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 1,674 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a study of 1216 pregnancies, 427 (35%) patients reported hand symptoms. Symptoms of the same quality and distribution were reported by 40 (30%) of 132 control subjects within the previous year, and although invariably mild, these symptoms suggest that pregnancy may aggravate a pre-existing condition. Fewer than 20% of the 427 affected patients described a classic median-nerve symptom distribution (carpal tunnel syndrome), while 12% of patients described an ulnar-nerve distribution, which is thought to represent a genuine and previously underestimated occurrence of ulnar-nerve neuropathy in pregnancy. In 69% of patients, hand symptoms were generalized. Most symptoms were bilateral, commenced in the third trimester and resolved soon after delivery. There was a significant correlation of hand symptoms in pregnancy with the presence of preeclampsia, tight rings, the weight at confinement, the birth weight and a history of premenstrual bloating. Operative intervention was not required for any patient.
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PMID:Survey of hand symptoms in pregnancy. 369 40

Gastrointestinal motor dysfunction, intestinal pseudo-obstruction syndromes, and hollow visceral neuropathy and myopathy were previously considered functional bowel diseases but are now recognized to be organic disorders. They may alter the muscle of the intestinal wall or the nerves of the myenteric plexus, or both. Their symptoms of chronic unexplained abdominal pain, abdominal distention and bloating, early satiety, nausea, vomiting, and alternating diarrhea and constipation are the most common and perhaps the most difficult problems encountered by gastroenterologists. New intestinal recording devices assess motility and allow objective classification of neuromuscular disease, permitting accurate diagnosis and better treatment.
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PMID:Neuromuscular diseases of the gastrointestinal tract. Specific disorders that often get a nonspecific diagnosis. 787 32

Small bowel motility disorders may result in prolonged or accelerated transit and present clinically with such symptoms as nausea, vomiting, bloating, pain or altered bowel movements. These disorders result from derangements of neuromuscular control affecting extrinsic nerves, enteric plexuses or smooth muscle, or from structural disorders that may be congenital or acquired. Diagnosis depends on exclusion of mechanical obstruction or structural disease and assessment of motor function by measurement of transit and intestinal pressure profiles, and a search for the underlying disorder causing a neuropathy or myopathy. Management of stasis syndromes is based on restoration of good nutrition, treatment of bacterial overgrowth, prokinetic agents, antiemetics and surgery for localized disease. Patients with fast transit disorders require opioid agonists and, rarely, second-line treatments such as verapamil, clonidine or octreotide.
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PMID:Small bowel motility disorders. 799 64

Familial visceral neuropathy is a rare cause of chronic intestinal pseudo-obstruction. It is characterized by progressive destruction of the gastrointestinal myenteric plexus resulting in dysmotility and associated early satiety, post-prandial bloating, recurrent nausea and vomiting, abdominal distension, chronic diarrhea, weight loss, and malnutrition. In its varying forms, there may be neuronal destruction in other parts of the peripheral and central nervous system. We report on four siblings who presented in their third or fourth decades with initial clinical features of chronic intestinal pseudo-obstruction and eventual progressive diffuse neuronal disease, characterized by leukoencephalopathy and peripheral neuropathy. Within 5 yr of presentation, all four patients died from inanition and sepsis, despite aggressive nutritional support. Their clinical and pathological features are characteristic of familial visceral neuropathy of the autosomal recessive form. This presentation may represent a unique syndrome characterized by a tetrad of polyneuropathy, ophthalmoplegia, leukoencephalopathy, and intestinal pseudo-obstruction.
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PMID:Familial visceral neuropathy as part of a diffuse neuronal syndrome: four fatal cases in one sibship. 817 58

First, it is important to find out whether the patient is complaining of infrequent defaecation, excessive straining at defaecation, abdominal pain or bloating, a general sense of malaise attributed to constipation, soiling, or a combination of more than one symptom. Second, one must decide if there is a definable abnormality as a cause of the symptom(s). Is the colon apparently normal or is its lumen widened (megacolon)? Is the upper gut normal or is there evidence of neuropathy or myopathy? Is the ano-rectum normal or is there evidence of a weak pelvic floor, mucosal prolapse, major rectocele, an internal intussusception or solitary rectal ulcer? Is there any systemic component such as hypothyroidism, hypercalcaemia, neurological or psychiatric disorder or relevant drug therapy? Choice of treatment will depend on this clinical evaluation. The range of treatments available is: Reassurance and stop current treatment: Patients with a bowel obsession may take laxatives or rectal preparations regularly without need. Increase dietary fibre: Most cases of 'simple' constipation respond to increased dietary fibre, possibly with an added supplement of natural bran. Toilet training and altered routine of life: Young people particularly may need to recognise the call to stool and alter their daily routine to permit and encourage regular defaecation. Medicinal bulking agent: Ispaghula, methyl cellulose, concentrated wheat germ or bran, and similar preparations are useful when patients with a normal colon find it difficult to take adequate dietary fibre. These preparations increase the bulk of stool and soften its consistency. They may be useful for those patients with the constipated form of irritable bowel syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical management of constipation. 823 32

Autonomous neuropathy in patients with diabetes is associated with dysmotility and abdominal discomfort. The disturbances resemble to some extent those seen in patients with functional dyspepsia. To gain further insight into the disorders, we compared patients with long-standing diabetes, patients with functional dyspepsia, and healthy individuals with respect to abdominal symptoms, width of gastric antral area, and autonomic nerve function. We investigated 42 type I diabetic outpatients by structured interview for abdominal discomfort, ultrasonography of the gastric antrum, assessment of vagal and sympathetic nerve function by respiratory sinus arrhythmia and skin conductance, and measurement of blood sugar and HbA1c. Immediately after a standard meal of soup with meat, 21 (50%) of the 42 patients with diabetes complained of abdominal discomfort (pain, bloating, fullness), which was significantly less frequent (95% CI of difference 0.03-0.5) than previously seen in patients with functional dyspepsia (76%), and significantly more frequent (95% CI of difference 0.3-0.6) than that seen in healthy individuals (4%). Bloating was the most marked postprandial complaint. Mean fasting antral area was significantly wider in patients with diabetes (mean 4.9 cm2, SD 1.7) compared to healthy individuals (mean 3.5 cm2, SD 1.2), 95% CI of difference 0.6-2.2 cm2. Mean postprandial antral area was 14.8 cm2 (SD 4.6) in the patients with diabetes, which is insignificantly wider than in patients with functional dyspepsia (mean 13.0 cm2, SD 4.0) but significantly wider (95% CI of difference 1.9-6.5 cm2) than that seen in healthy individuals (mean 10.6 cm2, SD 3.8). The mean respiratory sinus arrhythmia was 0.7 beats/min (SD 0.7) in the patients with diabetes, which was insignificantly lower than that seen in patients with functional dyspepsia (2.1 beats/min, SD 4.5), and significantly lower (99% CI of difference 3.8-7.1 beats/min) compared to healthy individuals (6.2 beats/min, SD 3.8). It is concluded that patients with diabetes have a wider gastric antrum and more discomfort after a meal than healthy individuals. Compared to patients with functional dyspepsia, patients with diabetes have a wider postprandial antrum but fewer symptoms. The very low vagal tone seen in patients with diabetes may play an important role in the pathogenesis of their gastric motility disturbance and postprandial abdominal discomfort.
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PMID:Wide gastric antrum and low vagal tone in patients with diabetes mellitus type 1 compared to patients with functional dyspepsia and healthy individuals. 856 73

Celiac disease develops from an autoimmune response to specific dietary grains that contain gluten. Diagnosis can be made based on the classical presentation of diarrhea, fatty stools, and abdominal bloating and cramping, as well as the presence of specific serum antibodies. In addition, gluten ingestion has increasingly been found to be associated with other conditions not usually correlated with gluten intolerance. The subsequent diversity of the clinical presentation in these cases can complicate decision-making and delay treatment initiation in conditions such as ataxia, headaches, arthritis, neuropathy, type 1 diabetes mellitus, and others. This review explores the etiology and pathology of celiac disease, presents support for the relationship between gluten and other diseases, and provides effective screening and treatment protocols.
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PMID:Celiac disease and gluten-associated diseases. 1616 73

Celiac disease is a gastrointestinal disorder characterized by inflammation, leading to injury to the mucosal lining of the small intestine. The inflammation occurs when gliadin, a protein found in such gluten-containing foods as wheat, rye, and barley, is ingested by genetically susceptible individuals. The mucosal damage and subsequent malabsorption of nutrients leads to various complications. Researchers estimate that more than 2 million people in the United States have celiac disease-a prevalence that is greater than was previously believed. Approximately 60,000 Americans are diagnosed annually with celiac disease. Until recently, diagnosis has been complicated by the fact that the indicators of celiac disease are nonspecific. However, because of the development of new, easy-to-administer serology tests, diagnosis has become much less complicated. After conducting a review of the literature, the authors recommend a serologic testing sequence for diagnosis of celiac disease and urge that adults and children with an assortment of symptoms be tested for this disease. Common signs and symptoms of celiac disease include anemia, arthralgia, fatigue, infertility, neuropathy, and weight loss, in addition to such gastrointestinal symptomatology as abdominal pain, anorexia, bloating, constipation, and diarrhea. The only treatment for patients with celiac disease remains a gluten-free diet.
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PMID:New strategies for diagnosis and management of celiac disease. 1658 82

Diabetes is associated with several changes in gastrointestinal (GI) motility and associated symptoms such as nausea, bloating, abdominal pain, diarrhoea and constipation. The pathogenesis of altered GI functions in diabetes is multifactorial and the role of the enteric nervous system (ENS) in this respect has gained significant importance. In this review, we summarize the research carried out on diabetes-related changes in the ENS. Changes in the inhibitory and excitatory enteric neurons are described highlighting the role of loss of inhibitory neurons in early diabetic enteric neuropathy. The functional consequences of these neuronal changes result in altered gastric emptying, diarrhoea or constipation. Diabetes can also affect GI motility through changes in intestinal smooth muscle or alterations in extrinsic neuronal control. Hyperglycaemia and oxidative stress play an important role in the pathophysiology of these ENS changes. Antioxidants to prevent or treat diabetic GI motility problems have therapeutic potential. Recent research on the nerve-immune interactions demonstrates inflammation-associated neurodegeneration which can lead to motility related problems in diabetes.
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PMID:Diabetes and the enteric nervous system. 1797 Oct 27

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.
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PMID:Gastric electrical stimulation for the treatment of diabetic gastroparesis. 2274 75


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