Shortbowelsyndrome is at once a surgical, medical, and a disorder, with potential for life-threatening complications as well as eventual independence from artificial nutrition. Navigating through the diagnostic and therapeutic decisions is ideally accomplished by a multidisciplinary team comprised of nutrition, pharmacy, social work, medicine, and surgery. Early identification of patients at risk for long-term PN-dependency is the first step towards avoiding severe complications. Close monitoring of nutritional status, steady and early introduction of enteral nutrition, and aggressive prevention, diagnosis and treatment of infections such as line sepsis, and bacterial overgrowth can significantly improve prognosis. Intestinal transplantation is an emerging treatment that may be considered when intestinal failure is irreversible and children are suffering from serious complications related to TPN administration.
Damage control and gastrointestinal surgery have come a long way from the first reported case of an enterocu- taneous fistula to advances in Intestinal transplant and vacuum assisted therapy. Everything we have known in between such as intestinal resections, enteral/parenteral nutrition, delayed abdominal wall closure and intestinal reconstruction have all lead to an exponential increase in our knowledge of gastrointestinal surgery. One area that still remains a significant challenge and clinical dilemma to the general surgeon is intestinal failure in shortbowelsyndrome. Not only does the anatomical complexity of shortbowelsyndrome offer difficulties in the definite reconstruction, but also the accompanying intestinal failure increases patient morbidity and mortality. There are no current algorithms or systematic approaches to these daunting clinical scenarios and although sur- gery has come a long way, there is still room for determining optimal approaches. Therefore, it is critical to keep researching new ways to treat these patients. A relatively new horizon in managing intestinal failure in shortbowelsyndrome is the use of biomarkers. Here we present a short review on the possible future treatment. The aim of this paper is to provide a pathway for future research into the treatment of this complex area of general surgery. Key words: shortbowelsyndrome; bowel failure; biomarkers; citrulline; apoprotein(a); rehabilitation.
The symptoms of intestinal carcinoid tumour are non- specific and vague, generally consisting of periodical abdominal pain as a major symptom, along with intesti- nal obstruction, intermittent diarrhoea, and gastrointesti- nal bleeding [1,5,10]. Intestinal obstruction, due to a desmoplastic reaction from the tumour causing local mesenteric fibrosis, can lead to the need of surgery and to the incidental finding of a carcinoid tumour . The inci- dence of carcinoid syndrome is variable, reported to occur in 1.6–18% of cases, depending on the location of the pri- mary tumour, local tumour extension, and the secretion of serotonin and other amines [2,5,10,11]. Therefore, ileal carcinoids are more likely to develop the syndrome with almost 90% of patients with carcinoid syndrome having a small bowel carcinoid . Whilst the development of hepatic metastasis has been a common established pre- requisite for the development of carcinoid syndrome, it is not essential [2,11]. Despite the fact that serotonin is almost always present in carcinoid syndrome, the classical symptoms of the syndrome, flushing, diarrhoea, intesti- nal cramps, heart valves lesions, asthma and wheezing are thought to be caused by other amines, with one example being flushing caused by bradykinin [2,11]. Nevertheless, as many as 40–60% of patients are asymptomatic and as the symptoms are often non-specific, this may lead to a delay in diagnosis with a range from 2–20 years. In one series, the median delay for abdominal carcinoid tumours was 5.5 years, with a maximum delay of 22 years, although 12% had no delay . At diagnosis, 10% had only a primary tumour, 20% had lymph node metastases, 41% liver metastases, 16% carcinomatosis, and 13% had extra-abdominal metastases. These findings correlate with other studies [6,11].
Hepatorenal syndrome is complication of advanced cirrhosis characterized by renal failure, changes in systemic blood pressure, and increased activity of en- dogenous vasoactive systems. Renal failure is due to severe renal vasoconstriction developing in the late stages of cirrhosis. The pathogenesis of hepatorenal syndrome is the result of an extreme underfilling of the arterial circulation secondary to an arterial vasodila- tion located in the splanchnic circulation. This under- filling triggers a compensatory response with activa- tion of vasoconstrictor systems. The diagnosis of hepa- torenal syndrome is based on established diagnostic criteria aimed at excluding nonfunctional causes of re- nal failure. The prognosis of patients with hepatorenal syndrome is very poor. Liver transplantation is the best option in selected patients, but it is not always ap- plicable due to the short survival expectancy and do- nor shortage. Pharmacological therapies based on the use of vasoconstrictor drugs (terlipressin, midodrine, octreotide or noradrenline) are the most promising in aims of successfully offering a bridge to liver trans- plantation. Prevention of hepatorenal syndrome with albumin infusion is recommended in patients with spontaneous bacterial peritonitis and with pentoxifyl- line in patients with acute alcoholic hepatitis.
The diagnosis of OSA was based on the results of a sleep test, in accordance with the guidelines of the Spanish national consensus on apnea-hypopnea syndrome . All participating centers used the same model of polygraph (Embletta; ResMed, Australia) for the diagnosis of OSA. Oronasal flow, thoracoabdominal movements, ECG, and pulse oximetry were recorded. Apnea is defined as an absence of airflow lasting ! 10 seconds. Hypopnea is defined as a reduction in airflow lasting ! 10 seconds and is associated with oxygen desaturation. Oxygen desaturation (ODI) is considered as a decrease in SaO2 >4%. The apnea-hypopnea index is defined as the number of apneas and hypopneas per hour of sleep. The extent of self-reported sleepiness/ drowsiness was analyzed using the Spanish version of the ESS test . Echocardiographic evaluations and Killip classification were performed routinely at hospital admission. During hospitalization, we evaluated the severity of ACS and each patient’s short-term prognosis, in terms of the ejection fraction, the Killip score, the number of affected vessels, the average and
This cross-sectional study in a representative sample of the Spanish population aged ≥ 40 years found a prevalence of 0.01% for Brugada type 1 pattern, 1.01% for long QTc interval defined as ≥ 470 ms or 0.42% when defined as ≥ 480 ms, and 0.18% for short QTc. Consequently, we found that electrocardiographic abnormalities associated with SCD were present in a nonnegligible percentage of the general population. Based on the results, it was estimated that 0.6% to 1.2% of the population ≥ 40 years old has an electrocardiographic pattern associated with a higher risk of SCD. If patients with borderline QTc and Brugada type 2 pattern are also considered, this percentage would be nearly 10%.
The main ﬁ ndings of the present study can be summarized as follows: (1) Short- and long-term prognosis depends on the trigger of TTS; (2) patients with an emotional trigger have a better prognosis, whereas those with physical stress have the worst; (3) not all physical triggers inﬂuence the prognosis of patients in the same way, with those triggered by hypoxia presenting a worse evolution in the short and long term; (4) incidence of physical, emotional, and unidenti ﬁ able triggers are similar; and (5) age > 70 years, shock on admission, left ventricular ejection fraction < 30%, and diabetes mellitus were also independent predictors of mortality during the follow-up. Initial studies had suggested that TTS is predominantly preceded by emotional triggers. 15,16 Subsequent studies have proven that this syndrome may also be triggered by physical factors or even without any evident preceding trigger. 17–19 Some previous studies have shown that TTS related to physical stress could have a worse prognosis. 13,19,20 Recently, a classi ﬁ cation for TTS has been proposed based on its possible prognostic implications. 13 The reason for this differentiation was to facilitate the identi ﬁ cation and moni- toring of phenotypes that could be related to a worse short- and long-term prognosis. Our current data con ﬁ rm this point, showing a higher mortality in the group of TTS related to physical stress and a better survival rate in the group with emotional stress. In addition, our data add more information regarding the different types of physical triggers that exist showing a different prognosis. However, the reason for the difference in mortality still remains unclear. Although several hypotheses have been proposed to explain the mechanism of TTS, catecholamine release by the central nervous system is considered to have a central role in the pathophysiology of TTS. 2,21–23 Some researchers advocate for a differentiation in the pathophysiological mechanism that triggers TTS. On the one hand, emotional triggers may have a phasic nature, and Table 3. Multiple Cox Regression for Long-Term Mortality
represented flares in disease activity. CE yielded ne- gative findings in approximately 48% of symptomatic patients, which, the authors interpreted as symptoms caused by other diseases (bacterial overgrowth, irritable bowelsyndrome, etc.) CE yielded negative findings in approximately 48% of symptomatic patients, which the authors interpreted as symptoms caused by other diseases (bacterial overgrowth, irritable bowelsyndrome …). Accordingly, they believe that the use of CE avoided unnecessary treatments, and recommended that every patient with Crohn’s disease should undergo CE early in the evolution of the disease, in order to have an accurate evaluation of disease extension. Nevertheless, this study has a retrospective design and does not describe a follow up, so the results must be interpreted with caution  .
Patients affected with FXS have more than 200 repeats of the CGG trinucleotide. On the other hand, premutation carriers (55 to 200 repeats) although are not affected with the classic FXS phenotype, can have other medical, psychiatric and neurological problems. In the last 15 years multiple advances have been made in the description of genetic characteristics, function of the protein encoded by the FMR1 gene (FMRP), pharmacological management and the description, in carriers of the premutation, of the Fragile X associated Tremor/Ataxia Syndrome (FXTAS) and fragile X-associated primary ovarian insufficiency (FXPOI) 3-5 .
This is a good descriptive study in which the authors analyze effect of short- term exposure of nitrogen dioxide in patients with the clinical syndrome of heart failure with preserved and depressed left ventricular ejection fraction. The re- sults are interesting and suggest that other aspects, as the exposure of nitrogen dioxide can contribute to pathophysiology of the heart failure with preserved ejection fraction. These data are of public health importance.
2.1. Subjects. We recruited a sample of 120 subjects (60 female; mean age 33.4 ± 7.4, range 20–45) who exhibited bilateral short hamstring syndrome (SLR test = 80 ∘ or less) [31–33]. Sample size was calculated using Ene 3.0 software (Autonomic University of Barcelona, Spain) and calculations were based on detecting between-group mean differences of 7 ∘ at postdata . Assuming a standard deviation of 8 ∘ when comparing 2 means, an alpha level of 0.05, and desired power of 90%, a sample size of 29 subjects per group was generated. We increased the sample size by 25% (40 per group) to increase statistical power. Exclusion criteria were hamstring injury within the past year, exceeding 80 ∘ in the initial SLR test, verbal report of performing regular lower extremity muscle stretching exercises, history of neck trauma (whiplash), neck symptoms, history of fracture in any part of the body, history of growth disorders, history of neurological or orthopedic disorders, diagnosis of herniated disk, low back pain in the last 6 months, and body mass index (BMI) lower than 20 Kg/cm 2 or higher than 30 Kg/cm 2 . We chose the BMI range as an exclusion criterion to allow for better identification of body landmarks and introduce some degree of homogeneity for subject body type. Subjects were recruited from the general population via advertisements in local newspapers. All subjects signed an informed consent before they were included in the study, and all procedures were conducted according to the Declaration of Helsinki. The period of recruitment was from January 2009 to June 2011. Figure 1 provides a flowchart of subject recruitment during the study.
33. Andresen V, Busciglio I, Grudell A, Burton D, McKinzie S, Foxx-Orenstein A, Zinsmeister AR, Currie MG, Kurtz C, Camilleri M. Effects of a novel, first-in-class guanylate cyclase-C activator, linaclotide acetate (MD- 1100), on gastrointestinal and colonic transit and bowel habits in patients with constipation-predominant irritable bowelsyndrome (C- IBS). Dig Dis Week 2007 Abs 532.
17. Lea R, Houghton LA, Calvert EL, Larder S, Gosalkorale WM, et al. Gut focused hypnotherapy normalizes disorders rectal sensitivity in patients with irritable bowelsyndrome. Aliment Pharmacol Ther 2003;17:635-642. 18. Lydiard RB. Anxiety and the irritable bowelsyndrome. Psychiatr Ann
Irritable bowelsyndrome (IBS) is a functional gastrointestinal disorder of uncertain etiology. Several studies have proposed the possible role of intestinal parasites in the pathogenesis of IBS. We aimed to summarize the epidemiological studies that describe a possible link between intestinal parasites and IBS, with special interest in endemic areas for intestinal parasitism such as South America. A comprehensive review of the literature was conducted by using the keywords: irritable bowelsyndrome, intestinal parasites, protozoan infection, soil-transmitted helminths and South America. Giardia lamblia may cause IBS symptoms that can persist several years after effective treatment. Dientamoeba fragilis can cause IBS-like symptoms, but low sensitive parasitological techniques may fail to detect it. Entamoeba histolytica can cause a chronic non-dysenteric colitis, but several studies have failed to find an association with IBS. The role of Blastocystis hominis in IBS remains controversial. In addition, epidemiological studies evaluating the effect of soil-transmitted helminths in IBS are scant. Symptoms elicited by intestinal parasites may resemble to those in IBS, especially in endemic areas such as South America, where both the prevalence of IBS and intestinal parasitism are high. Whether these organisms are the cause or contributing factors in IBS remains a subject of study. Routine parasitological examination of stools in individuals who full-fit the criteria for IBS should be included upon initial assessment in endemic countries. Key words: Irritable bowelsyndrome; Intestinal diseases, parasitic; Protozoan infections; Helminthiasis; South America (source: MeSH NLM).