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)

Motility-like dyspepsia, a clinical subgroup of functional dyspepsia, refers to the cluster of symptoms which suggests an underlying motility disturbance of the upper gut. Characteristic symptoms, in addition to upper abdominal pain or discomfort, are nausea, vomiting, early satiety, anorexia, postprandial abdominal bloating and excessive repetitive postprandial belching. Patients with concomitant symptoms of irritable bowel syndrome are currently excluded from this clinical entity. Delayed gastric emptying of solids and/or liquids, postprandial antral hypomotility and antroduodenal incoordination, gastric myoelectrical arrhythmias and dysfunction of visceral afferents are the major alterations in upper gut sensorimotor activity which have been described. An empirical trial of medical therapy is warranted if there are no "alarm" symptoms at presentation. If symptoms are not relieved after 2-4 weeks, then investigations of the upper gastrointestinal tract, preferably by endoscopy, to exclude the presence of organic disease, is advisable. Management approaches are then reassurance, dietary manipulations and attention to psychosocial aspects. Prokinetic agents appear to be useful as short-term medical therapy in some patients, but optimum long-term treatment strategies, including the use of medications which may improve a diminished tolerance to gut distension, are not established.
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PMID:Motility-like dyspepsia. Current concepts in pathogenesis, investigation and management. 144 83

The frequency and severity of physical and emotional menstrual symptoms were investigated with a cross-sectional study of 502 women not seeking treatment for menstrual symptoms. The most frequent symptoms were abdominal bloating, backache, headache, constipation, low abdominal pain, fatigue and symptoms related to depression. Some symptoms increased during the late luteal phase, and others were related to the women's life-style. Lack of schooling and living in rural areas were associated with headache, backache, sadness, insecurity, restlessness and weakness. Women from urban areas with more schooling had more breast tenderness, abdominal pain, irritability, depression, aggressiveness and increased sexual desire. Younger women had increased appetite, lack of concentration, insecurity, desire to be alone, weakness and dissatisfaction with their looks. Heavier women had more leg cramps, swollen feet, lack of coordination and polydipsia. Menstrual symptoms seem to be determined by the interplay of the menstrual cycle with biologic factors and life-style.
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PMID:Association of physical and emotional symptoms with the menstrual cycle and life-style. 833 24

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

Fatal meningoencephalitis caused by equine herpesvirus-1 (EHV-1) was diagnosed in a reticulated giraffe (Giraffa camelopardalis reticulate). The giraffe died following a history of stumbling, incoordination, and abdominal pain. Gross examination of the brain revealed asymmetric edema and red-brown discoloration, predominantly within the telencephalon. Microscopically, there was perivascular lymphohistiocytic cuffing, multifocal gliosis, and neuronal necrosis in the cerebrum. Necrotic neurons contained acidophilic intranuclear inclusions. EHV-1 was isolated from the brain of the giraffe, and polymerase chain reaction was positive on sections of the brain. Immunohistochemistry using an EHV-1-specific antibody identified positive staining in neurons, astrocytes, and endothelial cells. The giraffe had been housed with a group of zebras that were serologically positive for EHV-1 and suspected as the source of infection. This raises concerns for cross-species transmission of EHV-1 when housing equids together with other species in zoologic collections.
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PMID:Fatal herpesvirus encephalitis in a reticulated giraffe (Giraffa camelopardalis reticulata). 1696 58