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 31-year-old male had a sudden onset of painful swelling in the penile root region. He then developed necrosis of the penis and further a progressive, chemotherapy-resistant ulcer which involved the perineal region also. Histologically there was evidence of neither malignancy nor specific inflammation, but there were granulomatous tissues with cellular infiltration and scattered vascular necrosis. Examination of the nose suggested gangrenous rhinitis with perforation of the nasal septum. X-ray examination revealed that the nasal septum and conchae had disappeared. Chest roentgenogram also revealed increased hilar shadows in both fields of the chest. Routine laboratory examinations showed slight albuminuria and a normal BUN level. Positive findings included leucocytosis, hyper-gamma-globulinemia, accelerated ESR, positive RA and CRP tests. The patient's death was caused by bleeding from gastric ulcer and pulmonary failure.
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PMID:A case of Wegener's granulomatosis with necrosis of the penis. 98 29

Cimetidine is a histamine H2-receptor antagonist. Widely it is prescribed, and then various side effects have been increasingly recognized. Acute renal failure as a result of acute interstitial nephritis is one of the most important adverse effect. We report a case of biopsy-proven acute interstitial nephritis following cimetidine therapy. Farther more, we review other reported cases of cimetidine-induced acute interstitial nephritis, and discuss the clinical features and a role of immunological mechanisms of these cimetidine-induced disorders. A 52-year-old woman was admitted because of fever and protenuria. A month before admission, she developed gastric ulcer and was given cimetidine 600mg orally a day by a near physician. Laboratory data on admission included the following: white blood cell count, 14700/microliters; eosinophils, 6%; BUN, 50.7mg/dl; Cr, 7.6mg/dl; CRP, 34.0mg/dl. All drugs were discontinued because we suspected drug-induced acute renal failure, especially by cimetidine. Renal biopsy performed on day 3 showed interstitial nephritis with lymphocyte infiltration which was composed mainly of T cell. T4/T8 ratio was determined to be 1. There was neither predominance of helper nor cytotoxic cells in T cell subpopulation. We reviewed 22 cases reported and discussed the features of cimetidine-induced interstitial nephritis. The most important thing is to monitor renal function periodically with the suspicion of this disorder. On the detection of abnormality of laboratory data, cimetidine should be discontinued.
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PMID:[A case of acute interstitial nephritis and nonoliguria acute renal failure induced by cimetidine]. 129 77

To test the possible participation of activated leukocytes in the pathogenesis of gastric ulcer, plasma levels of polymorphonuclear leukocyte-elastase-alpha 1-proteinase inhibitor complex (PMN-EC), a discerning indicator for the activation of leukocytes, were determined in patients with gastric ulcer. Plasma levels of PMN-EC in patients with gastric ulcer (185.2 +/- 21.6 micrograms/l, mean +/- S.E.M.) were significantly higher than those in normal healthy subjects (67.6 +/- 4.4 micrograms/l, p less than 0.01). On the other hand, plasma levels of C-reactive protein and sialic acid increased in only 17.8% and 7.1% of patients with gastric ulcer, respectively. No significant correlation was observed between PMN-EC and the plasma levels of CRP or sialic acid. Plasma levels of PMN-EC decreased with the healing of the ulcerative lesion as judged by gastro-endoscopic observation. These findings suggested that activation of leukocytes might deeply be correlated with the pathologic mechanism of gastric ulceration and the measurement of PMN-EC might be useful for monitoring the patients with gastric ulcer.
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PMID:[Plasma concentration of polymorphonuclear leukocyte elastase-alpha 1-proteinase inhibitor complex in patients with gastric ulcer]. 223 51

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