Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 62-year-old man developed recurrent TIAs presenting as mild unconsciousness, dysarthria and weakness of the right upper extremity lasting for 15 to 20 minutes. He was found to have severe iron deficiency anemia (hemoglobin: 5.5-5.9g/dl; hematocrit: 18.4-19.5%) which insidiously developed through the chronic bleeding from the gastric ulcer. He had slight hypertension (184/86mmHg), but no orthostatic hypotension. DSA and MR angiography showed severe stenosis at the origin of the bilateral internal carotid arteries and of the left vertebral artery. There was also hypoplasia of the right vertebral artery. Blood circulation detected by 123I-IMP-SPECT was markedly decreased in the whole brain and in the right hemisphere of the cerebellum. TIA was, however, completely disappeared following to the recovery of anemia. The present case suggested that the presence of severe anemia accelerated the occurrence of hemodynamic TIA (regional cerebral anemic hypoxia), which is probably the consequence of the reduced oxygen-transporting capacity of the blood.
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PMID:[Hemodynamic TIA associated with severe anemia--a case report]. 799 47

The patient was a 72-year-old man who had a history of subtotal gastrectomy for gastric ulcer at age of 37 years. He had no familial history of hereditary disorders. In 1980 he noticed mild ataxic gait which exaggerated while he closed eyes. The symptoms increased gradually, and four years later he noticed hypoesthesia of his soles. In 1983 he was admitted to the National Center Hospital for Mental, Nervous and Muscular Disorders for the first time. Neurological examination revealed dysarthria, ataxic gait, disturbance of coordination to a slight degree, and muscle strength of the upper and lower limbs were in normal range. Mild hypoesthesia of pain and temperature sensation, and marked decrease of deep sensation and vibration of the lower extremities were demonstrated. Romberg sign was positive. EMG studies revealed low amplitude of action potential and normal motor nerve conduction velocity. Biopsy of the sural nerve showed marked decrease of both large and small myelinated fibers. In 1998 he was admitted second time for the further examination. Laboratory examination including routine blood examination, blood chemistry including CRP, TPHA, vitamin B1, B2, B12, A, E, K, hexosaminidase A in leucocyte were in normal range. CSF was normal. Genetic studies including SCA 1, 2, 3, 6, DRPLA, CMT1A, CMTX 1 were all negative. MCV of lower limbs was in normal range, though SCV was not evoked in the upper and lower limbs. MRI studies showed mild atrophy of the bilateral lobulus of the cerebellum which was not so much changed in the last 5 years. The clinical symptoms revealed dominant posterior column disturbance, ataxia and sensory neuropathy. These combination was not described in the previous literature, and this case may be a new variant of the spinocerebellar degeneration.
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PMID:[A case with posterior column ataxia associated with cerebellar ataxia and sensory neuropathy]. 1061 59

A 74-year-old man noted dysarthria and right hemiparesis. His history included a gastric ulcer 2 years previously, and he had gradually lost 10 kg over a 2-year period due to appetite loss. He daily consumed 120 mg of alcohol. Upon arrival, he had clear consciousness and stable vital signs. He was malnourished. Neurologic findings included a positive finding of Barre sign in the right hand and dysarthria. A venous blood gas analysis demonstrated the following: pH 7.059; PCO2, 21.5 mm Hg; PO2, 59.1 mm Hg; HCO(3-), 5.8 mmol/L; base excess, -22.7 mmol/L; lactate,17 mmol/L; and glucose, 4 mg/dL. After the administration of an infusion of thiamine and glucose, his abnormal neurologic findings subsided completely. Head magnetic resonance image (MRI; diffusion weighted image) disclosed 3 spotty, high-intensity signals in the brain. The main results of biochemical analyses of the blood collected on arrival were as follows: hemoglobin, 5.5 g/dL; glucose, 5 mg/dL; aspartate aminotransferase, 89 IU/L. He was admitted for further examination and was diagnosed as having alcoholic ketoacidosis with hypoglycemic encephalopathy and anemia due to colon cancer.
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PMID:A patient with clear consciousness even with a glucose level of 5 mg/dL (0.2 mmol/L). 2652 Nov 93