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)

The purpose of this paper is to describe 2 siblings who had a generalized neurological disease which presented as intestinal pseudoobstruction. The siblings had 40-year histories of abdominal pain, distention, and vomiting as well as gait ataxia, small, irregular, poorly reactive pupils, dysarthria, absent deep tendon reflexes, and impaired vibratory and position senses. Compared with age-matched controls, they had inappropriate blood pressure responses to phenylephrine, the Valsalva maneuver, and upright posture, lack of sweating on warming, and pupillary denervation hypersensitivity. Radiographs revealed hyperactive, nonpropulsive contractions of a dilated esophagus and small intestine and extensive colonic diverticulosis. Esophageal manometry recorded repetitive, spontaneous, nonperistaltic waves and positive Mechyolyl tests. Postmortem examinations showed degeneration of the myenteric plexuses of the esophagus, small intestine, and colon of both patients. Myenteric plexus neurons were significantly reduced in number compared with 7 controls. About one-third of the siblings' neurons contained round, eosinophilic intranuclear inclusions, which, by histochemistry, were composed of protein by lacked RNA, DNA, carbohydrate, and fat. By electron microscopy the inclusions consisted of an irregular array of nonviral, nonmembrane-bounded filaments. Neurons and glial cells of the brain, spinal cord, dorsal root, and celiac plexus ganglia contained identical intranuclear inclusions. Intestinal smooth muscle was normal. These 2 siblings represent a unique disease in which degeneration of the myenteric plexus resulted in hyperactive but uncoordinated smooth muscle activity and the clinical syndrome of intestinal pseudoobstruction, the presenting manifestation of their neurological disease.
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PMID:A familial neuronal disease presenting as intestinal pseudoobstruction. 21 42

Clinical observations on ciguatera were collected between 1964 and 1977 on 3,009 patients from several South Pacific island groups. Patients generally presented with neurologic symptoms such as parasthesia, vertigo, and ataxia, in addition to gastrointestinal symptoms such as diarrhea, abdominal pain, nausea, and vomiting. Patients with this illness usually became symptomatic less than 24 hours after ingestion of the fish and most patients (76.8%) developed symptoms in less than 12 hours. Significant differences in certain symptoms were noted between Melanesian and Polynesian ethnic groups, suggesting a susceptibility difference, or a difference in the nature of the toxin found in different areas of the Pacific. Being poisoned multiple times appeared to result in a clinically more severe illness than disease observed in patients experiencing ciguatera for the first time.
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PMID:Clinical observations on 3,009 cases of ciguatera (fish poisoning) in the South Pacific. 57 66

Bajiaolian (Dysosma pleianthum), one species in the Mayapple family, has been widely used as a general remedy and for the treatment of snake bite, weakness, condyloma accuminata, lymphadenopathy and tumours in China for thousands of years. However, the textbooks of traditional Chinese medicine mention little about the toxicity of Bajiaolian. Within 1 year, the authors saw five people who manifested nausea, vomiting, diarrhoea, abdominal pain, thrombocytopenia, leucopenia, abnormal liver function tests, sensory ataxia, altered consciousness and persistant peripheral tingling or numbness after drinking infusions made with Bajiaolian. The herb was recommended by either traditional Chinese medical doctors or herbal pharmacies for postpartum recovery and treatment of a neck mass, hepatoma, lumbago and dysmenorrhoea. Podophyllotoxin is one of the main ingredients of the Bajiaolian root. The clinical manifestations observed in our patients were consistent with podophyllum intoxication. Podophyllotoxin intoxication usually results from the accidental ingestion or topical application of podophyllum resin. However, these cases of Bajiaolian intoxication were iatrogenic and results from 'therapeutic doses' of Bajiaolian cited in the textbooks of traditional Chinese medicine.
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PMID:Podophyllotoxin intoxication: toxic effect of Bajiaolian in herbal therapeutics. 136 Nov 36

A 23 year old male developed abdominal pain, diarrhoea, and vomiting several hours after poisoning with acute triphenyltin intoxication in a suicide attempt. Severe ataxia, dysmetria, nystagmus, and blurring of vision soon supervened. Disturbance of consciousness and confusion developed 12 days later and lasted for two months. A delayed sensorimotor polyneuropathy was shown by electrophysiological studies to be due to axonal degeneration and demyelination. The neuropathy rapidly recovered after consciousness was regained.
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PMID:Acute triphenyltin intoxication: a case report. 750 Jan 18

The currently recognized toxic effects of quinine in humans are identified and the problems of management of overdosage of quinine are discussed. Quinine, available therapeutically as sulphate or hydrochloride salts, also is widely used in tonic water, and there are several case reports of allergic reactions to the drug when a patient has consumed the drug in this way. Another unintentional source of poisoning is its use as an adulterant in heroin for "street" use. This appears to be a problem in the US. Quinine, termed a "general protoplasmic poison" is toxic to many bacteria, yeasts, and trypanosomes, as well as to malarial plasmodia. Quinine has local anesthetic action but also is an irritant. The irritant effects may be responsible in part for the nausea associated with its clinical use. In addition it has a mild antipyretic effect. Several features are common to both an acute single overdose in self-poisoning and accumulation of quinine during therapy for malaria: together they are termed cinchonism. Auditory symptoms, gastrointestinal disturbances, vasodilatation, sweating, and headache occur with moderately elevated plasma quinine concentration. As these rise, increasingly severe visual disturbances and then cardiac and neurologic features occur. Mild nausea may be the only symptom, but with large overdoses profuse vomiting, abdominal pain, and diarrhea may occur. These result from a combination of the local irritant effect of quinine on the gut and the central effects of quinine on the chemoreceptor trigger zone. Vasodilatation and sweating are well recognized, and tinnitus is common. Visual symptoms usually are delayed, and blindness may not be discovered for a day or more. Aspirin-sensitive patients, and others, may develop angioedema by nonimmunological mechanisms in response to drugs, and quinine has been reported to produce pseudo-allergic reactions in aspirin-sensitive patients. Quinine also can cause drug-induced thrombocytopenia and purpura. In patients suffering with malaria due to "Plasmodium falciparum," anemia and acute intravascular hemolysis with renal failure are recognized complications. There appears to be little evidence in the literature in support of the folk tradition of quinine as an inducer of abortion. Quinine is known to cause deterioration in patients with myasthenia gravis and erythema multiforme, to stimulate insulin release in patients receiving treatment for falicparum malaria, and to be responsible at times for ataxia following moderate overdosage. Clinically, quinine poisoning is observed in 3 situations: self-poisoning; accidentally; and following use of quinine in excessive doses in the hope of achieving abortion. Treatment courses are reviewed.
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PMID:Quinine toxicity. 354 70

A 12-year-old Standard-bred mare and a 21-year-old Quarter Horse gelding were treated for signs of abdominal pain and sweating. The mare also had muscle fasciculations, azotemia, and ataxia, and was euthanatized after signs of pain became refractory to analgesics. The gelding died when ventricular tachycardia developed during general anesthesia for exploratory celiotomy. Adrenal pheochromocytomas (bilateral in the mare), associated with retroperitoneal and intra-abdominal hemorrhage, were found on postmortem examination. Pheochromocytoma should be considered in older horses with signs of abdominal pain and sweating. Further consideration of pheochromocytoma should be afforded in older horses in which muscle fasciculations, ataxia, azotemia, and intraperitoneal hemorrhage are recognized. Identification, by per rectum palpation, of retroperitoneal swelling in the dorsal aspect of the abdomen also should alert the diagnostician to the possibility of a ruptured pheochromocytoma.
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PMID:Pheochromocytoma in two horses. 775 37

An 8-year-old 38-kg spayed female Golden Retriever was admitted for vomiting, signs of abdominal pain on palpation, ataxia, anorexia, and generalized weakness of 2 days' duration. Ten hours prior to onset of clinical signs, the dog was found standing in and drinking from large pools of an accidentally spilled herbicide that contained an octanoic acid ester of bromoxynil (3,5-dibromo-4-hydroxybenzonitrile) and an isooctyl ester of (2-methyl-4-chloro) phenoxyacetic acid (MCPA). Appendicular muscles were firm on palpation and persistent muscle contraction (myotonia > 1 minute duration) was found on muscle percussion, using a reflex hammer. Electrical activity indicative of myotonia was identified on electromyographic evaluation. With supportive treatment, the dog eventually recovered from suspected MCPA toxicosis. Although rare, MCPA toxicosis should be considered as a cause of acquired myotonia in dogs.
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PMID:Suspected herbicide toxicosis in a dog. 896 Jan 92

The disease is named after George H. Whipple who, in 1907, was the first to describe an intestinal "lipodystrophy". Although Whipple's disease is generally recognized as a multisystem chronic granulomatous disease, primarily involving the digestive system, it can also appear as a primary neurological disorder in rare cases. Most often it is manifested with loss of weight, diarrhea, malabsorption, abdominal pain, lymphadenopathy, cardiopathy, hyperpigmentation and hypotension. The presence of periodic acid-Schiff (PAS)-positive macrophages in biopsy specimens (not only jejunal) and demonstration of "Whipple's bacilli" visible by electron microscopy, are diagnostic signs of active Whipple's disease. Whipple's disease confined to the CNS is rare. It is rarely found in the differential diagnosis of patients with progressive neurological deterioration. The most common neurological picture includes progressive dementia, external ophalmoplegia, myoclonus, seizures, ataxia, hypothalamic dysfunction (sleep disorders, hyperphagia, polydipsia) and meningitis. Oculofacial-skeletal myorhythmia as a movement disorder, associated with Whipple's disease, is reported. Fulminant course of cerebral Whipple's disease is unusual and unfavourable. The confusing and nonspecific clinical appearance is typical for primary CNS involvement. It has recently been suggested that CNS involvement occurs in all cases, although only 10-20% of patients may show it. The CNS is the most common site of disease relapse. The CT scans and MRI of the brain are often normal, but may show cortical/subcortical atrophy, hydrocephalus, focal or intracerebral mass lesions. The cerebrospinal fluid can sometimes contain PAS-positive macrophages. Brain biopsy is suggested as a diagnostic method in cases of high suspicion of CNS Whipple's disease. However, the lesions are frequently inaccessible and false negative. Without extended antibiotic therapy, the course of Whipple's disease is lethal. Now, the prognosis is good, although the optimal antimicrobial regimen is not clearly established. Initial parenteral therapy (tetracycline, penicilline, streptomycine, chloramphenicol, ampicilline) and peroral long-term treatment with trimetoprime-sulphametoxasole, are recommended. As CNS relapse of Whipple's disease may occur after several years, long-term treatment should include antibiotics that are able to cross the blood-brain barrier. The CNS relapse, in contrast to the systemic ones, is resistant to the treatment. Appropriate therapy instituted earlier in the course of the disease is associated with a better neurological outcome. Early recognition can be critical in Whipple's disease because of irreversible neurological sequelae seen later in the course of this potentially treatable condition. In cases with high clinical suspicion in which Whipple's disease cannot be diagnosed with procedures such as jejunal biopsy, antibiotic therapy is recommended. Recovery of an established neurological deficit may rarely occur. Longterm follow-up studies would help to identify the optimal antibiotic regimen and duration of treatment.
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PMID:[Neurologic disorders in Whipple's disease]. 910 28

We studied 13 patients with lipoamide dehydrogenase (LAD) deficiency, originating from seven Ashkenazi Jewish families. Their disease was characterized by recurrent attacks of vomiting, abdominal pain, and encephalopathy accompanied by elevated liver transaminases, prolonged prothrombin time, and occasionally associated with lactic and ketoacidemia or with myoglobinuria. Two patients who presented neonatally suffered from residual neurological damage with attention deficit hyperactive disorder, mild ataxia, motor incoordination, muscle hypotonia, and weakness. Nine patients who presented in early childhood or later suffered from exertional fatigue between decompensation episodes but were otherwise asymptomatic. Two patients died because of intractable metabolic acidosis and multi-organ failure. In all patients LAD activity was reduced to 8 to 21% of the control in muscle or lymphocytes. In four patients LAD protein in muscle was reduced to 20 to 60% of the control. Direct sequencing of the cDNA of the LAD gene showed that 12 of the 14 mutated alleles carried the G229C mutation and two carried an insertion mutation 105insA (Y35X). The patients who presented neonatally and had more severe sequelae were compound heterozygotes for the two mutations; patients who presented in early childhood or later were homozygous for the G229C mutation. Using an allele-specific oligonucleotide hybridization technique, nine heterozygotes for the G229C mutation were identified among 845 anonymous individuals of Ashkenazi Jewish origin disclosing a carrier rate of 1:94. Because of the significant morbidity associated with the disease, screening for the G229C mutation among Ashkenazi Jewish couples should be considered.
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PMID:Molecular basis of lipoamide dehydrogenase deficiency in Ashkenazi Jews. 993 85

The ASPCA National Animal Poison Center managed 29 cases of ingestion of commercially available macadamia nuts in dogs during a 5-y period. Clinical signs included, from most to least, weakness, depression, vomiting, ataxia, tremor, hyperthermia, abdominal pain, lameness, stiffness, recumbency, and pale mucous membranes. The onset of clinical signs was reported as < 12 h in 79% of the cases. The duration of clinical signs for the majority of cases was < 24 h. The amount of macadamia nuts ingested was estimated in 72% of the calls with a mean of 11.7 g/kg bw. In an attempt to reproduce the syndrome, 4 dogs were gavaged with 20 g macadamia nuts/kg bw in a water slurry. The experimentally dosed dogs developed weakness, manifested by the inability to rise 12 h after dosing, mild central nervous system depression, vomiting, and hyperthermia, with rectal temperatures up to 40.5 C. Mild elevations in serum triglycerides and serum alkaline phosphatase were detected. Lipase values peaked sharply at 24 h and returned to normal by 48 h after dosing. Other serum biochemical and electrolyte determinations were unremarkable. Serum lipoprotein electrophoresis determinations were unchanged from baseline. The mechanism of the syndrome is unknown. All field and experimental dogs recovered uneventfully within 1 to 2 d whether treated by a veterinarian or not.
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PMID:Weakness, tremors, and depression associated with macadamia nuts in dogs. 1067 81


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