Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022104 (irritable bowel syndrome)
 8,033 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperparathyroidism is a common cause of hypercalcemia. The hypercalcemia usually is discovered during a routine serum chemistry profile. Often, there has been no previous suspicion of this disorder. In most patients initially believed to be asymptomatic, previously unrecognized symptoms resolve with surgical correction of the disorder. The symptoms of hyperparathyroidism are vague and often similar to symptoms of depression, irritable bowel syndrome, fibromyalgia or stress reaction. Complications of primary hyperparathyroidism include peptic ulcers, nephrolithiasis, pancreatitis and dehydration. Surgical management is usually indicated. When medical management is used, routine monitoring for clinical deterioration is recommended. Preoperative localization of adenomas with technetium Tc 99m sestamibi scan is possible but may be unnecessary. An experienced surgeon should perform the parathyroidectomy.
 ...
PMID:Hyperparathyroidism. 957 20

All cases of diarrhea involve increased fecal excretion of water. Understanding the mechanisms of infectious diarrhea requires review of the physiology of water and electrolyte absorption. Every day, 8 to 9 liters of fluid flow into the intestine, most of it reabsorbed in the small bowel. There are 2 main types of infectious diarrhea: secretory noninvasive diarrhea, such as cholera, due to impairment of water absorption mechanisms in the small bowel and inducing watery stools and dehydration; and enteroinvasive diarrhea, due to alteration of the colonic mucosa, inducing dysentery. Most cases of infectious diarrhea are acute. Some pathogens, mainly parasites, can induce chronic diarrhea. A HIV serology is then warranted. Some patients develop chronic irritable bowel syndrome after acute gastroenteritis.
 ...
PMID:[Pathophysiology of tropical diarrhea]. 1732 66

Local or village chickens are the major source of poultry products in less developed countries, but information is limited on their susceptibility or resistance to diseases. In this work, 6-week-old local Nigerian chickens, pullets and broilers were used. One day before infection the mean body weight of the broilers was more than twice that of the pullets and local chickens. The bursa: body weight (B:BW) indices of the pullets and local chickens were similar, but were significantly higher than those of broilers. Following inoculation intraocularly with pathogenic infectious bursal disease virus (IBDV) drowsiness, drop in feed and water consumption, and diarrhoea were observed among the local chickens and pullets on day 2 post inoculation (p.i.) and in the broilers on day 3 p.i. Body weight losses from 1 to 11 days p.i. were significantly higher in the local chickens and pullets than in the broilers, total mortalities being 17.6, 50.0 and 61.51% in broilers, pullets and local chickens, respectively. Necropsy showed that dehydration and proventricular haemorrhages occurred most frequent in the local chickens. The response correlated with the B:BW indices on day 14 p.i. This showed that local Nigerian chickens are more susceptible to IBD than broilers and slightly more susceptible than pullets, explaining earlier reports that mortality due to IBD was higher in pullets or light breeds of chicken than in broilers or heavy breeds.
 ...
PMID:Comparative study of the resistance or susceptibility of local Nigerian and exotic chickens to infectious bursal disease. 1848 82

The two most clinically serious eating disorders are anorexia nervosa and bulimia nervosa. A drive for thinness and fear of fatness lead patients with anorexia nervosa either to restrict their food intake or binge-eat then purge (through self-induced vomiting and/or laxative abuse) to reduce their body weight to much less than the normal range. A drive for thinness leads patients with bulimia nervosa to binge-eat then purge but fail to reduce their body weight. Patients with eating disorders present with various gastrointestinal disturbances such as postprandial fullness, abdominal distention, abdominal pain, gastric distension, and early satiety, with altered esophageal motility sometimes seen in patients with anorexia nervosa. Other common conditions noted in patients with eating disorders are postprandial distress syndrome, superior mesenteric artery syndrome, irritable bowel syndrome, and functional constipation. Binge eating may cause acute gastric dilatation and gastric perforation, while self-induced vomiting can lead to dental caries, salivary gland enlargement, gastroesophageal reflux disease, and electrolyte imbalance. Laxative abuse can cause dehydration and electrolyte imbalance. Vomiting and/or laxative abuse can cause hypokalemia, which carries a risk of fatal arrhythmia. Careful assessment and intensive treatment of patients with eating disorders is needed because gastrointestinal symptoms/disorders can progress to a critical condition.
 ...
PMID:Gastrointestinal symptoms and disorders in patients with eating disorders. 2649 70

Cyclic vomiting syndrome (CVS) is a functional disorder characterized by stereotypical episodes of intense vomiting separated by weeks to months. Although it can occur at any age, the most common age at presentation is 3-7 years. There is no gender predominance. The precise pathophysiology of CVS is not known but a strong association with migraine headaches, in the patient as well as the mother indicates that it may represent a mitochondriopathy. Studies have also suggested the role of an underlying autonomic neuropathy involving the sympathetic nervous system in its pathogenesis. CVS has known triggers in many individuals and avoiding these triggers can help prevent the onset of the episodes. It typically presents in four phases: a prodrome, vomiting phase, recovery phase and an asymptomatic phase until the next episode. Complications such as dehydration and hematemesis from Mallory Wise tear of the esophageal mucosa may occur in more severe cases. Blood and urine tests and abdominal imaging may be indicated depending upon the severity of symptoms. Brain magnetic resonance imaging and upper gastrointestinal endoscopy may also be indicated in certain circumstances. Management of an episode after it has started ('abortive treatment') includes keeping the patient in a dark and quiet room, intravenous hydration, ondansetron, sumatriptan, clonidine, and benzodiazepines. Prophylactic treatment includes cyproheptadine, propranolol and amitriptyline. No mortality has been reported as a direct result of CVS and many children outgrow it over time. A subset may develop other functional disorders like irritable bowel syndrome and migraine headaches.
...
PMID:Cyclic Vomiting Syndrome: A Functional Disorder. 2677 Aug 96

Very-early-onset inflammatory bowel disease (VEO-IBD) has a distinct phenotype and should be considered a specific entity. VEO-IBD presents with very severe clinical pictures and is frequently known by an indeterminate colitis whose clinical remission is unmanageable. This study examines the case of a neonate with VEO-IBD, not responding to medical and surgical treatment. A 7-day-old Iranian female neonate presented with severe bloody diarrhea, poor feeding, abdominal distention, and dehydration suggesting severe proctocolitis due to an allergy to the protein in cow's milk. The condition did not respond to the elimination of diet for 1 month. Infections, celiac disease, and cystic fibrosis were excluded. Immunological investigations were negative, but antineutrophil cytoplasmic antibodies were positive. Due to the neonate's persistent symptoms and failure to thrive, upper and lower endoscopies were performed, showing ulcerative colitis. At the age of 4 months, she presented with signs and symptoms of toxic colitis and acute intestinal perforation, which prompted an emergency laparotomy. Due to the necrosis of the colon, hemicolectomy and colostomy were done. The patient was resuscitated and rehabilitated and was given glucocorticoid and mesalamine. We believe that the incidence of this problem is increasing, as is shown by the rise in the number of children under 10 years old being diagnosed. These patients require more aggressive therapeutic interventions than older IBD patients to achieve complete remission because they are more likely to have extensive colonic disease.
 ...
PMID:Neonatal Presentation of Unremitting Inflammatory Bowel Disease. 2989 52

Blastocystis sp. is a unicellular parasitic microorganism commonly found in the gastrointestinal tracts of humans and animals. It causes symptomatic or asymptomatic infection and its route of transmission is via fecal-oral. High prevalence of Blastocystis infection in developing countries is usually due to poor hygiene practices, exposure to animals infected with the parasite and intake of contaminated water or food. Blastocystis infected individuals often suffer from diarrhea, abdominal pain, nausea, and stomach bloating. Even though pathogenicity of Blastocystis is unclear, it is commonly associated with irritable bowel syndrome. In this review, we have analysed the evidence that shows the association between this microorganism and gastrointestinal disorders. There have been a number of studies which showed that the pathogenicity of Blastocystis is related to its different STs. The pathogenicity is speculated to be due to cysteine proteases formation which stimulates mucosal cells to release interleukin-8 which has been associated with extreme dehydration and gut inflammation. In vitro studies on human colonic epithelial cells revealed that incubation of Blastocystis modulated the host immune response by stimulating the formation of pro-inflammatory cytokines and granulocyte macrophage colonystimulating factor. Metronidazole is found to be the first-line drug of choice. Another treatment option is the combination therapy with trimethoprim/sulfamethoxazole.
 ...
PMID:Blastocystis sp., Parasite Associated with Gastrointestinal Disorders: An Overview of its Pathogenesis, Immune Modulation and Therapeutic Strategies. 3008 27

Several intestinal secretagogues became available for the patients with irritable bowel syndrome. We report a case of symptomatic hyponatremia after lubiprostone ingestion. A male patient was visiting our office to manage chronic kidney disease. He suffered chronic hepatitis (type C), which was successfully treated with asunaprevir and daclatasvir. He took lubiprostone due to constipation, and then watery diarrhoea was frequently developed. Next morning, he came to our hospital due to consciousness disturbance. Physical examination showed dehydration and laboratory data exhibited hyponatremia (110 mEq/L). Subsequent treatment against hypovolemic hyponatremia recovered his consciousness without any sequels. This case suggests that intestinal secretagogues can accompany severe electrolyte disturbance. Potential mechanisms for hyponatremia were discussed.
 ...
PMID:Symptomatic hyponatremia: a rare but reversible adverse reaction of lubiprostone. 3218 6

The aim of this study was to investigate the use of a standardized animal model subjected to antibiotic treatment, and the effects of this treatment on the course of dextran sodium sulphate (DSS)-induced colitis in mice. By decontamination with selective antibiotics and observation of pathogenesis of ulcerative colitis (UC) induced chemically by exposure of mice to various concentrations of DSS, we obtained an optimum animal PGF model of acute UC manifested by mucin depletion, epithelial degeneration and necrosis, leading to the disappearance of epithelial cells, infiltration of lamina propria and submucosa with neutrophils, cryptitis, and accompanied by decreased viability of intestinal microbiota, loss of body weight, dehydration, moderate rectal bleeding, and a decrease in the selected markers of cellular proliferation and apoptosis. The obtained PGF model did not exhibit changes that could contribute to inflammation by means of alteration of the metabolic status and the induced dysbiosis did not serve as a bearer of pathogenic microorganisms participating in development of ulcerative colitis. The inflammatory process was induced particularly by exposure to DSS and its toxic action on compactness and integrity of mucosal barrier in the large intestine. This offers new possibilities of the use of this animal model in studies with or without participation of pathogenic microbiota in IBD pathogenesis.
 ...
PMID:Innovative Animal Model of DSS-Induced Ulcerative Colitis in Pseudo Germ-Free Mice. 3327 73