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Gastroparesis is a chronic disorder of gastric motility characterized by delayed gastric empting in the absence of mechanical obstruction, which can lead to symptoms of nausea, vomiting, bloating, abdominal pain, postprandial fullness and weight loss. Although there are many etiologies, the primary causes are diabetes or are idiopathic. The mainstay of treatment is dietary and drug therapies. However, many patients will continue to suffer intractable symptoms despite these treatments. Gastric neurostimulation with the Enterra Therapy system has been approved for use under the Humanitarian Device Exemption by the US FDA. The device produces pulses of electrical stimulation that are delivered to the stomach continuously. One randomized clinical trial and multiple nonrandomized unblinded clinical trials and case series have documented improvement of symptoms in intractable diabetic and idiopathic gastroparesis. The purpose of this article is to introduce the Enterra Therapy gastric neurostimulator. Gastroparesis and its pathophysiology will be discussed in this clinical context to enhance the understanding of the device and its development. We will analyze the device in detail, its placement and the results of studies evaluating its efficacy.
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PMID:Enterra Therapy: gastric neurostimulator for gastroparesis. 2042 May 55

Human intestinal microbiota create a complex polymicrobial ecology. This is characterised by its high population density, wide diversity and complexity of interaction. Any dysbalance of this complex intestinal microbiome, both qualitative and quantitative, might have serious health consequence for a macro-organism, including small intestinal bacterial overgrowth syndrome (SIBO). SIBO is defined as an increase in the number and/or alteration in the type of bacteria in the upper gastrointestinal tract. There are several endogenous defence mechanisms for preventing bacterial overgrowth: gastric acid secretion, intestinal motility, intact ileo-caecal valve, immunoglobulins within intestinal secretion and bacteriostatic properties of pancreatic and biliary secretion. Aetiology of SIBO is usually complex, associated with disorders of protective antibacterial mechanisms (e.g. achlorhydria, pancreatic exocrine insufficiency, immunodeficiency syndromes), anatomical abnormalities (e.g. small intestinal obstruction, diverticula, fistulae, surgical blind loop, previous ileo-caecal resections) and/or motility disorders (e.g. scleroderma, autonomic neuropathy in diabetes mellitus, post-radiation enteropathy, small intestinal pseudo-obstruction). In some patients more than one factor may be involved. Symptoms related to SIBO are bloating, diarrhoea, malabsorption, weight loss and malnutrition. The gold standard for diagnosing SIBO is still microbial investigation of jejunal aspirates. Non-invasive hydrogen and methane breath tests are most commonly used for the diagnosis of SIBO using glucose or lactulose. Therapy for SIBO must be complex, addressing all causes, symptoms and complications, and fully individualised. It should include treatment of the underlying disease, nutritional support and cyclical gastro-intestinal selective antibiotics. Prognosis is usually serious, determined mostly by the underlying disease that led to SIBO.
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PMID:Small intestinal bacterial overgrowth syndrome. 2057

Gastrointestinal dysmotility presenting as nausea, vomiting, bloating, diarrhea, constipation or abdominal pain is seen in diabetic patients. Oxidative stress has recently been recognized as a significant player in the pathogenesis of gastrointestinal complications of diabetes. In this issue of Neurogastroenterology and Motility, a team of investigators from Emory University led by Dr. Srinivasan present new evidence on the effect of oxidative stress in the diabetic colon. They show in diabetic patients, increased oxidative stress is associated with loss of the inhibitory neuronal subpopulation of enteric neurons, and that the neuronal loss can be reversed in-vitro by anti-oxidant lipoic acid. This new information adds to the accumulating evidence on the deleterious effect of oxidative stress in the gastrointestinal tract and highlights the opportunity to develop newer therapies focused on augmenting anti-oxidant defenses in the gastrointestinal tract in diabetic patients.
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PMID:Oxidative stress: key player in gastrointestinal complications of diabetes. 2093 47

Irritable bowel syndrome (IBS) is a common chronic disorder with a prevalence ranging from 5 to 10 percent of the world's population. This condition is characterised by abdominal discomfort or pain, altered bowel habits, and often bloating and abdominal distension. IBS reduces quality of life in the same degree of impairment as major chronic diseases such as congestive heart failure and diabetes and the economic burden on the health care system and society is high. Abnormalities have been reported in the neuroendocrine peptides/amines of the stomach, small- and large intestine in patients with IBS. These abnormalities would cause disturbances in digestion, gastrointestinal motility and visceral hypersensitivity, which have been reported in patients with IBS. These abnormalities seem to contribute to the symptom development and appear to play a central role in the pathogenesis of IBS. Neuroendocrine peptides/amines are potential tools in the treatment and diagnosis of IBS. In particular, the cell density of duodenal chromogranin A expressing cells appears to be a good histopathological marker for the diagnosis of IBS with high sensitivity and specificity.
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PMID:Irritable bowel syndrome: the role of gut neuroendocrine peptides. 2265 78

Diabetic gastroparesis is a component of autonomic neuropathy, and is the most common manifestation of gastrointestinal neuropathy. Diabetes is responsible for about one quarter of gastroparesis. The upper gastrointestinal symptoms are often non-specific and dominated by nausea, vomiting, early satiety, fullness, bloating. We also have to look for diabetic gastroparesis in case of metabolic instability, such as postprandial hypoglycaemia. The pathophysiology of diabetic gastroparesis is complex, partly due to a vagus nerve damage, but also to changes in secretion of hormones such as motilin and ghrelin. A decrease in the stem cell factor (SCF), growth factor for cells of Cajal (gastric pacemaker), was found in subjects with diabetic gastroparesis. These abnormalities lead to an excessive relaxation in the corpus, a hypomotility of antrum, a desynchronization antrum-duodenum-pylorus, and finally an abnormal duodenal motility. The treatment of diabetic gastroparesis is based on diabetes control, and split meals by reducing the fiber content and fat from the diet. The antiemetic and prokinetic agents should be tested primarily in people with nausea and vomiting. Finally, after failure of conventional measures, the use of gastric neuromodulation is an effective alternative, with well-defined indications. Introduced in the 1970s, this technology works by applying electrical stimulation continues at the gastric antrum, particularly in patients whose gastric symptoms are refractory to other therapies. Its efficacy has been recently reported in different causes of gastroparesis, especially in diabetes. Gastric emptying based on gastric scintigraphy, gastrointestinal symptoms, biological markers of glycaemic control and quality of life are partly improved, but not normalized. Finally, a heavy nutritional care is sometimes necessary in the most severe forms. The enteral route should be preferred (nasojejunal and jejunostomy if possible efficiency). However, in case of failure especially in patients with small bowel neuropathy, the long-term parenteral nutrition is sometimes required.
Diabetes Metab 2012 Nov
PMID:Gastric electrical stimulation for the treatment of diabetic gastroparesis. 2274 75

Pancreatic exocrine insufficiency (PEI) is often observed in patients with pancreatic diseases, including chronic pancreatitis, cystic fibrosis, and tumors, or after surgical resection. PEI often results in malnutrition, weight loss and steatorrhea, which together increase the risk of morbidity and mortality. Therefore, nutritional interventions, such as low-fat diets and pancreatic enzyme replacement therapy (PERT), are needed to improve the clinical symptoms, and to address the pathophysiology of pancreatic exocrine insufficiency. PERT with delayed-release pancrelipase is now becoming a standard therapy for pancreatic exocrine insufficiency because it significantly improves the coefficients of fat and nitrogen absorption as well as clinical symptoms, without serious treatment-emergent adverse events. The major adverse events were tolerable gastrointestinal tract symptoms, such as stomach pain, nausea, and bloating. Fibrosing colonopathy, a serious complication, is associated with high doses of enzymes. Several pancrelipase products have been approved by the US Food and Drug Administration in recent years. Although many double-blind, placebo-controlled trials of pancrelipase products have been conducted in recent years, these studies have enrolled relatively few patients and have often been less than a few weeks in duration. Moreover, few studies have addressed the issue of pancreatic diabetes, a type of diabetes that is characterized by frequent hypoglycemia, which is difficult to manage. In addition, it is unclear whether PERT improves morbidity and mortality in such settings. Therefore, large, long-term prospective studies are needed to identify the optimal treatment for pancreatic exocrine insufficiency. The studies should also examine the extent to which PERT using pancrelipase improves mortality and morbidity. The etiology and severity of pancreatic exocrine insufficiency often differ among patients with gastrointestinal diseases or diabetes (type 1 and type 2), and among elderly subjects. Finally, although there is currently limited clinical evidence, numerous extrapancreatic diseases and conditions that are highly prevalent in the general population may also be considered potential targets for PERT and related treatments.
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PMID:Pancrelipase: an evidence-based review of its use for treating pancreatic exocrine insufficiency. 2293 95

The rhizomes of Zingiber officinale Roscoe (Zingiberaceae), commonly known as ginger is an important kitchen spice and also possess a myriad health benefits. The rhizomes have been used since antiquity in the various traditional systems of medicine to treat arthritis, rheumatism, sprains, muscular aches, pains, sore throats, cramps, hypertension, dementia, fever, infectious diseases, catarrh, nervous diseases, gingivitis, toothache, asthma, stroke and diabetes. Ginger is also used as home remedy and is of immense value in treating various gastric ailments like constipation, dyspepsia, belching, bloating, gastritis, epigastric discomfort, gastric ulcerations, indigestion, nausea and vomiting and scientific studies have validated the ethnomedicinal uses. Ginger is also shown to be effective in preventing gastric ulcers induced by nonsteroidal anti-inflammatory drugs [NSAIDs like indomethacin, aspirin], reserpine, ethanol, stress (hypothermic and swimming), acetic acid and Helicobacter pylori-induced gastric ulcerations in laboratory animals. Various preclinical and clinical studies have also shown ginger to possess anti-emetic effects against different emetogenic stimuli. However, conflicting reports especially in the prevention of chemotherapy-induced nausea and vomiting and motion sickness prevent us from drawing any firm conclusion on its effectiveness as a broad spectrum anti-emetic. Ginger has been shown to possess free radical scavenging, antioxidant; inhibition of lipid peroxidation and that these properties might have contributed to the observed gastroprotective effects. This review summarizes the various gastroprotective effects of ginger and also emphasizes on aspects that warranty future research to establish its activity and utility as a gastroprotective agent in humans.
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PMID:A review of the gastroprotective effects of ginger (Zingiber officinale Roscoe). 2361 3

Diabetes mellitus affects virtually every organ system in the body and the degree of organ involvement depends on the duration and severity of the disease, and other co-morbidities. Gastrointestinal (GI) involvement can present with esophageal dysmotility, gastro-esophageal reflux disease (GERD), gastroparesis, enteropathy, non alcoholic fatty liver disease (NAFLD) and glycogenic hepatopathy. Severity of GERD is inversely related to glycemic control and management is with prokinetics and proton pump inhibitors. Diabetic gastroparesis manifests as early satiety, bloating, vomiting, abdominal pain and erratic glycemic control. Gastric emptying scintigraphy is considered the gold standard test for diagnosis. Management includes dietary modifications, maintaining euglycemia, prokinetics, endoscopic and surgical treatments. Diabetic enteropathy is also common and management involves glycemic control and symptomatic measures. NAFLD is considered a hepatic manifestation of metabolic syndrome and treatment is mainly lifestyle measures, with diabetes and dyslipidemia management when coexistent. Glycogenic hepatopathy is a manifestation of poorly controlled type 1 diabetes and is managed by prompt insulin treatment. Though GI complications of diabetes are relatively common, awareness about its manifestations and treatment options are low among physicians. Optimal management of GI complications is important for appropriate metabolic control of diabetes and improvement in quality of life of the patient. This review is an update on the GI complications of diabetes, their pathophysiology, diagnostic evaluation and management.
World J Diabetes 2013 Jun 15
PMID:Gastrointestinal complications of diabetes mellitus. 2377 73

Obesity is the most prevalent health problem affecting all age groups, and leads to many complications in the form of chronic heart disease, diabetes mellitus Type 2 and stroke. A systematic review about safety and efficacy of herbal medicines in the management of obesity in human was carried out by searching bibliographic data bases such as, PubMed, Scopus, Google Scholar, Web of Science, and IranMedex, for studies reported between 30th December 2008 to 23rd April 2012 on human or animals, investigating the beneficial and harmful effects of herbal medicine to treat obesity. Actually we limited our search to such a narrow window of time in order to update our article published before December of 2008. In this update, the search terms were "obesity" and ("herbal medicine" or "plant", "plant medicinal" or "medicine traditional") without narrowing or limiting search items. Publications with available abstracts were reviewed only. Total publications found in the initial search were 651. Total number of publications for review study was 33 by excluding publications related to animals study.Studies with Nigella Sativa, Camellia Sinensis, Crocus Sativus L, Seaweed laminaria Digitata, Xantigen, virgin olive oil, Catechin enriched green tea, Monoselect Camellia, Oolong tea, Yacon syrup, Irvingia Gabonensi, Weighlevel, RCM-104 compound of Camellia Sinensis, Pistachio, Psyllium fibre, black Chinese tea, sea buckthorn and bilberries show significant decreases in body weight. Only, alginate-based brown seaweed and Laminaria Digitata caused an abdominal bloating and upper respiratory tract infection as the side effect in the trial group. No other significant adverse effects were reported in all 33 trials included in this article.In conclusion, Nigella Sativa, Camellia Synensis, Green Tea, and Black Chinese Tea seem to have satisfactory anti-obesity effects. The effect size of these medicinal plants is a critical point that should be considered for interpretation. Although there was no report for side effect in these trials, we believe that safety of these plants still remains to be elucidated by further long-term studies.
J Diabetes Metab Disord 2013 Jun 19
PMID:A systematic review of anti-obesity medicinal plants - an update. 2377 75

While the symptoms of gastroparesis are common, an accurate diagnosis is based on a combination of those symptoms with a documented delay in gastric emptying. Typical symptoms include nausea, vomiting, early satiety, postprandial fullness, bloating, and abdominal discomfort. Patients with gastroparesis face many diagnostic and therapeutic challenges. The most common origins of gastroparesis are idiopathic causes and diabetes mellitus. The increased use of certain medications in medicine today, including opiates and drugs with anticholinergic properties, can alter gastrointestinal functions and mimic symptoms of gastroparesis. Accordingly, alternative explanations for symptoms and altered gastrointestinal function need to be considered. Numerous clinical sequelae, including weight loss and severe protein-calorie malnutrition, may be seen in advanced stages of gastroparesis. This article provides an overview of gut sensorimotor function to help the reader better understand the clinical presentation of patients with dyspepsia and those who may have accompanying delayed gastric emptying that meets criteria for gastroparesis. Techniques available for diagnosing motor dysfunction and the principles of gastroparesis management are reviewed. Nutrition recommendations and a review of pharmacologic agents, nonpharmacologic techniques, and novel treatment modalities are provided.
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PMID:Gastroparesis: from concepts to management. 2379 76


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