Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011168 (dysphagia)
 15,644 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Salivary gland dysfunction is uniformly detrimental to the oral cavity. Its effects on the GI tract have begun to be explored. Dry mouth is a common complaint among older adults, probably due to systemic disease and its therapy rather than the aging process per se. Evaluation of complaints of dry mouth should include medical history, sialometry and physical examination. Numerous medications can elicit drug-induced xerostomia. Patients who have received radiation therapy to the head and neck region often have permanent radiation-induced xerostomia, which has been linked to esophagitis. SS is an autoimmune systemic exocrinopathy resulting in irreversible salivary gland dysfunction. SS has numerous GI manifestations, including dysphagia, temporal defects of deglutition, esophageal dysmotility, gastritis, pancreatitis and liver disease. Management of salivary hypofunction is directed toward preserving the dentition and improving patient comfort. Drug-induced xerostomia is often correctable by altering the therapeutic modality.
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PMID:Interactions of the salivary and gastrointestinal systems. II. Effects of salivary gland dysfunction on the gastrointestinal tract. 191 20

Pancreatitis may be associated with thoracic complications, notably chronic massive pleural effusion (CMPE) and, rarely, pseudocysts with mediastinal extension (PME) and enzymatic mediastinitis (EM). Our personal experience with 14 cases of thoracic complications (nine CMPE, two PME associated with pleural effusion, and three EM of 670 patients who underwent surgery; of these, 191 had acute and 479 had chronic pancreatitis) during 16 years (1970-1986) is reported. In the patients with CMPE, the initial symptoms were progressive dyspnea eventually associated with cough and chest pain. In the PME cases, there was dysphagia associated with left subscapular pain and left chest pain. The initial signs in the patients with EM were sudden dyspnea, cyanosis, retrosternal pain, tachycardia, and acute heart failure. A fistula between the pancreatic ductal system and the pleural cavity in seven of the nine patients with CMPE was demonstrated by intraoperative pancreatography and/or cystography. On the contrary, preoperative endoscopic pancreatography demonstrated the sinus tract in only three of the seven. In both cases of PME, computed tomography (CT) provided a correct diagnosis that was confirmed at surgery. In the patients with EM, the diagnosis was suggested by the clinical appearance and was confirmed by the chest roentgenogram and by CT. All patients had operations after varying periods of unsuccessful 2-4-week-long conservative treatment. One patient with infected ascites died postoperatively. There were no thoracic recurrences of pancreatic disease among the other patients at a 10-month-10-year follow-up observation after surgery.
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PMID:Thoracic complications of pancreatitis. 275 44

Secondary achalasia is commonly due to cancer. Benign causes are rare and an association with pancreatitis has never been made. Our patient presented with clinical, manometric, endoscopic, and radiographic features of achalasia that occurred in conjunction with a pancreatic pseudocyst extending into the mediastinum. Documentation of this unique relationship was made on two occasions after episodes of complicated pancreatitis and was confirmed by restoration of normal esophageal function after drainage of the pseudocyst. Onset of dysphagia occurring in association with pancreatitis suggests the presence of a pseudocyst and secondary achalasia.
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PMID:Pancreatic pseudocyst as a cause for secondary achalasia. 290 23

Mediastinal pancreatic pseudocysts are rare complications occurring in the course of pancreatitis. Two patients are described with chronic alcoholic pancreatitis who developed mediastinal pancreatic pseudocysts. The most prominent clinical findings were, respectively, recurrent pericardial and pleural effusions and dysphagia. The elevated amylase values in serum and urine and in the pericardial and pleural effusions pointed to pancreatic disease. The mediastinal pancreatic pseudocysts were found preoperatively by ultrasound and endoscopic retrograde cholangiopancreatography. Surgery was performed. In one case the pseudocyst was treated by external drainage and in the other case by marsupialization into the left pleural space. In each case pancreaticojejunostomy was performed in addition. Etiology, symptoms, diagnosis and therapy in 32 published cases are discussed on the basis of experience with these two patients.
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PMID:[Mediastinal pancreatic pseudocysts. Report of 2 cases and review of the literature]. 662 29

There are increasing challenges for the practising gastroenterologist in treating AIDS-related gastrointestinal diseases. The differential diagnoses of dysphagia and odynophagia include cytomegalovirus (CMV) and herpes simplex virus (HSV) infection, non-specific aphthous ulceration and non-AIDS oesophageal diseases, especially reflux oesophagitis. Chronic subacute abdominal pain with nausea, vomiting, early satiety and weight loss is suggestive of an obstructive lesion caused by lymphoma or Kaposi's sarcoma. Severe acute abdominal pain can indicate pancreatitis or intestinal perforation due to cytomegalovirus. Right upper quadrant pain (with or without fever, vomiting or abnormal liver function tests with a cholestatic profile) is suggestive of hepatobiliary pathology including cholecystitis, cholangitis, acalculous cholecystitis and AIDS cholangiopathy. Diarrhoea is the most common gastrointestinal symptom of AIDS, affecting 50-90% of patients. Causes of AIDS diarrhoea include protozoa (Cryptosporidium parvum, Isospora belli, Enterocytozoon bieneusi, Septata intestinalis, Cyclospora spp, Entamoeba histolytica and Giardia lamblia), bacteria (Mycobacterium avium-intracellulare, Clostridium difficile, Salmonella, Shigella and Campylobacter jejuni), and viruses (CMV, HSV and possibly HIV). Chronic diarrhoea, malnutrition and weight loss can shorten the life-span of patients with AIDS. Elemental diets, isotonic formulas, medium chain triglycerides and total parenteral nutrition have been tried with little success in AIDS patients with severe diarrhoea and wasting.
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PMID:AIDS and the gut. 805 32

A careful history can localize gastrointestinal motility disorders and suggest appropriate diagnostic tests. Dysphagia, odynophagia, heartburn and reflux have esophageal origins. The same symptoms occur in achalasia, a classic motor disorder of the lower esophageal sphincter, which can be diagnosed by barium swallow, endoscopy and esophageal motility studies. Nausea, vomiting, anorexia, bloating and abdominal pain are symptoms of motor disorders of the stomach and small intestine. When these symptoms are accompanied by unexplained right upper quadrant pain, elevated liver enzyme levels and unexplained recurrent pancreatitis, the diagnosis of impaired biliary motility is suggested. Colorectal motility disorders may present as abdominal pain, diarrhea, constipation and/or fecal incontinence. If symptoms do not resolve with dietary changes and appropriate medications and the anatomy is normal on lower gastrointestinal studies, colorectal motility studies may be indicated.
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PMID:Gastrointestinal motility disorders. 859 65

A fatal case of acute pancreatitis is reported. On account of difficulty in eating caused by persistent dysphagia and heartburn, the clinical condition of a 39-year-old man who had been a heavy drinker deteriorated rapidly. He was taken to a hospital in an ambulance in an unconscious state. Based on the endoscopic examination and blood chemistry data, the diagnosis of hemorrhagic esophagitis and hepatic failure was made. Treatment including fluid infusion was unsuccessful and he died on the second hospital day. Based on a strong suspicion that the pathologic change in the esophagus may have been chemical esophagitis caused by corrosives of some type, the police ordered an administrative autopsy. The postmortem examination revealed marked necrosis in the pancreas and in the abdominal fatty tissue including the omentum and the mesentery. The necrotic areas in the pancreas were accompanied by only a slight degree of hemorrhage. The cause of death was diagnosed as acute pancreatitis. The pathologic change in the esophagus was identified as Candida esophagitis. Alcohol abuse and malnutrition caused by esophagitis were both considered to be factors which lead to the acute fatal pancreatitis.
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PMID:Death caused by undiagnosed acute pancreatitis. 869 55

Cholelithiasis and gastroesophageal reflux are both very common diseases that may occur simultaneously. Management of asymptomatic gallstones is still controversial. Because severe complications due to gallstones may occur incidental cholecystectomy during nonrelated abdominal surgery may be offered to patients with coexisting gallbladder disease. The aim of this study was to assess the clinical outcome of patients after laparoscopic fundoplication and incidental cholecystectomy for cholelithiasis compared with the outcome of patients after fundoplication alone. We conducted a retrospective chart review and prospective analysis using a questionnaire of the clinical outcome of patients who underwent laparoscopic fundoplication and incidental cholecystectomy from June 1991 to January 2000 in comparison with sex- and age-matched patients who had antireflux surgery alone. Sixty-seven (6.3%) of 1065 patients had a laparoscopic cholecystectomy at the time of laparoscopic antireflux surgery; 101 (75%) of 134 answered the questionnaire. The mean follow-up time was 4.6 years. Laparoscopic cholecystectomy did not influence surgical morbidity or mortality. Postoperative symptom score (1-10) did not show a statistically significant difference regarding bloating, diarrhea, abdominal pain, nausea, vomiting, biliary problems, jaundice, pancreatitis, dysphagia for liquids and solid, heartburn, regurgitation, and chest pain when the two groups were compared. We conclude that incidental cholecystectomy during laparoscopic antireflux surgery is safe and does not appear to influence the clinical outcome of the antireflux procedure.
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PMID:Incidental cholecystectomy during laparoscopic antireflux surgery. 1213 45

Mitochondriopathies (MCPs) are either due to sporadic or inherited mutations in nuclear or mitochondrial DNA located genes (primary MCPs), or due to exogenous factors (secondary MCPs). MCPs usually show a chronic, slowly progressive course and present with multiorgan involvement with varying onset between birth and late adulthood. Although several proteins with signalling, assembling, transport, enzymatic function can be impaired in MCP, most frequently the activity of the respiratory chain (RC) protein complexes is primarily or secondarily affected, leading to impaired oxygen utilization and reduced energy production. MCPs represent a diagnostic challenge because of their wide variation in presentation and course. Systems frequently affected in MCP are the peripheral nervous system (myopathy, polyneuropathy, lactacidosis), brain (leucencephalopathy, calcifications, stroke-like episodes, atrophy with dementia, epilepsy, upper motor neuron signs, ataxia, extrapyramidal manifestations, fatigue), endocrinium (short stature, hyperhidrosis, diabetes, hyperlipidaemia, hypogonadism, amenorrhoea, delayed puberty), heart (impulse generation or conduction defects, cardiomyopathy, left ventricular non-compaction heart failure), eyes (cataract, glaucoma, pigmentary retinopathy, optic atrophy), ears (deafness, tinnitus, peripheral vertigo), guts (dysphagia, vomiting, diarrhoea, hepatopathy, pseudo-obstruction, pancreatitis, pancreas insufficiency), kidney (renal failure, cysts) and bone marrow (sideroblastic anaemia). Apart from well-recognized syndromes, MCP should be considered in any patient with unexplained progressive multisystem disorder. Although there is actually no specific therapy and cure for MCP, many secondary problems require specific treatment. The rapidly increasing understanding of the pathophysiological background of MCPs may further facilitate the diagnostic approach and open perspectives to future, possibly causative therapies.
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PMID:Mitochondriopathies. 1500 63

C1 inhibitor (C1-INH) is a serine protease inhibitor (serpins) that inactivates several different proteases in the complement, contact, coagulation, and fibrinolytic systems. By its C-terminal part (serpin domain), characterized by three beta-sheets and an exposed mobile reactive loop, C1-INH binds, and blocks the activity of its target proteases. The N-terminal end (nonserpin domain) confers to C1-INH the capacity to bind lipopolysaccharides and E-selectin. Owing to this moiety, C1-INH intervenes in regulation of the inflammatory reaction. The heterozygous deficiency of C1-INH results in hereditary angioedema (HAE). The clinical picture of HAE is characterized by bouts of local increase in vascular permeability. Depending on the affected site, patients suffer from disfiguring subcutaneous edema, abdominal pain, vomiting and/or diarrhoea for edema of the gastrointestinal mucosa, dysphagia, and dysphonia up to asphyxia for edema of the pharynx and larynx. Apart from its genetic deficiency, there are several pathological conditions such as ischemia-reperfusion, septic shock, capillary leak syndrome, and pancreatitis, in which C1-INH has been reported to either play a pathogenic role or be a potential therapeutic tool. These potential applications were identified long ago, but controlled studies have not been performed to confirm pilot experiences. Recombinant C1-INH, produced in transgenic animals, has recently been produced for treatment of HAE, and clinical trials are in progress. We can expect that the introduction of this new product, along with the existing plasma derivative, will renew interest in exploiting C1-INH as a therapeutic agent.
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PMID:C1 inhibitor: molecular and clinical aspects. 1626 49


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