal management of thyroid dysfunction in diabetic patients and provide recommendations for assessing and treating these disorders during therapy with antidiabetic drugs. An algorithm for a correct approach of these disorders when linked is also provided.

Hypertensive disorders of pregnancy (HDP) as a group of medical complications in pregnancy are believed to be associated with an increased risk of poor fetal growth, but the influence on offspring’s body composition is not clear. The aim of the present study was to evaluate the association between maternal hypertensive disorders of pregnancy and overweight status in the offspring of mothers with gestational diabetes mellitus (GDM). A cross-sectional study among 1263 GDM mother-child pairs was performed in Tianjin, China. General linear models and logistic regression models were used to assess the associations of maternal hypertension in pregnancy with anthropometry and overweight status in the offspring from birth to 1–5 years old. Offspring of GDM mothers who were diagnosed with hypertensive disorders during pregnancy had higher mean values of Z scores for birth weight for gestational age and birth weight for length, and higher mean values of Z scores for weight for age, weight for length/height, and body mass index for age at 1–5 years old than those of GDM mothers with normal blood pressure during pregnancy. Maternal hypertensive disorders of pregnancy were associated with increased risks of large for gestational age (OR 1.74, 95%CI 1.08–2.79) and macrosomia (OR 2.02, 95%CI 1.23–3.31) at birth and childhood overweight/obesity at 1–5 years old age (OR 1.88, 95%CI 1.16–3.04). For offspring of mothers with GDM, maternal hypertension during pregnancy was a risk factor for macrosomia at birth and childhood overweight and obesity, and controlling the maternal hypertension may be more important for preventing large for gestational age babies and childhood obesity.

The purpose of this study, was to determine whether hypoxia preconditioning can protect corneal stromal cells from UV stress and cytokine mediated apoptosis. Two models were implemented. First, primary cultured bovine corneal fibroblasts were preconditioned with 0.5–1.5% O2 for 4 hr and stressed with UV-irradiation or stimulation of Fas receptor. Second, bovine eyes were preconditioned with 0.5% O2 for 4 hr and stressed by epithelial scraping to induce anterior keratocyte apoptosis. Cell fate was analyzed at 4 hr after stress using quantitative TUNEL or condensed nuclei assays. Cell apoptotic rates in hypoxia preconditioned groups were significantly lower (50–80%) than that of normoxia control groups. Hypoxia prevented the degradation of the transcription factor HIF-1α. CoCl2 (100–200 μM), a chemical inducer of HIF-1α, also produced strong protection against UV and Fas induced apoptosis. Moreover, hypoxia preconditioned media protected cells against UV-induced apoptosis. These findings demonstrate that hypoxia preconditioning has a generalized protective effect against stromal fibroblast and keratocyte apoptosis and suggest that HIF-1α mediated expression and secretion of protective factors is involved.

To determine why a subgroup of coasted patients developed moderate/severe ovarian hyperstimulation syndrome (OHSS) in an assisted reproduction setting. Retrospective study of 2948 in-vitro fertilization/intracytoplasmic sperm injection (IVF/ICSI) treatment cycles with 327 patients requiring coasting. Long protocol gonadotrophin releasing hormone analogue (GnRH-a) regimen was used and serum estradiol (E2) checked when ≥20 follicles were noted on follicular tracking. Coasting was initiated when leading three follicles were ≥15mm with E2 ≥1635pg/ml. The incidence of moderate/severe OHSS was 10.4% in coasted patients (equivalent 1.15% of the total IVF/ICSI cycles in the Center). Coasted patients who subsequently developed OHSS showed a significantly higher number of retrieved oocytes, higher serum E2 level on the day of human chorionic gonadotrophin (hCG) administration, and multiple pregnancies. No significant differences were noted with female age, BMI, cause of infertility, gonadotrophin dosage, coasting duration, and % of E2 drop. Moderate/severe OHSS might be predicted in coasted patients by a combination of total oocyte numbers and E2 level on the day of hCG. Multiple pregnancies also significantly increased the risk.

Tea has anecdotally been associated with stress relief, but this has seldom been tested scientifically. To investigate the effects of 6 weeks of black tea consumption, compared with matched placebo, on subjective, cardiovascular, cortisol and platelet responses to acute stress, in a parallel group double-blind randomised design. Seventy-five healthy nonsmoking men were withdrawn from tea, coffee and caffeinated beverages for a 4-week wash-out phase during which they drank four cups per day of a caffeinated placebo. A pretreatment laboratory test session was carried out, followed by either placebo (n = 38) or active tea treatment (n = 37) for 6 weeks, then, a final test session. Cardiovascular measures were obtained before, during and after two challenging behavioural tasks, while cortisol, platelet and subjective measures were assessed before and after tasks. The tasks induced substantial increases in blood pressure, heart rate and subjective stress ratings, but responses did not differ between tea and placebo treatments. Platelet activation (assessed using flow cytometry) was lower following tea than placebo treatment in both baseline and post-stress samples (P < 0.005). The active tea group also showed lower post-task cortisol levels compared with placebo (P = 0.032), and a relative increase in subjective relaxation during the post-task recovery period (P = 0.036). Compared with placebo, 6 weeks of tea consumption leads to lower post-stress cortisol and greater subjective relaxation, together with reduced platelet activation. Black tea may have health benefits in part by aiding stress recovery.