Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertrophic pyloric stenosis (IHPS) is the most common abdominal abnormality requiring surgery in infants. It occurs due to the hypertrophic and hyperplasia of the muscular layers of the pyloric. The usual age of clinical presentation is about three weeks of life. The most important symptom is non bilious emesis, intermittent or after each feeding. From march 1996 to June 2001, 21 infants, 20 males and 1 female, were subjected to ultrasonographic, radiographic exams and after diagnosis to the pyloromyotomy extramucosa. Ultrasonography was the study of choice used to identify hypertrophic pyloric stenosis; the markers to analyse were the length and the overall diameter of the pyloric canal and the muscle thickness of the wall. The results showed that a length of the pyloric canal 20 +/- 6 mm, a diameter 13.6 +/- 2.5 mm and a muscle thickness 4.1 +/- 1 mm are diagnostics for hypertrophic pyloric stenosis.
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PMID:Muscle thickness in infants hypertrophic pyloric stenosis. 1291 45

This study aimed to evaluate the effectiveness of oral atropine in the management of IHPS. Cases were diagnosed clinically and confirmed sonographically. Atropine was given orally from the outset at a dose of 0.18 mg/kg/day in eight divided doses, increased daily by 1/4th of the commencing dose till vomiting ceased. Ultrasonographic evaluation of pyloric muscle thickness and length was done at the commencement of treatment, after completion of treatment and at 3, 6, 9, 12 and 15 months follow up. Oral atropine was effective in 11/12 (91.06%) cases. Vomiting ceased in 14 to 21 days in all cases. One case required initial 7 days of i.v. treatment followed by 18 days oral treatment to stop vomiting. USG evidence of normalization of pylorus was observed in all these cases, 3-15 months after completion of treatment. We conclude that oral atropine proved to be a simple, effective, safe, very cheap and acceptable treatment option for IHPS.
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PMID:Oral atropine sulfate for infantile hypertrophic pyloric stenosis. 1592 95

Migraine attacks are characterized by unilateral throbbing, pulsating headache associated with nausea, vomiting, photophobia, phonophobia and allodynia. Peripheral sensitization is an acute, chemical-induced form of functional plasticity, which converts high-threshold nociceptors into low-threshold sensory neurons. This form of sensitization occurs when the nerve terminals (meningeal nociceptors) of the neurons of the trigeminal ganglion are soaked with the "inflammatory" soup (prostaglandin E2, bradykinin, serotonin and cytokines) along the vasculature of the cerebral dura mater. Peripheral sensitization in migraine attacks is explained clinically by intracranial hypersensitivity (the headache worsens during coughing or physical activity) and by a throbbing element in the pain of migraine (sensitized nociceptors become hyperresponsive to the otherwise innocuous and unperceived rhythmic fluctuation in intracranial pressure produced by normal arterial pulsation). The essence of central sensitization is that the second-order neurons in the trigeminocervical complex become hyperexcitable. The altered behavior of the second-order neurons is based on the increased glutamate sensistivity of the NMDA receptors and the neuronal nitric oxide synthase activity stimulated by nitric oxide. This process is explained clinically by face and scalp ollodynia and by neck stiffness (extracranial tenderness).
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PMID:[The mechanism of peripheral and central sensitization in migraine. A literature review]. 1973 14

Oxaliplatin, an anti-cancer chemotherapeutic agent used for the treatment of colorectal cancer, commonly causes gastrointestinal side-effects such as constipation, diarrhoea, nausea, and vomiting. Damage to enteric neurons may underlie some of these gastrointestinal side-effects, as the enteric nervous system (ENS) controls functions of the bowel. In this study, neuronal loss and changes to the structure and immunoreactivity of myenteric neuronal nitric oxide synthase (nNOS) neurons were examined in colonic segments from mice following exposure to oxaliplatin ex vivo and following repeated intraperitoneal injections of oxaliplatin over 3 weeks in vivo, using immunohistochemistry and confocal microscopy. Significant morphological alterations and increases in the proportion of NOS-immunoreactive (IR) neurons were associated with both short-term oxaliplatin exposure and long-term oxaliplatin administration, confirming that oxaliplatin causes changes to the myenteric neurons. Long-term oxaliplatin administration induced substantial neuronal loss that was correlated with a reduction in both the frequency and propagation speed of colonic migrating motor complexes (CMMCs) in vitro. Similar changes probably produce some symptoms experienced by patients undergoing oxaliplatin treatment.
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PMID:Effects of oxaliplatin on mouse myenteric neurons and colonic motility. 2348 39

Postsynaptic density (PSD) proteins in excitatory synapses are relatively immobile components, while there is a structured organization of mobile scaffolding proteins lying beneath the PSDs. For example, shank proteins are located further away from the membrane in the cytosolic faces of the PSDs, facing the actin cytoskeleton. The rationale of this organization may be related to important roles of these proteins as "exchange hubs" for the signaling proteins for their migration from the subcortical cytosol to the membrane. Notably, PSD95 have also been demonstrated in prejunctional nerve terminals of nitrergic neuronal varicosities traversing the gastrointestinal smooth muscles. It has been recently reported that motor proteins like myosin Va play important role in transcytosis of nNOS. In this review, the hypothesis is forwarded that nNOS delivered to subcortical cytoskeleton requires interactions with scaffolding proteins prior to docking at the membrane. This may involve significant role of "shank," named for SRC-homology (SH3) and multiple ankyrin repeat domains, in nitric oxide synthesis. Dynein light chain LC8-nNOS from acto-myosin Va is possibly exchanged with shank, which thereafter facilitates transposition of nNOS for binding with palmitoyl-PSD95 at the nerve terminal membrane. Shank knockout mice, which present with features of autism spectrum disorders, may help delineate the role of shank in enteric nitrergic neuromuscular transmission. Deletion of shank3 in humans is a monogenic cause of autism called Phelan-McDermid syndrome. One fourth of these patients present with cyclical vomiting, which may be explained by junctionopathy resulting from shank deficit in enteric nitrergic nerve terminals.
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PMID:Molecular handoffs in nitrergic neurotransmission. 2570 21

Development of infantile hypertrophic pyloric stenosis during postoperative period in EA with TEF is rare. Postoperative vomiting or feeding intolerance in EA is more common which is due to esophageal stricture, gastroesophageal reflux and esophageal dysmotility. A typical case of IHPS also presents with non-bilious projectile vomiting at around 3-4 weeks of life. The diagnosis of infantile hypertrophic pyloric stenosis in this subset is usually delayed because of its rarity. We report a case of IHPS in postoperative EA and emphasize on high index of suspicion to avoid any delay in diagnosis with its metabolic consequences.
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PMID:Infantile Hypertrophic Pyloric Stenosis in Postoperative Esophageal Atresia with Tracheoesophageal Fistula. 2629 Aug 14

A 24-day old female Nigerian neonate presented with protracted vomiting, fever and dehydration but without palpable abdominal tumour or visible gastric peristalsis. There was no derangement of serum electrolytes. The initial working diagnosis was Late-Onset Sepsis but abdominal ultrasonography showed features consistent with the diagnosis of IHPS. This case report highlights the atypical presentation of this surgical condition and the need to investigate cases of protracted vomiting in the newborn with at least, ultrasonography to minimize complications and reduce the risk of mortality in a resource-poor setting.
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PMID:Infantile hypertrophic pyloric stenosis with unusual presentations in Sagamu, Nigeria: a case report and review of the literature. 2764 52

Gastrointestinal (GI) side-effects of chemotherapy present a constant impediment to efficient and tolerable treatment of cancer. GI symptoms often lead to dose reduction, delays and cessation of treatment. Chemotherapy-induced nausea, bloating, vomiting, constipation, and/or diarrhea can persist up to 10 years post-treatment. We have previously reported that long-term 5-fluorouracil (5-FU) administration results in enteric neuronal loss, acute inflammation and intestinal dysfunction. In this study, we investigated whether the cytoprotectant, BGP-15, has a neuroprotective effect during 5-FU treatment. Balb/c mice received tri-weekly intraperitoneal 5-FU (23 mg/kg/d) administration with and without BGP-15 (15 mg/kg/d) for up to 14 days. GI transit was analyzed via in vivo serial X-ray imaging prior to and following 3, 7, and 14 days of treatment. On day 14, colons were collected for assessment of ex vivo colonic motility, neuronal mitochondrial superoxide, and cytochrome c levels as well as immunohistochemical analysis of myenteric neurons. BGP-15 did not inhibit 5-FU-induced neuronal loss, but significantly increased the number and proportion of choline acetyltransferase (ChAT)-immunoreactive (IR) and neuronal nitric oxide synthase (nNOS)-IR neurons in the myenteric plexus. BGP-15 co-administration significantly increased mitochondrial superoxide production, mitochondrial depolarization and cytochrome c release in myenteric plexus and exacerbated 5-FU-induced colonic inflammation. BGP-15 exacerbated 5-FU-induced colonic dysmotility by reducing the number and proportion of colonic migrating motor complexes and increasing the number and proportion of fragmented contractions and increased fecal water content indicative of diarrhea. Taken together, BGP-15 co-treatment aggravates 5-FU-induced GI side-effects, in contrast with our previous findings that BGP-15 alleviates GI side-effects of oxaliplatin.
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PMID:Co-treatment With BGP-15 Exacerbates 5-Fluorouracil-Induced Gastrointestinal Dysfunction. 3113 44

Gastroparesis is a disorder where the stomach empties contents too slowly into the small intestine with associated symptoms of nausea, vomiting, postprandial fullness, bloating, early satiety and/or abdominal pain. It is a well-established fact that the female gender is more susceptible to developing gastroparesis compared to males, although the significance and rationale behind this gender inequality remains an unresolved mystery. Several hypotheses have been proposed including an intrinsically slower stomach in females, elevated levels of sex steroid hormones, loss of neuronal nitric oxide (nNOS) expression, and possibly due to altered serotonergic signaling. Recently, our group investigated gender-associated differences in the number of interstitial cells of Cajal in the antral and pyloric smooth muscle of diabetic patients with severe refractory gastroparesis and found there was no significant difference between the 2 genders. Targeting these gender-specific mechanisms may lead towards future therapeutic options that might alleviate and/or prevent gastroparesis. Furthermore, a better-understanding of the sex-related differences in gastroparesis can allow medical practitioners to better tailor treatment options for their patients. This article will attempt to explain why females are more vulnerable to developing gastroparesis by examining the pathogenesis and molecular basis of gender-related factors that have been identified to play a role in the gender disparity of this entity.
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PMID:Gender-Related Differences in Gastroparesis. 3252 95