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)

A 37-year-old man, previously submitted to colectomy for ulcerative pancolitis unresponsive to medical therapy, presented with nausea, vomiting, epigastric pain, and bloody diarrhea. An upper gastrointestinal endoscopy revealed mucosal friability, petechiae, and erosions throughout the duodenum, whereas prestomal ileum showed large ulcers and pseudopolyps. Histologically, a dense inflammation chiefly composed of lymphocytes and plasma cells with few neutrophils was detected. No bacteria, protozoa, and fungi could be detected. Despite intensive care, intra-1194 venous antibiotics and steroids, the patient died of diffuse intravascular coagulation and multiorgan failure. At post-mortem examination severe ulcerative lesions were observed scattered throughout the duodenum up to the distal ileum. The dramatic clinical presentation with fatal outcome, the widespread ulcers throughout the intestine, and the histological picture are peculiar features in our patient which can not be ascribed to any type of the ulcerative jejunoenteritis so far reported. Patients with pancolitis and diffuse ileal involvement do not necessarily have Crohn's disease but rather may have ulcerative colitis.
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PMID:Fatal ulcerative panenteritis following colectomy in a patient with ulcerative colitis. 1038 95

There have frequently been doubts as to the relevance of food allergy, in particular as far as the involvement of the intestinal tract is concerned. Several studies, however, have confirmed the existence of allergic reactions in the gut, with an estimated prevalence of about 1-2% in adults. Clinical symptoms are unspecific and include nausea, vomiting, abdominal pain, cramping and diarrhea. Intestinal mast cells, as well as intestinal eosinophils, have been shown to be involved in the pathogenesis of food-allergy-related enteropathy. In addition to classical IgE-dependent degranulation, further agonists have been demonstrated for mast cell activation, for example IL-4. The methods used to confirm the diagnosis of intestinal allergy are still insufficient. Until now, blinded oral challenge procedures with food antigens have been accepted as the 'gold standard' in diagnosing food allergy, although these tests have practical problems. Therefore, new test systems have been developed, such as endoscopic provocation tests, that may improve diagnostic procedures. Elimination diet still presents the main basis of therapy. Aspects to be focused on in the future are the role fo IgE-independent allergic mechanisms in intestinal allergy, the impact of cross-reactivity with other allergens and the relationship to other inflammatory bowel diseases such as Crohn's disease, ulcerative colitis, celiac disease and irritable bowel syndrome.
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PMID:Allergy and the gut. 1082 17

A patient with a fulminant amebic colitis coexisting with intestinal tuberculosis had a sudden onset of crampy abdominal pain, mucoid diarrhea, anorexia, fever and vomiting with signs of positive peritoneal irritation. Fulminant amebic colitis occurring together with intestinal tuberculosis is an uncommon event and may present an interesting patho-etiological relationship. The diagnosis was proven by histopathologic examination of resected specimen. Subtotal colectomy including segmental resection of ileum, about 80 cm in length, followed by exteriorization of both ends, was performed in an emergency basis. Despite all measures, the patient died on the sixth postoperative day. The exact relationship of fulminant amebic colitis and intestinal tuberculosis is speculative but the possibility of a cause and effect relationship exists. Fulminant amebic colitis may readily be confused with other types of inflammatory bowel disease, such as idiopathic ulcerative colitis, Crohn's disease, perforated diverticulitis and appendicitis with perforation. This report draws attention to the resurgence of tuberculosis and amebiasis in Korea, and the need for the high degree of caution required to detect it.
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PMID:Toxic amebic colitis coexisting with intestinal tuberculosis. 1119

BACKGROUND: Eosinophilic gastritis is related to eosinophilic gastroenteritis, varying only in regards to the extent of disease and small bowel involvement. Common symptoms reported are similar to our patient's including: abdominal pain, epigastric pain, anorexia, bloating, weight loss, diarrhea, ankle edema, dysphagia, melaena and postprandial nausea and vomiting. Microscopic features of eosinophilic infiltration usually occur in the lamina propria or submucosa with perivascular aggregates. The disease is likely mediated by eosinophils activated by various cytokines and chemokines. Therapy centers around the use of immunosuppressive agents and dietary therapy if food allergy is a factor. CASE PRESENTATION: The patient is a 31 year old Caucasian female with a past medical history significant for ulcerative colitis. She presented with recurrent bouts of vomiting, abdominal pain and chest discomfort of 11 months duration. The bouts of vomiting had been reoccurring every 7-10 days, with each episode lasting for 1-3 days. This was associated with extreme weakness and cachexia. Gastric biopsies revealed intense eosinophilic infiltration. The patient responded to glucocorticoids and azathioprine. The differential diagnosis and molecular pathogenesis of eosinophilic gastritis as well as the molecular effects of glucocorticoids in eosinophilic disorders are discussed. CONCLUSIONS: The patient responded to a combination of glucocorticosteroids and azathioprine with decreased eosinophilia and symptoms. It is likely that eosinophil-active cytokines such as interleukin-3 (IL-3), granulocyte macrophage colony stimulating factor (GM-CSF) and IL-5 play pivotal roles in this disease. Chemokines such as eotaxin may be involved in eosinophil recruitment. These mediators are downregulated or inhibited by the use of immunosuppressive medications.
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PMID:Eosinophilia in a patient with cyclical vomiting: a case report. 1514 61

Ulcerative colitis seldom associated with nutritive and/or salicylate allergy. Authors present a case of both allergic events at the course of the disease. In 1996 a 19-year-old girl was referred with a history of blood in stool as well as diarrhoea, suggesting ulcerative proctitis. Biopsy revealed ulcerative colitis of the rectum mucosa with eosinophilic infiltration and 20% peripheral eosinophilia was found. Allergic origin and worm infection were ruled out, and after tinidazol treatment, four year elapsed without any signs or symptoms. In December 2000 blood in stools and upper abdominal complaints developed without peripheral eosinophilia. Gastroscopy and biopsy showed a mild chronic gastritis. Olsalazine, budesonide enema and famotidin treatment were started, but then later changed to mesalazine and pantoprazol, because of the constant stomach complaints. The next five months passed without any symptoms. The patient had to break off her seashore journey in July 2000 because of stomach complaints, vomiting and exsiccosis. Peripheral eosinophilia (27.3%) was evident. Gastroscopy revealed erosive ulcers and the biopsy showed eosinophilic gastritis. Biopsies from the jejunum, duodenum and antrum as well as enteroscopy and biopsies from the rectum showed mild eosinophilic infiltration. An allergy test proved the presence of IgE against salicylate, egg protein, seafood protein and the lymphocyte transformation test was also positive against salicylate. Oral food challenges proved to be negative and the amino-salicylate treatment was stopped. After a temporary symptom free period, bloody stools reappeared in May 2003; the peripheral eosinophilia still existed, but had decreased (22.2%). Esomeprazol, and methyl-prednisolone containing enema (40 mg/day/2 weeks) followed by budesonide enema twice a week resulted in a symptom free period and peripheral eosinophilia became almost normalised (6.2%). The authors report a case having ulcerative proctitis first, than nutritive and salicylate allergy with eosinophilic gastritis and a proctitis flare-up thereafter.
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PMID:[Ulcerative colitis and eosinophilic corpus gastritis]. 1562 70

Campylobacter jejuni is the most common cause of community-acquired acute bacterial diarrhea. Campylobacter diarrhea is usually accompanied by fever and abdominal pain. Campylobacter diarrhea is usually watery. Nausea, vomiting, headache, and myalgias may also be present. Tenesmus is a common feature. The majority of patients with Campylobacter diarrhea have some component of segmental colitis, usually beginning in the small bowel and progressing distally to the cecum and colon. C. jejuni is a rare cause of pancolitis. Community-acquired colitis may be caused by C. jejuni or other enteric pathogens, for example, Shigella, Entamoeba, Yersinia, Escherichia coli 0157:H7, Clostridium difficile colitis, ischemic colitis, or idiopathic ulcerative colitis. We present a case of C. jejuni pancolitis in an elderly woman. Differential diagnosis is included in the discussion. The patient's C. jejuni pancolitis was successfully treated with a 7-day course of oral moxifloxacin.
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PMID:Campylobacter jejuni pancolitis mimicking idiopathic ulcerative colitis. 1602 51

Leukocytapheresis (LCAP) is a therapeutic strategy for extra corporeal immunomodulation that has been used to treat several immunological disorders, including ulcerative colitis (UC), with encouraging results, inducing remission in steroid-resistant patients. However, we have experienced some complications during or after LCAP therapy. Common adverse effects include fever, chills, nausea, vomiting, and hypotension. One of the reasons for these adverse effects might be the use of nafamostat mesilate (NM) as an anticoagulant. In the present study, 75 patients with UC were divided into two groups, an NM group and a dalteparin sodium (DS) group. The clinical efficacy of these treatments, improvement after treatment, changes in leukocyte differential count, and adverse effects after LCAP therapy were then compared. The clinical efficacy, improvement after treatment, and changes in leukocyte classification were not significantly different between the two groups, while some adverse effects were observed in the NM group but not in the DS group. In conclusion, LCAP therapy is a useful therapy for patients with moderate to severe UC who fail to respond to glucocorticoid therapy, however, a safe anticoagulant should be used to avoid its related adverse effects.
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PMID:Leukocytapheresis for ulcerative colitis: a comparative study of anticoagulant (nafamostat mesilate vs. dalteparin sodium) for reducing clinical complications. 1655 37

Mesalazine is a first-line drug in pediatric inflammatory bowel disease, and is effective as primary treatment and maintenance therapy. It's usually well tolerated, but various side effects have been described. A 15-year-old female with ulcerative colitis developed polyuria, polydipsia, vomiting, and fatigue. She was receiving mesalazine (500 mg, thrice daily, p.o.) and prednisolone for 4 months. She was detected as acute tubular injury as she had dehydration, acidosis, hypostenuria, hematuria, proteinuria, low levels of potassium, uric acid and bicarbonate. These findings were attributed to interstitial nephritis as a side effect of mesalazine, however as renal biopsy was disapproved by the parents, it was not confirmed. After discontinuation of mesalazine her renal tubular functions improved. Potassium and phosphorus supplements were stopped after 7 months, although she had to continue bicarbonate supplementation. We conclude that regular renal screening is important in patients receiving 5-ASA therapy to prevent rare but serious complications, such as interstitial nephritis sometimes leading to chronic renal failure.
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PMID:Acute tubular injury associated with mesalazine therapy in an adolescent girl with inflammatory bowel disease. 1740 67

Background. A 61-year-old woman who had undergone an ileostomy closure 10 days previously presented to a tertiary medical center with abdominal pain, vomiting, diarrhea, dehydration, and oliguria. The patient had undergone a staged total proctocolectomy with ileal-pouch-anal anastomosis and a loop ileostomy 8 months previously to treat her steroid-refractory ulcerative colitis.Investigations. Physical examination, abdominal and pelvic CT scan, blood laboratory tests, pouch endoscopy, and fecal testing for Clostridium difficle toxins A and B.Diagnosis. Fulminant C. difficile-associated pouchitis and enteritis, which led to Psuedomonas aeruginosa septicemia, intravascular coagulopathy, acute renal failure, hemorrhagic ascites and respiratory failure and eventual death.Management. Intravenous hydration, aggressive therapy with oral and intravenous antibiotics, supportive care, hemodialysis, and intubation.
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PMID:Fulminant Clostridium difficile-associated pouchitis with a fatal outcome. 1965 2

Reversible posterior leukoencephalopathy syndrome (RPLS) is recently described disorder with typical radiological findings in the posterior regions of the cerebral hemisphere and cerebellum. Its clinical symptoms include headache, decreased alertness, mental abnormalities, such as confusion, diminished spontaneity of speech, and changed behavior ranging from drowsiness to stupor, seizures, vomiting and abnormalities of visual perception like cortical blindness. RPLS is caused by various heterogeneous factors, the commonest being hypertension, followed by non-hypertensive causes such as eclampsia, renal diseases and immunosuppressive therapy. We presented nine patients with RPLS who had primary diagnoses such as acute post-streptococcal glomerulonephritis, idiopathic hypertension, the performing of intravenous immunoglobulin for infection with crescentic glomerulonephritis, erythrocyte transfusion for severe iron deficiency, L: -asparaginase treatment for acute lymphoblastic leukemia and performing of granulocyte-colony stimulating factor for ulcerative colitis due to neutropenia. Early recognition of RPLS as complication during different diseases and therapy in childhood may facilitate precise diagnosis and appropriate treatment.
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PMID:Reversible posterior leukoencephalopathy syndrome in childhood: report of nine cases and review of the literature. 1980 87


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