Gastrointestinal Failure Research Articles

Prescription regularity of famous veteran traditional Chinese medicine Doctor Yu Guoyou for treating gastrointestinal failure based ondata mining

Gastrointestinal failure is a kind of severe systemic inflammatory response, and often complicated with multiple organ dysfunction syndrome. Integrated traditional Chinese and Western medicine have a better curative effect in treating it. This study collected the famous veteran TCM physician Yu Guoyou's 175 prescriptions for treating 89 cases of gastrointestinal failure, calculated the frequency of traditional Chinese medicines and their categories, and analyzed the medication regularity with system clustering method, so as to summarize Yu's frequently used drugs and prescriptions. The results showed the top three most frequently used drugs aremagnolia bark, bitter orange, and rhubarb, which are components of Xiaochengqi decoction; Among the traditional Chinese medicines, medicines of tonifying deficiency, regulating qi, clearing heat, eliminating phlegm and dissipating dampness are most commonly used. Among the tonic medicines, those for tonifying Qi accounted for 2/3, which was the largest proportion; At the same time, some new prescriptions and new drug combinations were excavated and could be used as the reference for clinical medication. According to the findings, when differentiating syndromes of gastrointestinal failure, Yu regards the spleen and stomach Qi deficiency as the root cause and the heat toxin, blood stasis, Qi stagnation and dampness as the symptoms. In the treatment of gastrointestinal function failure, Yu gives priority to strengthening spleen, regulating Qi and purgation, prescribes medicines for dissolving blood stasis and detoxication, dissipating dampness, clearing heat and eliminating phlegm according to syndrome types. In other words, the treatment is based on syndrome differentiation, and the prescription is modified according to symptoms. In particular, Yu attaches importance to stomach-Qi recuperation and gastrointestinal function recovery in the process of treatment.

Perioperative use of nonsteroidal anti-inflammatory drugs and the risk of anastomotic failure in emergency general surgery.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used analgesic and anti-inflammatory adjuncts. Nonsteroidal anti-inflammatory drug administration may potentially increase the risk of postoperative gastrointestinal anastomotic failure (AF). We aim to determine if perioperative NSAID utilization influences gastrointestinal AF in emergency general surgery (EGS) patients undergoing gastrointestinal resection and anastomosis. Post hoc analysis of a multi-institutional prospectively collected database was performed. Anastomotic failure was defined as the occurrence of a dehiscence/leak, fistula, or abscess. Patients using NSAIDs were compared with those without. Summary, univariate, and multivariable analyses were performed. Five hundred thirty-three patients met inclusion criteria with a mean (±SD) age of 60 ± 17.5 years, 53% men. Forty-six percent (n = 244) of the patients were using perioperative NSAIDs. Gastrointestinal AF rate between NSAID and no NSAID was 13.9% versus 10.7% (p = 0.26). No differences existed between groups with respect to perioperative steroid use (16.8% vs. 13.8%; p = 0.34) or mortality (7.39% vs. 6.92%, p = 0.84). Multivariable analysis demonstrated that perioperative corticosteroid (odds ratio, 2.28; 95% confidence interval, 1.04-4.81) use and the presence of a colocolonic or colorectal anastomoses were independently associated with AF. A subset analysis of the NSAIDs cohort demonstrated an increased AF rate in colocolonic or colorectal anastomosis compared with enteroenteric or enterocolonic anastomoses (30.0% vs. 13.0%; p = 0.03). Perioperative NSAID utilization appears to be safe in EGS patients undergoing small-bowel resection and anastomosis. Nonsteroidal anti-inflammatory drug administration should be used cautiously in EGS patients with colon or rectal anastomoses. Future randomized trials should validate the effects of perioperative NSAIDs use on AF. Therapeutic study, level III.

Activated Braf induces esophageal dilation and gastric epithelial hyperplasia in mice.

Germline mutations in BRAF are a major cause of cardio-facio-cutaneous (CFC) syndrome, which is characterized by heart defects, characteristic craniofacial dysmorphology and dermatologic abnormalities. Patients with CFC syndrome also commonly show gastrointestinal dysfunction, including feeding and swallowing difficulties and gastroesophageal reflux. We have previously found that knock-in mice expressing a Braf Q241R mutation exhibit CFC syndrome-related phenotypes, such as growth retardation, craniofacial dysmorphisms, congenital heart defects and learning deficits. However, it remains unclear whether BrafQ241R/+ mice exhibit gastrointestinal dysfunction. Here, we report that BrafQ241R/+ mice have neonatal feeding difficulties and esophageal dilation. The esophagus tissues from BrafQ241R/+ mice displayed incomplete replacement of smooth muscle with skeletal muscle and decreased contraction. Furthermore, the BrafQ241R/+ mice showed hyperkeratosis and a thickened muscle layer in the forestomach. Treatment with MEK inhibitors ameliorated the growth retardation, esophageal dilation, hyperkeratosis and thickened muscle layer in the forestomach in BrafQ241R/+ mice. The esophageal dilation with aberrant skeletal-smooth muscle boundary in BrafQ241R/+ mice were recovered after treatment with the histone H3K27 demethylase inhibitor GSK-J4. Our results provide clues to elucidate the pathogenesis and possible treatment of gastrointestinal dysfunction and failure to thrive in patients with CFC syndrome.

OR60: Gastrointestinal Organ Failure Symptoms Included in Sofa Scores Improve Mortality Prediction in the ICU: A Mathematical Approach

OR60: Gastrointestinal Organ Failure Symptoms Included in Sofa Scores Improve Mortality Prediction in the ICU: A Mathematical Approach

Brain micro-inflammation at specific vessels dysregulates organ-homeostasis via the activation of a new neural circuit.

Impact of stress on diseases including gastrointestinal failure is well-known, but molecular mechanism is not understood. Here we show underlying molecular mechanism using EAE mice. Under stress conditions, EAE caused severe gastrointestinal failure with high-mortality. Mechanistically, autoreactive-pathogenic CD4+ T cells accumulated at specific vessels of boundary area of third-ventricle, thalamus, and dentate-gyrus to establish brain micro-inflammation via stress-gateway reflex. Importantly, induction of brain micro-inflammation at specific vessels by cytokine injection was sufficient to establish fatal gastrointestinal failure. Resulting micro-inflammation activated new neural pathway including neurons in paraventricular-nucleus, dorsomedial-nucleus-of-hypothalamus, and also vagal neurons to cause fatal gastrointestinal failure. Suppression of the brain micro-inflammation or blockage of these neural pathways inhibited the gastrointestinal failure. These results demonstrate direct link between brain micro-inflammation and fatal gastrointestinal disease via establishment of a new neural pathway under stress. They further suggest that brain micro-inflammation around specific vessels could be switch to activate new neural pathway(s) to regulate organ homeostasis.

Research advances in liver diseases associated with parenteral nutrition

For patients with gastrointestinal dysfunction or failure, although parenteral nutrition can maintain nutrition and save their lives, lack of food stimulus during the fasting period can cause abnormal secretion of gastrointestinal fluid, bile, and pancreatic juice, which may result in the abnormal secretion of a series of enzymes and lead to the development of various liver diseases. Recent research has focused on the prevention and treatment of such diseases, and this article reviews the research advances in recent years.

N-3 polyunsaturated fatty acid-enriched lipid emulsion improves Paneth cell function via the IL-22/Stat3 pathway in a mouse model of total parenteral nutrition

Total parenteral nutrition (TPN) is a life-saving therapy for patients with gastrointestinal dysfunction or failure. Long-term TPN impairs gut barrier function and contributes to infections and poor clinical outcomes. However, the underlying mechanisms of TPN-related gut barrier damage have not been fully elucidated, and effective measures are still rare. Here, we compared the effects of a predominantly n-6 polyunsaturated fatty acids emulsion (PUFAs; Intralipid) and a lipid emulsion containing n-3 PUFAs (Intralipid plus Omegaven) on antimicrobial peptides produced by Paneth cells. Our results show for the first time that n-3 PUFAs markedly ameliorated intestine atrophy, and increased protein levels of lysozyme, RegIIIγ, and α-cryptdin 5, and their mRNA expression, compared to the n-6 PUFAs emulsion. Importantly, our study reveals that downregulation of IL-22 and phosphorylated Stat3 (p-Stat3) is associated with Paneth cell dysfunction, which may mediate TPN-related gut barrier damage. Lastly, n-3 PUFAs upregulated levels of IL-22 and increased the p-Stat3/Stat3 ratio in ileal tissue, suggesting that n-3 PUFAs improve Paneth cell function through activation of the IL-22/Stat3 pathway. Therefore, our study provides a cogent explanation for the beneficial effects of n-3 PUFAs, and indicates the IL-22/Stat3 pathway as a promising target in the treatment of TPN-related gut barrier damage.

Cirrhosis and Complications of Portal Hypertension

Cirrhosis is the most advanced stage of all the different types of chronic liver diseases. It is defined as a diffuse disorganization of normal hepatic structure by extensive fibrosis associated with regenerative nodules. Hepatic fibrosis is potentially reversible if the causative agent is removed. However, advanced cirrhosis leads to major alterations in the hepatic vascular bed and is usually irreversible. Cirrhosis is a progressive and severe clinical condition associated with considerable morbidity and high mortality. It leads to a wide spectrum of characteristic clinical manifestations, mainly attributable to hepatic insufficiency and portal hypertension. Major complications of portal hypertension include ascites, gastrointestinal (GI) variceal bleeding, hepatic encephalopathy (HE), renal failure, and bacterial infections. In recent years, major advances in the understanding of the natural history and pathophysiology of cirrhosis and the treatment of its complications have led to improved management, quality of life, and life expectancy of patients with this disease. Cirrhosis is also a risk factor for developing hepatocellular carcinoma (HCC). Decompensated cirrhosis carries a poor short-term prognosis; thus, orthotopic liver transplantation (OLT) should always be considered in suitable candidates. This chapter describes the epidemiology, etiology and genetic factors, pathogenesis, diagnosis, general management, and treatment of cirrhosis. Complications of cirrhosis are discussed, including ascites, spontaneous bacterial peritonitis, dilutional hyponatremia, hepatorenal syndrome, variceal bleeding, hepatopulmonary syndrome and postpulmonary hypertension, HE, and HCC. Indications and contraindications for liver transplantation are described. Figures show liver biopsy results and ultrasound images in cirrhosis from hepatitis C, a patient with tense ascites, transjugular intrahepatic portosystemic shunting (TIPS), large esophageal varices with red spots, and HCC. Tables outline the main causes of cirrhosis and the diagnostic methods for identifying them, the Child-Pugh score, diagnostic criteria for hepatorenal syndrome, grades of HE, and indications for liver transplantation.This chapter contains 6 highly rendered figures, 8 tables, 73 references.

Cirrhosis and Complications of Portal Hypertension

Cirrhosis is the most advanced stage of all the different types of chronic liver diseases. It is defined as a diffuse disorganization of normal hepatic structure by extensive fibrosis associated with regenerative nodules. Hepatic fibrosis is potentially reversible if the causative agent is removed. However, advanced cirrhosis leads to major alterations in the hepatic vascular bed and is usually irreversible. Cirrhosis is a progressive and severe clinical condition associated with considerable morbidity and high mortality. It leads to a wide spectrum of characteristic clinical manifestations, mainly attributable to hepatic insufficiency and portal hypertension. Major complications of portal hypertension include ascites, gastrointestinal (GI) variceal bleeding, hepatic encephalopathy (HE), renal failure, and bacterial infections. In recent years, major advances in the understanding of the natural history and pathophysiology of cirrhosis and the treatment of its complications have led to improved management, quality of life, and life expectancy of patients with this disease. Cirrhosis is also a risk factor for developing hepatocellular carcinoma (HCC). Decompensated cirrhosis carries a poor short-term prognosis; thus, orthotopic liver transplantation (OLT) should always be considered in suitable candidates. This chapter describes the epidemiology, etiology and genetic factors, pathogenesis, diagnosis, general management, and treatment of cirrhosis. Complications of cirrhosis are discussed, including ascites, spontaneous bacterial peritonitis, dilutional hyponatremia, hepatorenal syndrome, variceal bleeding, hepatopulmonary syndrome and postpulmonary hypertension, HE, and HCC. Indications and contraindications for liver transplantation are described. Figures show liver biopsy results and ultrasound images in cirrhosis from hepatitis C, a patient with tense ascites, transjugular intrahepatic portosystemic shunting (TIPS), large esophageal varices with red spots, and HCC. Tables outline the main causes of cirrhosis and the diagnostic methods for identifying them, the Child-Pugh score, diagnostic criteria for hepatorenal syndrome, grades of HE, and indications for liver transplantation.This chapter contains 6 highly rendered figures, 8 tables, 73 references.

Etiology and grading treatment of gastrointestinal failure

Gastrointestinal failure is often secondary to a variety critically illness such as sepsis, severe hypoxia and severe gastrointestinal diseases and characterized gastrointestinal mucous lesion, dysfunction of gastrointestinal motility and barrier.It is a pivotal factor influencing the outcome of critically ill patients.Early diagnosis and appropriate treatment is important to improve the outcome of patients, but for a long time there was no unified definition and standard of diagnosis and also no consensus of therapeutic regimen because of lacking specific criteria of assessment.In recent years, the new conception of acute gastrointestinal injury with its four grades of severity and therapeutic regimen based on the grades were proposed in adult ICU field which is worth learning for pediatrician.In this review, the etiology of gastrointestinal failure and the new concepts on its different grades and grading treatment were discussed. Key words: Acute gastrointestinal injury; Gastrointestinal failure; Etiology; Grading treatment,

WITHDRAWN: Nutrition support for bone marrow transplant patients.

This is an update of the original Cochrane review published in Issue 2, 2002. Bone marrow transplantation involves administration of toxic chemotherapy and infusion of marrow cells. After treatment, patients can develop poor appetite, mucositis and gastrointestinal failure, leading to malnutrition. To prevent this, parenteral nutrition (PN) support is often first choice but is associated with increased risk of infection. Enteral nutrition (EN) is an alternative, as is addition of substrates. To determine efficacy of EN or PN support for patients receiving bone marrow transplant. Search of The Cochrane Library, MEDLINE, EMBASE and CINAHL in November 2000 and subsequently June 2006. RCTs that compared one form of nutrition support with another, or control, for bone marrow transplant patients. Twenty nine studies were identified. Data were collected on participants' characteristics; adverse effects; neutropaenia; % change in body weight; graft versus host disease; and survival. In two studies (82 participants) glutamine mouthwash reduced number of days patients were neutropenic (6.82 days, 95%CI (1.67 to 11.98) P = 0.009) compared with placebo. Three studies reported (103 participants) that patients receiving PN with glutamine had reduced hospital stay, 6.62 d (95%CI 3.47 to 9.77, P = 0.00004) compared with patients receiving standard PN. However, in the update a further study was added (147 participants) which altered the pooled results: duration in hospital may be increased for those who receive PN with additional glutamine - 0.22 days (95%CI (1.29 to 1.72). Two other studies reported that (73 participants) patients receiving PN plus glutamine had reduced incidence of positive blood cultures (OR 0.23, 95%CI 0.08 to 0.65, P = 0.006) compared to those receiving standard PN. However, a study from the update (113 participants in total) showed the odds of having a positive blood culture have increased but are still less likely if the patient receives PN with glutamine compared to standard PN (OR 0.46, 95%CI 0.20 to 1.04). When patients were given PN versus IV hydration, (25 participants) patients receiving PN had a higher incidence of line infections (OR 21.23, 95%CI 4.15 to 108.73, P = 0.0002) compared to those receiving standard IV fluids. The update identified one study which recognised that (55 participants) those who received IV were likely to spend less time in hospital, 3.30 days (95%CI -0.38 to 6.98, P = 0.08), although this result was not significant. As reported in the original review there remains no evaluable data to properly compare PN with EN. In this update an additional study that compared PN and Glutamine versus standard PN showed that the certain benefits of parenteral nutrition with added glutamine compared to standard PN for reducing hospital stay are no longer definite. When PN with glutamine is compared with standard PN, patients may not leave hospital earlier, but do have reduced incidence of positive blood cultures, than those receiving standard PN. Where possible use of intravenous fluids and oral diet should be considered as a preference to parenteral nutrition, however, in the event of a patient suffering severe gastrointestinal failure even with a trial of enteral feeding, PN with the addition of glutamine could be considered.

Inflammatory Bowel Disease and Current Treatment Options in Dogs

Inflammatory Bowel Disease (IBD) is an idiopathic and chronic gastrointestinal failure of cats, dogs and some farm animals such as horses. Since the long and difficult classical therapy of the disease has various side effects such as malignancy and lymphoma, new therapeutic methods are needed. However, a safe and standardized treatment protocol has not been developed, yet. Therefore, IBD treatment is still a big dilemma for both veterinary and human medicine. In this review, IBD and new possible therapeutic alternatives were evaluated for dogs.

The Impact of Central Venous Catheters on Pediatric Venous Thromboembolism.

The use of central venous catheters (CVCs) in children is escalating, which is likely linked to the increased incidence of pediatric venous thromboembolism (VTE). In order to better understand the specific risk factors associated with CVC-VTE in children, as well as available prevention methods, a literature review was performed. The overall incidence of CVC-VTE was found to range from 0 to 74%, depending on the patient population, CVC type, imaging modality, and study design. Throughout the available literature, there was not a consistent determination regarding whether a particular type of central line (tunneled vs. non-tunneled vs. peripherally inserted vs. implanted), catheter material, insertion technique, or insertion location lead to an increased VTE risk. The patient populations who were found to be most at risk for CVC-VTE were those with cancer, congenital heart disease, gastrointestinal failure, systemic infection, intensive care unit admission, or involved in a trauma. Both mechanical and pharmacological prophylactic techniques have been shown to be successful in preventing VTE in adult patients, but studies in children have yet to be performed or are underpowered. In order to better determine true CVC-VTE risk factors and best preventative techniques, an increase in large, prospective pediatric trials needs to be performed.

Common chemotherapeutic agents modulate fatty acid distribution in human hepatocellular carcinoma and colorectal cancer cells.

Introduction: Cancer cells are critically correlated with lipid molecules, particularly fatty acids, as structural blocks for membrane building, energy sources, and related signaling molecules. Therefore, cancer progression is in direct correlation with fatty acid metabolism. The aim of this study was to investigate the potential effects of common chemotherapeutic agents on the lipid metabolism of hepatocellular carcinoma (HCC) and colorectal cancer (CRC) cells, with a focus on alterations in cellular fatty acid contents. Methods: Human HepG2 and SW480 cell lines as HCC and CRC cells were respectively cultured in RPMI-1640 medium supplemented with non-toxic doses of 5-fluorouracil and doxorubicin for 72 hours. Oil Red O dye was used to estimate intracellular lipid vacuole intensity. Fatty acid analysis of isolated membrane phospholipids and cytoplasmic triglycerides (TG) was performed by gas-liquid chromatography (GLC) technique. Results: Oil red O staining represented significantly higher lipid accumulation and density in cancer cells after exposure to the chemotherapeutic agents as compared to non-treated control cells. Doxorubicin and 5-fluorouracil treatment promoted the channeling of saturated fatty acids (SFAs) from phospholipids to triglyceride pool in both HepG2 (+5.91% and +8.50%, P < 0.05, respectively) and SW480 (+37.41% and +5.73%, P < 0.05, respectively) cell lines. However, total polyunsaturated fatty acid content was inversely shifted from TG to phospholipid fraction after doxorubicin and 5-fluorouracil incubation of HepG2 (+58.89% and +29.13%, P < 0.05, respectively) and SW480 (+19.20% and +14.65%, P < 0.05, respectively) cells. Conclusion: Our data showed that common chemotherapeutic agents of HCC and CRC can induce significant changes in cellular lipid accumulation and distribution of fatty acids through producing highly saturated and unsaturated lipid droplets and membrane lipids, respectively. These metabolic side effects may be associated with gastrointestinal cancers treatment failure.

HMGB1 as a new biomarker of celiac disease in children: A multicenter study

ObjectiveDespite the availability of specific sierology and point-of-care tests, the phenotypic heterogeneity and the symptoms fluctuation as well as the “open-window” existing among the late and silent forms cause often a delayed celiac disease (CD) diagnosis. Recently, it has been reported that high mobility group box 1 (HMGB1) mediates inflammation and gastrointestinal barrier failure. The aim of this study was to detect serum HMGB1 levels at CD diagnosis and to evaluate the relationship between serum HMGB1 levels and clinical and histologic phenotypes. Methods49 CD children and 44 healthy children were enrolled. Specific antitissue transglutaminase type 2, antideaminated form of gliadin antibodies, serum HMGB1 levels, and typical histopathological changes in duodenal mucosa were performed in all patients. Mucosal lesions were classified according to Marsh classification. In relation to clinical presentation, we classified patients into: typical, atypical and silent forms. ResultsSerum HMGB1 levels were significantly higher in those with CD than those in the healthy control group (P < 0.001). Significant differences in serum HMGB1 levels were detected in children with typical CD form compared to both children with atypical CD form (P < 0.001) and children with silent CD form (P < 0.001). By using the Marsh classification, significant differences were found between subjects with grade 3 B-B1 and 3 C-B2 and villous atrophy, respectively (P < 0.05). On the contrary, no significant differences in serum HMGB1 levels in subgroups of children with grade 3 A compared to grade 3 B-B1 were detected. ConclusionsHMGB1 is upregulated at diagnosis in all CD children, especially in typical form, and reflecting the histologic severity of disease.

AIMing to block tissue damage

Radiation Damage Ionizing radiation kills actively dividing cells such as those in the gut and in the bone marrow. Hu et al. found a pathological role for the protein AIM2 in irradiation-induced tissue damage. AIM2 is best known for its role in sensing double-stranded DNA in the cytoplasm and alerting the body to infections. It seems that AIM2 also senses DNA damage caused by radiation and then triggers intestinal epithelial cells and bone marrow cells to die. Deficiency in AIM2 protected mice from irradiation-induced gastrointestinal syndrome and hematopoietic failure. Science , this issue p. [765][1] [1]: /lookup/doi/10.1126/science.aaf7532

Parenteral Nutrition in Patients with Advanced Cancer and Gastrointestinal Failure or Obstruction

&lt;p class="cco-body"&gt;&lt;span lang="EN-GB"&gt;Malnutrition in patients with advanced cancer and gastrointestinal failure (ACGIF) is inevitable. This is a prospective study of a cohort of patients with ACGIF who were treated by home parenteral nutrition (HPN).&lt;/span&gt;&lt;/p&gt;&lt;p class="cco-body"&gt;&lt;span lang="EN-GB"&gt;Included were all patients with ACGIF treated with HPN since January 2003. Data concerning the primary disease, demographics, functional capacity, and PN-related complications were obtained.&lt;/span&gt;&lt;/p&gt;&lt;p class="cco-body"&gt;&lt;span lang="EN-GB"&gt;125 patients, age's 60±12.9 years, were included. Seven (6%) had KPS&amp;lt;50. Median survival was 3.2 months. Cumulative survival&lt;/span&gt;&lt;span lang="EN-GB"&gt;was 0.95, 0.50, 0.25, and 0.09 at two weeks, three and six months, and one year after initiation of HPN, respectively. Multivariate analysis revealed higher mortality associated with male gender (HR 1.48 95% CI 1.03-2.14; p&amp;lt;0.05), albumin level&amp;lt;2.5 gr% (HR 1.73 95% CI 1.18-2.54 p&amp;lt;0.05), and low functional capacity (KPS&amp;lt;50) (HR 2.63 95% CI 1.21-5.74; p&amp;lt;0.05). Survival was not associated with age or BMI.&lt;/span&gt;&lt;/p&gt;&lt;p class="cco-body"&gt;&lt;span lang="EN-GB"&gt;More than 50% of patients survived more than three months, and more than 95% survived longer than two weeks. We cautiously suggest that HPN has prolonged survival and prevented starvation-related manifestations. The decision to initiate HTPN must be reached based on individual considerations, taking into account patient’s preferences. &lt;/span&gt;&lt;/p&gt;&lt;p&gt; &lt;/p&gt;

Trefoil factor 3 related to gastrointestinal failure in pediatric critical illness

To determine the relationship between the serum concentration of trefoil factor 3 (TFF3) and gastrointestinal failure (GIF) in pediatric critical illness in order to provide knowledge for disease management. We enrolled 137 cases and divided them into three groups, including a control group (group A), critical illness without GIF (group B), and critical illness with GIF (group C). The serum TFF3 concentration was determined by ELISA and compared among the groups. Serum TFF3 concentrations measured before the occurrence of GIF in group C were significantly higher than in groups A and B (P<0.01). Under the conditions of GIF in group C, serum TFF3 concentration was significantly related to the gastrointestinal tract function score (r=-0.712). Cox's proportional hazards model analysis showed that the serum TFF3 concentrations at the time of occurrence of GIF, and 48hours later, could be used as prognostic factors in critically ill pediatric patients with GIF (r=1.443 and 1.872, respectively). TFF3 may play an important role in predicting GIF in pediatric critical illness and has a protective function in the mucosal repair process.

Association between acute gastrointestinal injury grading system and disease severity and prognosis in critically ill patients: A multicenter, prospective, observational study in China

PurposeThis prospective study investigated the association between disease severity and acute gastrointestinal injury (AGI) grade and between prognosis and AGI. MethodsIn 12 teaching hospitals in China, patients in intensive care units who had received a diagnosis of AGI were enrolled (N = 196). Their demographics, body mass index, Acute Physiology and Chronic Health Evaluation II score, Sepsis-related Organ Failure Assessment score, mechanical ventilation, acute kidney injury, intensive care unit stay, and 7-day and 28-day mortality were recorded. ResultsOf the 196 AGI patients, 90, 64, 29, and 13 were classified as grades I, II, III, and IV, respectively. Acute Physiology and Chronic Health Evaluation II scores independently predicted grades III and IV; acute kidney injury independently predicted grade III. The 28-day mortality rates of grades I and II were similar, as were those of grades III and IV. The mortality rate of patients with grades I + II (gastrointestinal dysfunction) was significantly lower than that of patients with grades III + IV (gastrointestinal failure). ConclusionDifferentiating AGI as gastrointestinal dysfunction or gastrointestinal failure appears to be more valid for predicting prognosis than the AGI 4-grade system.

Serum ghrelin and PYY enterohormones during acute critical illness: A prospective observational trial

Introduction Gastrointestinal failure during critical illness is associated with decreased intake and limited tolerance to enteral feeding. Enterohormones like ghrelin and PYY could play a role in these dysfunctions. This study aimed at defining: – the time course of serum ghrelin and PYY during the first 5 days of stay; – correlations with limited tolerance to enteral feeding. Material and methods Thirty consecutive patients (age: 56.4 ± 16.4; BMI: 26.3 ± 4.5) and 10 fasting healthy volunteers (age: 34.1 ± 6.8; BMI: 23.1 ± 4.2) were included. In patients, blood was sampled for 5 consecutive days and once in the control group. Blood samples were immediately centrifuged at 3000 × g for 10 minutes at 4 °C. Ghrelin samples were acidified to pH 4 and then all samples were stored at –80 °C until processing. Ghrelin and PYY serum concentrations were measured using a commercial ELISA test. Enteral feeding intolerant patients were defined as patients with at least one episode of high gastric residual volume (> 250 mL) and/or diarrhea (> 200 mL of liquid stools/day). Comparisons between continuous variables were done using ANOVA and the Wilcoxon U -test as appropriated. Alpha error was set at 5%. Results The incidence of intolerance among patients was 41.4%. Mean gastric residual volume (millilitres) was higher in intolerant than in tolerant patients ( P P = 0.03) and than controls (53.5 pg/mL [17.5–191.7 pg/mL] vs. 6.4 pg/mL [0.35–18.1 pg/mL]; P = 0.02). Daily PYY serum concentration was higher in intolerant than in tolerant patients, specifically on days 2 (median (IQR): 103.2 pg/mL [23.2–193.6 pg/mL] vs. 16.9 pg/mL [3.9–54 pg/mL]; P = 0.02) and day 5 (103.2 pg/mL [23.2–193.6 pg/mL] vs. 16.9 pg/mL [3.9 to 54 pg/mL]; P = 0.02). Controls had a significantly higher serum ghrelin concentration than either tolerant patients (median (IQR): 1435.7 pg/mL [1335.5–1775.5 pg/mL] vs. 219.4 pg/mL [84–420.5 pg/mL]; P P = 0.004). Unexpectedly, serum ghrelin concentration was higher in intolerant compared to tolerant patients (median (IQR): 283.5 pg/mL [92–1002.5 pg/mL] vs. 219.4 pg/mL [84–420.5 pg/mL]; P = 0.02). No difference in serum ghrelin concentration between tolerant compared to intolerant patients was found from day 1 to day 5. Conclusions In critically ill patients, mean serum concentration of ghrelin and PYY significantly differ from that of healthy controls. These findings support a role of enterohormones in the critical illness-associated gastrointestinal failure.