Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 65-year-old man visited our hospital with complaints of tingling sensation in the distal parts of his extremities and dysuria, which first appeared 2 months before admission. He had no abnormal findings on physical examination. Neurological examination revealed sensory impairment of glove and stocking type, mild motor weakness and muscular atrophy in the proximal parts of arms and legs, and absent tendon reflexes in knees and ankles. Fasciculation was observed on his shoulders and upper extremities, and myokymia on the abdominal wall and bilateral calves. He had hyponatremia, which was proved to be caused by SIADH. Anti-acetylcholine receptor antibody, anti-GM1 ganglioside antibody and anti-galactocerebroside antibody were detected in the serum. Chest X-ray showed mass shadows in the mediastinum, which were confirmed as malignant thymoma by needle biopsy. Orthostatic hypotension, neurogenic bladder and anhidrosis were observed by the autonomic function tests. Lesions responsible for orthostatic hypotension and SIADH were suspected in the afferent fibers from baroreceptors, since an reactive increase of plasma arginine vasopressin to orthostatic hypotension was blunted and reflex hypertension in the cold pressor test was well-preserved, while overshoot in Valsalva's maneuver was absent. It is important that afferent baroreceptor dysfunction may be associated with paraneoplastic neurological syndrome, since lesions in acute autonomic neuropathy are usually in the efferent fibers.
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PMID:[A case of paraneoplastic autonomic and sensorimotor neuropathy with dysfunction in the afferent limb of baroreflex arc]. 840 86

We report a 54-year-old man with X-linked bulbospinal muscular atrophy (BSMA) with bilateral abductor vocal cord paralysis. He noticed distal weakness in the lower limbs at age 20. In the following 18 years the weakness and atrophy of his leg muscles increased gradually. He has complained of stridors during respiratory tract infection and snored heavily during sleep since his age of 50. He was admitted to our hospital for the progressive stridors during meals. His two brothers were said to have similar complaints. Physical examination showed gynecomastia, hypertension and inspiratory stridor. Neurologic examination revealed distal muscular atrophy in his four extremities, especially more severe in bilateral lower limbs. Deep tendon reflexes were absent in all extremities. His tongue was slightly atrophic with fasciculation. Neurological diagnosis was made by family history, neurological findings, electromyography and a CAG repeat expansion in the androgen receptor gene. Lungs and diaphragm were normal on the chest radiograph. Cranial MRI including brain stem was also normal. Direct laryngoscopy showed a complete paralysis of both vocal cords in paramedian position. Tracheostomy was done right away; his respiratory distress showed prompt improvement after the tracheostomy. No previous report of bilateral vocal cord paralysis in BSMA has been found. Life expectancy in BSMA patients with vocal cord paralysis may be shortened because of respiratory distress or asphyxia. Of clinical importance is a careful assessment of vocal cord function in BSMA patients.
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PMID:[A case of X-linked bulbospinal muscular atrophy with bilateral abductor vocal cord paralysis]. 890 90

We often have cases of insecticide poisoning where the patient is unconscious and the causal substances are unknown. We report an 83-year-old unconscious man who had apparently ingested several agricultural chemicals, possibly organophosphate or carbamate. According to his family, there were three kinds of containers of agricultural chemicals with their caps opened around him. When he was transferred to our hospital, he presented hypertension, hypersalivation, and muscle fasciculation. His pupils were markedly miotic. In order to identify the substances ingested we used a gas chromatographymass spectrometer (GCMS) using his gastric content. Within 30 minutes we were able to identify the causal substance as methomyl, one of the popular carbamates, thereby eliminating the need to use pralidoxime (PAM). GCMS makes it possible to identify unknown substances quickly and accurately and is therefore extremely useful in deciding the appropriate treatment.
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PMID:[A case of carbamate poisoning in which GCMS was useful to identify causal substance and to decide the appropriate treatment]. 1180 2

Epidemiological studies suggest that chronic adult diseases, such as type 2 diabetes and hypertension, can be programmed during fetal and early postnatal life. The nervous system regions governing vegetative functions and the hypothalamic-pituitary-adrenal axis are particularly sensitive to the perinatal nutritional status. Despite recent reports demonstrating that the activity of the sympathoadrenal system can be altered by early life events, the effects of maternal nutrient restriction on the adrenal medulla remain unknown. Using a rat model of maternal perinatal 50% food restriction (FR50) from the second week of gestation until weaning, immunohistochemical experiments revealed alterations in chromaffin cell aggregation and in nerve fiber fasciculation in the adrenal medulla of FR50 pups. These morphological changes were associated with enhanced circulating levels of catecholamines after decapitation (epinephrine by 55% and norepinephrine by 41%). Using macroarrays, we identified several genes whose expression was affected by maternal nutrient restriction. Semiquantitative RT-PCR confirmed the overexpression of four genes involved in neuroendocrine differentiation and neuronal plasticity (chromogranin B, growth-associated protein 43, neurofilament 3, and Slit2) in the adrenal glands of FR50 rats. Using in situ hybridization, we showed that these genes are solely expressed in the adrenal medulla. Together, our results suggest that perinatal maternal undernutrition markedly alters the differentiation of the adrenal medulla during postnatal life, resulting in enhanced activity of chromaffin cells at weaning. These alterations may persist in adulthood and participate to the programming of chronic adult diseases.
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PMID:Maternal perinatal undernutrition alters neuronal and neuroendocrine differentiation in the rat adrenal medulla at weaning. 1649 7

Chemical restraint is an important tool for the management and medical care of both captive and free-ranging rhinoceroses. Current anesthetic protocols for the white rhinoceros (Ceratotherium simum) are reported to cause varying degrees of hypertension, tachycardia, muscular stiffness and fasciculation, acidosis, and, most importantly, respiratory depression with resulting hypoventilation, hypoxia, and hypercapnea. To assist in the assessment and development of new and improved anesthetic techniques for the white rhinoceros, the following cardiopulmonary reference parameters for standing, unrestrained white rhinoceroses were generated (mean +/- standard error [minimum maximum]): heart rate = 39 +/- 0.8 beats/min (32-42), respiratory rate = 19 +/- 0.6 breaths/min (16-23), corrected indirect systolic blood pressure = 160 +/- 2.9 mm Hg (146-183), corrected indirect diastolic blood pressure = 104 +/- 2.3 mm Hg (88-117), corrected indirect mean blood pressure = 124 +/- 2.2 mm Hg (108-135), end tidal CO2 = 45.1 +/- 0.7 mm Hg (41.7-48.0), rectal temperature = 36.8 +/- 0.1 degrees C (36.6-37.2), arterial blood pH = 7.391 +/- 0.007 (7.346-7.431), arterial partial pressure of oxygen = 98.2 +/- 1.4 mm Hg (90.2-108.6), arterial partial pressure of CO2 = 49.0 +/- 0.9 mm Hg (44.4-53.7), base excess = 3.5 +/- 0.4 mmol/L (1.9-5.9), bicarbonate = 29.3 +/- 0.4 mmol/L (27.3-32.2), and arterial hemoglobin oxygen saturation (SaO2) = 97.2 +/- 0.1% (96.6-98.0).
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PMID:Reference cardiopulmonary physiologic parameters for standing, unrestrained white rhinoceroses (Ceratotherium simum). 1793 45

Snake and spider bites, as well as scorpion sting envenoming, are neglected diseases affecting millions of people all over the world. Neurological complications vary according to the offending animal, and are often directly related to toxic effects of the venom, affecting the central nervous system, the neuromuscular transmission, the cardiovascular system, or the coagulation cascade. Snake bite envenoming may result in stroke or muscle paralysis. Metalloproteinases and other substances (common in vipers and colubrids) have anticoagulant or procoagulant activity, and may induce ischemic or hemorrhagic strokes. The venom of elapids is rich in neurotoxins affecting the neuromuscular transmission at either presynaptic or postsynaptic levels. The clinical picture of scorpion sting envenoming is dominated by muscle weakness associated with arterial hypertension, cardiac arrythmias, myocarditis, or pulmonary edema. These manifestations occur as the result of release of catecholamines into the bloodstream or due to direct cardiac toxicity of the venom. Cerebrovascular complications have been reported after the sting of the Indian red scorpion. Intracranial hemorrhages occur in the setting of acute increases in arterial blood pressure related to sympathetic overstimulation, and cerebral infarctions are related to either cerebral hypoperfusion, consumption coagulopathy, vasculitis, or cardiogenic brain embolism. Three main syndromes result from spider bite envenoming: latrodectism, loxoscelism, and funnel-web spider envenoming. Latrodectism is related to neurotoxins present in the venom of widow spiders. Most cases present with headache, lethargy, irritability, myalgia, tremor, fasciculation, or ataxia. Loxoscelism is caused by envenoming by spiders of the family Sicariidae. It may present with a stroke due to a severe coagulopathy. The venom of funnel-web spiders also has neurotoxins that stimulate neurotransmitter release, resulting in sensory disturbances and muscle paralysis. Proper management of the envenomed patient, including prompt transport to the hospital, correction of the hemostatic disorder, ventilatory support, and administration of antivenom, significantly reduce the risk of neurological complications which, in turn, reduce the mortality and improve the functional outcome of survivors.
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PMID:Neurological effects of venomous bites and stings: snakes, spiders, and scorpions. 2382 24