Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cantharidin toxicosis in horses has become an increasing problem in certain regions of the United States. Toxicosis occurs when horses ingest alfalfa hay or products that are contaminated with "blister" beetles. Clinical signs may vary from depression to severe shock and death, depending upon the amount of toxin ingested. The most frequently observed signs include varying degrees of abdominal pain, anorexia, depression, and signs suggestive of oral irritation. Many horses make frequent attempts to void urine. Less commonly observed signs include synchronous diaphragmatic flutter and erosions of the oral mucosal surfaces. Clinical laboratory abnormalities suggestive of cantharidin toxicosis include persistent hypocalcemia and hypomagnesemia, development of hypoproteinemia, microscopic hematuria, and mild azotemia with inappropriate urine specific gravity. Chemical analysis for cantharidin is accomplished by evaluation of urine or stomach contents. Treatment of cantharidin toxicosis is symptomatic, but must include removal of toxin source. Gastrointestinal protectants, laxative, intravenous fluids, analgesics, diuretics, calcium gluconate, and magnesium are all included in the treatment regimen. Early and vigorous therapy is imperative if it is to be successful. In horses that remain alive for several days, persistence of elevated heart and respiratory rates and increasing serum creatine kinase concentration are associated with a deteriorating condition. Prevention is aimed at timely harvesting of alfalfa hay. Hay fields should be inspected for the presence of beetle clusters before harvesting. Involved areas of the field should not be harvested.
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PMID:Cantharidin toxicosis in horses. 268 72

Ninety-four consecutive patients (60 men and 34 women; mean age 68.5 +/- 11.5 years) with acute myocardial infarction (MI) were investigated retrospectively, in order to evaluate the prevalence, clinical features, and short-term course of the atypical forms (symptoms other than chest pain). An atypical MI was found in 30 patients, with a prevalence of 32% (95% confidence limits 27-36%). It was most prevalent in women above sixty-five years old (P < 0.05). Abdominal pain, paroxysmal dyspnea, and pulmonary edema were the most frequent symptoms (33%, 17%, 13%, respectively). No differences were observed between typical and atypical MI in regard to risk factors (hypercholesterolemia, arterial hypertension, diabetes mellitus, cigarette smoking) and history of MI, cerebrovascular disease, peripheral vascular disease, or chronic lung disease. Significantly fewer patients with atypical MI had a history of angina pectoris (P < 0.05). No differences were observed in regard to previous medication, except for antiarrhythmic drugs, more often used by atypical patients (P < 0.05). Location and severity of MI (as judged by ECG and peak levels of creatine kinase in the serum) were similar in both subgroups, as were the complications (34% typical and 50% atypical) and death rate (12.5% and 16.7%, respectively). In conclusion, atypical MI is not less severe than typical. This emphasizes the need for a high suspicion index in many different clinical settings, but particularly (although not exclusively) in elderly females, in the presence of abdominal pain or otherwise unexplained paroxysmal dyspnea.
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PMID:Prevalence, clinical features, and acute course of atypical myocardial infarction. 828 84

A 66-year-old man was hospitalized for abdominal pain and diarrhea of more than 10 times a day. He had been under regular medication with prednisolone for rheumatoid arthritis. On admission, laboratory data and clinical examination indicated inflammation, dehydration, acute renal failure with a high level of serum musculogenic enzyme (creatine kinase), and ileus. Salmonella enteritidis was isolated from his fecal and blood samples. The patient died within 24 hours after admission, and autopsy showed hemorrhagic necrotic enteritis localized to the ileum. Enterocolitis due to Salmonella enteritidis, which is usually an acute self-limited gastrointestinal illness, may occasionally be a serious and lethal disease.
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PMID:Fatality due to severe Salmonella enteritis associated with acute renal failure and septicemia. 937 24

This retrospective descriptive study aims to characterise and compare the clinical manifestations, course and outcome of 16 Oriental patients with adult-onset Still's disease diagnosed in the last 4 years with published data based on Western populations and another Oriental (Japanese) series. Like the Japanese, we found a female preponderance, an older age at onset, and fewer patients with abdominal pain, myalgia, sore throat and serositis compared to the Western series. A longer delay in diagnosis occurred in patients lacking either arthritis or rash at presentation. Most patients had mild hyponatraemia and 2 patients had overt syndrome of inappropriate anti-diuretic hormone secretion. All patients showed a dissociation of elevated aldolase with normal to low creatine kinase levels. Over 50% relapsed within a year from diagnosis and needed slow-acting anti-rheumatic drugs as steroid-sparing agents. Two were given intravenous pulse cyclophosphamide therapy for progressive pneumonitis. Outcome was generally good with minimal functional impairment and no mortality.
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PMID:Adult-onset Still's disease in an oriental population: manifestations, course and outcome in 16 patients. 958 68

This cohort descriptive study summarizes the epidemiological, clinical, and laboratory characteristics of the Rift Valley fever (RVF) epidemic that occurred in Saudi Arabia from 26 August 2000 through 22 September 2001. A total of 886 cases were reported. Of 834 reported cases for which laboratory results were available, 81.9% were laboratory confirmed, of which 51.1% were positive for only RVF immunoglobulin M, 35.7% were positive for only RVF antigen, and 13.2% were positive for both. The mean age (+/- standard deviation) was 46.9+/-19.4 years, and the ratio of male to female patients was 4:1. Clinical and laboratory features included fever (92.6% of patients), nausea (59.4%), vomiting (52.6%), abdominal pain (38.0%), diarrhea (22.1%), jaundice (18.1%), neurological manifestations (17.1%), hemorrhagic manifestations (7.1%), vision loss or scotomas (1.5%), elevated liver enzyme levels (98%), elevated lactate dehydrogenase level (60.2%), thrombocytopenia (38.4%), leukopenia (39.7%), renal impairment or failure (27.8%), elevated creatine kinase level (27.3%), and severe anemia (15.1%). The mortality rate was 13.9%. Bleeding, neurological manifestations, and jaundice were independently associated with a high mortality rate. Patients with leukopenia had significantly a lower mortality rate than did those with a normal or high leukocyte count (2.3% vs. 27.9%; odds ratio, 0.09; 95% confidence interval, 0.01-0.63).
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PMID:Rift Valley fever epidemic in Saudi Arabia: epidemiological, clinical, and laboratory characteristics. 1515 93

Nonocclusive mesenteric ischemia (NOMI) is a rare abdominal pathology caused by mucosal hypoperfusion without actual obstruction to the mesenteric arteries. We present a case of NOMI after a cardiopulmonary bypass operation. The patient was a 79-year-old woman with a history of hypertension and diabetes mellitus. A coronary bypass operation was performed with stable hemodynamic conditions, and continuous venovenous hemodialysis was performed on the second postoperative day because of renal insufficiency. After 24 h of hemodialysis, the hematocrit level increased from 29.1% to 36.1%. The patient had some vague abdominal pain on the third postoperative day with abnormal laboratory values: leukocytes 17.10 x 10(3)/microl, creatine kinase 1085 U/l, glutamic-oxyloacetic transaminase 6188 U/l, and lactate dehydrogenase 8695 U/l. Selective angiography showed diffuse stenosis of the superior mesenteric artery (SMA) without any occlusive findings on the major branches; the patient was therefore diagnosed with NOMI. An infusion of urokinase and prostaglandin E1 was started; however, disseminated intravascular coagulopathy had developed and the patient died on the 21st postoperative day as a result of multiple organ failure. The autopsy demonstrated extensive necrosis and hemorrhage in the small intestine without any occlusive findings on the major branches of the SMA.
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PMID:Nonocclusive mesenteric ischemia after cardiopulmonary bypass. 1555 39

Chlorophenoxy herbicides are used widely for the control of broad-leaved weeds. They exhibit a variety of mechanisms of toxicity including dose-dependent cell membrane damage, uncoupling of oxidative phosphorylation and disruption of acetylcoenzyme A metabolism. Following ingestion, vomiting, abdominal pain, diarrhoea and, occasionally, gastrointestinal haemorrhage are early effects. Hypotension, which is common, is due predominantly to intravascular volume loss, although vasodilation and direct myocardial toxicity may also contribute. Coma, hypertonia, hyperreflexia, ataxia, nystagmus, miosis, hallucinations, convulsions, fasciculation and paralysis may then ensue. Hypoventilation is commonly secondary to CNS depression, but respiratory muscle weakness is a factor in the development of respiratory failure in some patients. Myopathic symptoms including limb muscle weakness, loss of tendon reflexes, myotonia and increased creatine kinase activity have been observed. Metabolic acidosis, rhabdomyolysis, renal failure, increased aminotransferase activities, pyrexia and hyperventilation have been reported. Substantial dermal exposure to 2,4-dichlorophenoxy acetic acid (2,4-D) has led occasionally to systemic features including mild gastrointestinal irritation and progressive mixed sensorimotor peripheral neuropathy. Mild, transient gastrointestinal and peripheral neuromuscular symptoms have occurred after occupational inhalation exposure. In addition to supportive care, urine alkalinization with high-flow urine output will enhance herbicide elimination and should be considered in all seriously poisoned patients. Haemodialysis produces similar herbicide clearances to urine alkalinization without the need for urine pH manipulation and the administration of substantial amounts of intravenous fluid in an already compromised patient.
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PMID:Poisoning due to chlorophenoxy herbicides. 1557 61

An insidious onset of unexplained fever, weight loss, skin lesions, abdominal pain, and musculoskeletal pain should suggest the diagnosis of polyarteritis nodosa (PAN). However, familial Mediterranean fever (FMF) with protracted febrile myalgia (PFM) should be kept in mind in the differential diagnosis. In this report, 6 cases of PFM mimicking PAN are described. Patients presented with severe muscle and abdominal pain lasting longer than 4 weeks. Their common medical history included recurrent febrile abdominal pain or arthritis. Physical examination revealed hypertension together with severe muscle tenderness. Laboratory examination revealed high acute phase reactants, negative p-ANCA, normal creatine kinase, and complement levels. Duplex abdominal ultrasonography was normal. Four of 6 patients were hospitalized with initial diagnoses of PAN. Renal and mesenteric angiography performed in 1 patient was normal. Steroid therapy controlled all the severe symptoms including hypertension in all of the cases.FMF with PFM is important in the differential diagnosis of patients with suspected vasculitis especially when myalgia is present. Hypertension may be present as a result of sympathetic discharge because of severe myalgia. Because PFM rapidly responds to a short course of corticosteroids, a rapid diagnosis of PFM in FMF patients can reduce unnecessary workup and decrease the time patients have to suffer.
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PMID:Protracted febrile myalgia mimicking polyarteritis nodosa. 1863 21

A 14-year-old boy presented with fatigue and abdominal pain. Laboratory tests revealed a primary hypothyroidism with circulating auto-antibodies against thyroid peroxidase (TPO), anaemia and an elevated level of creatine kinase (CK). A diagnosis of auto-immune hypothyroidism with associated anaemia and myopathy was made. Thyroid hormone replacement therapy was started. However, six months later, he still complained of fatigue. He had unexpectedly varying thyroid function tests and the anaemia and the elevated level of CK persisted. Analysis of the other hormonal axes demonstrated a secondary adrenal insufficiency which was treated with hydrocortisone suppletion therapy. If a patient suffering from hypothyroidism does not respond appropriately to therapy or even deteriorates, adrenal insufficiency should always be considered. Patients with one type of auto-immune endocrinopathy have a greater risk at developing other types of auto-immune endocrinopathies.
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PMID:[Clinical reasoning and decision making in clinical practice: a boy with fatigue and abdominal pain]. 1978 3

Mutations in the dystrophin gene without disruption of the reading frame often lead to Becker muscular dystrophy, but a genotype/phenotype correlation is difficult to establish. Amino acid substitutions may disrupt binding capacities of dystrophin and have a major impact on the functionality of this protein. We have identified two brothers (ages 8 and 10 years) with very mild proximal weakness, recurrent abdominal pain, and moderately elevated serum creatine kinase levels. Gene sequencing revealed a novel mutation in exon 11 of the dystrophin gene (c.1280T>C) leading to a L427P amino acid substitution in repeat 1 of the central rod domain. Immunostaining of skeletal muscle showed weak staining of the dystrophin region encoded by exons 7 and 8 corresponding to the end of the actin-binding domain 1 and the N-terminal part of hinge 1. Spectrofluorescence and circular dichroism analysis of the domain repeat 1-2 (R1-2) revealed partial misfolding of the L427P mutated protein as well as a reduced refolding rate after denaturation. Based on computational homology models of the wild-type and mutated R1-2, a molecular dynamics study showed an alteration in the flexibility of the structure, which also strongly affects the conformational space available in the N-terminal region of the fragment. Our results suggest that this missense mutation hinders the dynamic properties of the entire N-terminal region of dystrophin.
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PMID:Novel mutation in spectrin-like repeat 1 of dystrophin central domain causes protein misfolding and mild Becker muscular dystrophy. 2245 24


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