Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008031 (chest pain)
 17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 63-year-old woman suddenly began to suffer from left chest pain. She gradually became unable to walk and was admitted to the emergency room at another hospital. When she became paraplegic in spite of steroid therapy, she was admitted to our hospital. Her affliction was diagnosed as anterior spinal artery syndrome because of flaccid paraplegia and dissociated sensory loss below the Th4 dermatome. Hematological study indicated a compensated DIC and hepatic enzyme abnormality, while the CSF examinations showed an elevation of protein and positive myelin basic protein (MBP) elevation. The initial MRI taken in the acute stage showed no abnormal signals on T1-weighted (T1) and Gd-enhanced images. The sagittal T2-weighted image (T2) revealed central high intensity (HI) with longitudinal extension from Th2 through the Th11 vertebral level. On axial T2, HI was located on the gray matter at the Th3 and Th4 vertebral level, the ventral two-thirds at the Th8 vertebral level, the central ventral side at the Th9 and Th10 vertebral level, and the entire cross section at the Th12 and L1. A follow-up MRI examination showed that the range of HI on the sagittal T2 had been reduced to 5 segments from Th6 through Th10 vertebral level. The T2 HI lesion on the axial aspect had become reduced so as to localize on the left ventral side at the Th8 vertebral level and on the central ventral side at Th9 and Th10.
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PMID:[Serial MRI study on a case of anterior spinal artery syndrome]. 1007 31

Despite established exposure limits and safety standards, and the availability of carbon monoxide (CO) alarms, each year 50,000 people in the United States visit emergency departments for CO poisoning. Carbon monoxide poisoning can occur from brief exposures to high levels of CO, or from longer exposures to lower levels. Common symptoms include headaches, nausea and vomiting, dizziness, general malaise, and altered mental status. Some patients may have chest pain, shortness of breath and myocardial ischemia, and may require mechanical ventilation and treatment of shock. Individuals poisoned by CO often go on to develop neurological problems, including cognitive sequelae, anxiety and depression, persistent headaches, dizziness, sleep problems, motor weakness, vestibular and balance problems, gaze abnormalities, peripheral neuropathies, hearing loss, tinnitus and Parkinsonian-like syndrome. While breathing oxygen hastens the removal of carboxyhemoglobin (COHb), hyperbaric oxygen (HBO2) hastens COHb elimination and favorably modulates inflammatory processes instigated by CO poisoning, an effect not observed with breathing normobaric oxygen. Hyperbaric oxygen improves mitochondrial function, inhibits lipid peroxidation transiently, impairs leukocyte adhesion to injured microvasculature, and reduces brain inflammation caused by the CO-induced adduct formation of myelin basic protein. Based upon three supportive randomized clinical trials in humans and considerable evidence from animal studies, HBO2 should be considered for all cases of acute symptomatic CO poisoning. Hyperbaric oxygen is indicated for CO poisoning complicated by cyanide poisoning, often concomitantly with smoke inhalation.
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PMID:Hyperbaric oxygen therapy for carbon monoxide poisoning. 2510 87

Despite established exposure limits and safety standards as well as the availability of carbon monoxide (CO) alarms, each year 50,000 people in the United States visit emergency departments for CO poisoning. Carbon monoxide poisoning can occur from brief exposures to high levels of CO or from longer exposures to lower levels. Common symptoms can include headaches, nausea and vomiting, dizziness, general malaise, and altered mental status. Some patients may have chest pain, shortness of breath, and myocardial ischemia, and may require mechanical ventilation and treatment of shock. Individuals poisoned by CO often develop brain injury manifested by neurological problems, including cognitive sequelae, anxiety and depression, persistent headaches, dizziness, sleep problems, motor weakness, vestibular and balance problems, gaze abnormalities, peripheral neuropathies, hearing loss, tinnitus, Parkinsonian-like syndrome, and other problems. In addition, some will have cardiac issues or other ailments. While breathing oxygen hastens the removal of carboxyhemoglobin (COHb), hyperbaric oxygen (HBO2) hastens COHb elimination and favorably modulates inflammatory processes instigated by CO poisoning, an effect not observed with breathing normobaric oxygen. Hyperbaric oxygen improves mitochondrial function, inhibits lipid peroxidation transiently, impairs leukocyte adhesion to injured microvasculature, and reduces brain inflammation caused by the CO-induced adduct formation of myelin basic protein. Based upon three supportive randomized clinical trials in humans and considerable evidence from animal studies, HBO2 should be considered for all cases of acute symptomatic CO poisoning. Hyperbaric oxygen is indicated for CO poisoning complicated by cyanide poisoning, often concomitantly with smoke inhalation.
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PMID:Carbon monoxide poisoning. 3217 57