Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018099 (gout)
5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study we examined 22 Hungarian male probands with gout and 105 of their first degree relatives. This was the first family study in Hungary in which the characteristics of distribution of gout and hyperuricaemia among patients with gout and their first degree relatives, as well as the possible correlation between the prevalence of the disease and MHC class I antigens was investigated. Our gout patients showed the following characteristics: (1) There was a typical onset after age 40, benign oligoarticular form of arthritis, underexcretion of uric acid, moderate hypertension without evidence of reduced renal function, and a relatively high frequency of hyperostosis. (2) The prevalence of hyperuricaemia and gout exceeded the general population level in the first degree relatives of our gout patients. (3) The distribution of MHC class I antigens among the first degree relatives of our patients with gout showed no characteristic patterns. (4) There was no correlation between HLA B27 antigens and prevalence of gout or hyperostosis in family sibling studies. (5) The high frequency of gout and hyperuricaemia, as well as the lack of characteristic HLA patterns among the first degree relatives of gout patients in our family studies, point to the possible cumulative effect of several genes and environmental factors in the etiopathogenesis of this disease.
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PMID:Clinical and family studies in Hungarian patients with gout. 129 17

The elderly constitute a high-risk group in which the benefit of treatment of hypertension is now obvious. The initial drug should be a low-dose diuretic, followed by a beta-blocker. At present there are no data favoring the use of an ultra low-dose diuretic, such as 12.5 mg hydrochlorothiazide, unless there is coexisting prediabetes or gout.
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PMID:Treatment of hypertension in the elderly--the end of the story? 129 73

We report a 55-year-old right-handed man with frontal lobe epilepsy manifesting recurrent speech arrest. He was known to have hypertension, hypertriglyceridemia, and gout. In the three days prior to admission, he had episodes of sudden inability to talk. These episodes lasted 10 to 30 seconds and recurred ten to twenty times a day. On admission, speech comprehension and other mental functions were normal, as were findings on neurologic examination. During the period of speech arrest, he understood spoken commands, and there was no abnormal motor activity or paresis. The episodes of speech arrest were thought to be short aphasic periods due to transient ischemic attacks in the left carotid territory. Computed tomography and magnetic resonance imaging demonstrated a small calcified lesion in the upper medial portion of the left frontal lobe. Left internal carotid angiography demonstrated no abnormal findings. After neuroradiological examination finished, he suddenly raised his right hand and followed it with his gaze and a right head turn. The EEG seizure pattern in which 20-25 Hz activity began in the left fronto-central region and spread rapidly to the right fronto-central region, which after about 8 seconds was replaced by 12-14 Hz flattening rhythmic polyspikes was detected 9 times within 60 minutes. It is most unusual for supplementary motor area seizure to present pure paroxysmal speech arrest without accompanying paroxysmal motor activity. As in our case, epileptic arrest of speech may be confused with a transient ischemic attack of the dominant hemisphere.
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PMID:[A case of frontal lobe epilepsy presenting with recurrent speech arrest]. 129 18

The study was undertaken to clinically assess the consequences of alcohol consumption in 'communal' drinking patients whose levels of alcohol consumption could not be determined accurately in grams of alcohol. The level of alcohol consumed by 100 adult 'communal' drinking medical patients per drinking session was scored on a scale 0-10. The score was based on a qualitative impression of how much alcohol was drunk, level of consciousness, behaviour and gait. The frequency of drinking days in a week was scored on a 0-7 scale. The duration of drinking in years prior to registration at the clinic was also recorded. The pattern of diseases among the drinkers was compared to that of 70 adult non-drinkers. The individual diseases were ranked to association with alcohol consumption by the Kruskal-Wallis Test. The drinkers attained a mean level score of 5.75 +/- 2.16, a frequency of 4.75 +/- 2.4 days but the duration of prior drinking varied greatly. Gout, dilated cardiomyopathy, epilepsy and hypertension ranked highest in that order to alcohol usage. Rheumatic heart disease and Diabetes mellitus ranked low. The probability significance were, for level score p = 0.005, frequency p = 0.016 and duration p = 0.001. This method was able to identify the morbid chronic medical diseases associated with alcohol usage in 'communal' drinkers. There is a need to evaluate it against a known screening instrument like the Alcohol Use Disorders Identification Test (AUDIT).
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PMID:A clinical assessment of the consequences of alcohol consumption in 'communal' drinkers in the Zimbabwean Midlands. 129 68

Lead may exert toxic effects on several organ systems, but those in the kidney are the most insidious. Acute lead nephropathy is characterized by proximal tubular dysfunction with the development of a Fanconi-type syndrome, alterations in mitochondrial structure and the development of cytosolic and nuclear inclusion bodies. Intracellular lead is associated with specific high affinity proteins and can also bind to metallothionein. Chronic lead nephropathy is irreversible and is typically accompanied by interstitial fibrosis, both hyperplasia and atrophy of the tubules, glomerulonephritis and, ultimately, renal failure. In addition, lead produces renal neoplasms in experimental animals. Chronic lead exposure is also implicated in the development of saturnine gout and hypertension. The metal interacts with renal membranes and enzymes and disrupts energy production, calcium metabolism, glucose homeostasis, ion transport processes and the renin-angiotensin system. This review summarizes the biochemical effects of lead on the kidney to understand the mechanisms of lead-induced nephropathy and other associated disorders.
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PMID:Lead nephrotoxicity and associated disorders: biochemical mechanisms. 131 92

Felodipine is a dihydropyridine calcium antagonist which may be administered once daily in an extended release (ER) formulation. As monotherapy in older patients with mild to moderate essential hypertension, felodipine ER once daily provides effective control of blood pressure (BP). The drug has also been effective, either as monotherapy or in combination with other antihypertensive medications, in comparisons with other antihypertensive agents, and does not adversely affect lipid profiles or, in patients with diabetes mellitus, glycaemic control. Results in patients with angina pectoris and congestive heart failure indicate a potential role for felodipine ER in these indications and data also suggest the drug reduces left ventricular hypertrophy. In addition, felodipine ER appears suitable for use in patients with concomitant respiratory disease, renal or hepatic dysfunction, cerebrovascular or peripheral ischaemic disease, or gout, making it particularly useful in the elderly who often have more than one significant clinical condition. Felodipine ER has generally been well tolerated by older patients in clinical trials, although further confirmation in the long term is desirable. Thus, felodipine ER effectively lowers BP in older patients with essential hypertension with the added convenience of once daily administration. It may be used as monotherapy or in combination with other antihypertensive agents and is a practical advance in the treatment of hypertension in the elderly.
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PMID:Felodipine. A review of the pharmacology and therapeutic use of the extended release formulation in older patients. 139 20

Four patients of pure gouty nephropathy are presented. Gout was of over five years duration and asymptomatic nephropathy manifested as non-oliguric acute renal failure. Diseases commonly associated with it like uric acid stones, urinary tract infections, hypertension, diabetes mellitus, hyperlipidemid, obesity and nephrosclerosis were absent. Reduction in serum uric acid level resulted in prompt improvement in renal functions. Early detection and control of hyperuricemia may help in restoration of renal functions.
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PMID:Non-oliguric acute renal failure in gout. 139 13

One way to prevent chronic renal failure (CRF) is to institute preventive measures against renal diseases in the general population. Patients with hereditary kidney diseases should have genetic counselling. Certain infections affecting or causing kidney diseases can be eradicated. People should be cautious in the use of analgesics and non-steroidal anti-inflammatory agents. Exposure to hydrocarbons, heavy metals and toxic gases should be avoided. Proper management of diabetes mellitus, gout, renal stones and hypertension can prevent renal damage. In patients with established renal disease, the following factors if treated or modified can prevent or ameliorate renal injury: glomerular hypertension, cell mediated proliferation, lipid induced proliferation, coagulation and thrombosis. Pregnancy in patients with renal disease should be well managed and termination advised if necessary. Reversible causes of renal failure as well as acute reversible elements can be removed or treated. Acute renal failure due to toxins can be avoided, although prevention requires awareness of association with renal failure. Prevention too depends on early detection of nephrotoxic injury like: greater awareness of hazards of environmental toxins, careful monitoring of dosage of nephrotoxic drugs and when possible, total avoidance of nephrotoxins should be the rule. Finally, in patients with glomerular disease, prevention or amelioration of glomerular damage with pharmacological agents have been achieved in some instances.
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PMID:Can therapeutic interventions prevent chronic renal failure? 141 97

A 73-year-old man was admitted with gait disturbance and dysarthria. He showed right-side cerebellar ataxia. Computed tomography of brain showed left thalamic bleeding. Nine months later, he was admitted again because of seizure and consciousness disturbance. He had a history of diabetes mellitus and gout for five years, but no hypertension. On physical examination the lungs and heart were normal. On neurological examination, he showed stupor,pupils and eye position were normal. He showed right hemiparesis and urinary incontinence. The deep tendon reflexes were (+) at the upper limbs and (2+) at the right knee and ankle. Blood pressure was 162/88 mmHg and glucose was 275 mg/dl. Other laboratory data were normal. Brain CT showed hemorrhage of the left frontal lobe. The cystatin C level in cerebrospinal fluid was 68 ng/ml. Therefore we suspected cystatin C deposit amyloid angiopathy. In this case, thalamic hemorrhage was initially thought to be amyloid angiopathy. In cases of cerebral hemorrhage in the elderly without hypertension, we must be considered amyloid angiopathy.
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PMID:[A case of recurrent cerebral hemorrhage considered to be cerebral amyloid angiopathy by cerebrospinal fluid examination]. 143 57

The performance of pharmacists in using an interactive computer-based patient simulation program and their attitudes toward the simulations are reported. The Institutional Patient Medication Simulation program is designed to enhance and evaluate the medication problem-solving skills of pharmacists. Each simulation consists of patient data-gathering, case question, and therapy decision modules with initial assessment and monitoring nodes. Five simulations were tested: gout, urinary-tract infection, congestive heart failure, antimicrobial prophylaxis in surgery, and hypertension. Pharmacists from nine hospitals were recruited for the study. Participants were asked to perform the simulations within a specified period and to complete attitudinal questionnaires. Of the 91 pharmacists who volunteered, 72 (79%) completed the simulations and the questionnaires. The practitioners indicated that the simulations adequately tested their knowledge and that they would recommend them to colleagues. Performance scores for data gathering were less than 70%, with no significant differences among the simulations. Case question scores exceeded 80% and again were consistent among simulations, whereas therapy decision scores were more variable, with the lowest scores being recorded for antimicrobial-related simulations. Pharmacists with more hospital experience tended to perform better. Pharmacists completing a patient simulation program found the simulations to be worthwhile. Performance scores indicated some difficulty in gathering patient data and showed that correct therapeutic decisions may not always occur even if adequate information is obtained.
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PMID:Computer-based patient simulations: hospital pharmacists' performance and opinions. 147 39


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