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)

Diuretics can result in various undesired biochemical changes, such as impotence, skin rashes, nausea, dizziness and lethargy as well as subjective side effects. The side effects are mostly predictable, their effects depending on both the circulatory blood volume and on the transport of water and solute in the renal tubules. Two of the commonest side effects are mild hypovolaemia, when any diuretic is used, and mild hypokalaemia when the non-potassium-sparing diuretics, such as thiazides and frusemide are used. Its occurrence is dose dependent and can be corrected by potassium supplements, but potassium-retaining diuretics, which also correct the often associated fall in serum magnesium, are preferable. Many reports link hypokalaemia with cardiac arrhythmias, but some dispute this association in the absence of the concomitant use of digoxin. Hyponatraemia rarely occurs, but can be life threatening. Calcium excretion is markedly reduced, but unlike other electrolyte disturbances from diuretics, this may be valuable: some suggest diuretics have an anti-osteoporotic action. Diuretics increase glucose and insulin resistance and should be used sparingly in diabetics. They rarely cause a non-ketotic hyperosmolar coma. Urate is raised, but clinical gout is not common. Cholesterol elevation has been reported in some studies, but long-term studies indicate that lipid changes are minor. Other rare side effects are not predictable from their pharmacological actions and these include the occurrence of skin rashes, thrombocytopenia, pancreatitis and interstitial nephritis; and ototoxicity from frusemide.
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PMID:Adverse reactions to diuretics. 148 14

Gross and microscopic changes in response to single po. doses of avicide 3-chloro-4-methyl benzamine HCl were studied in rooks (Corvus frugilegus L.) and pheasants (Phasianus colchicus L.). The observed changes followed a dose- and survival time related pattern and rooks were considerable more susceptible than pheasants to the toxicity of the compound. No effect was found in rooks and pheasants which survived safely 0.7 to 1.0 and 7.0 to 10.0 mg/kg doses, respectively. Early acute effect, in rooks died from 7.0 to 16.0 mg/kg within 16 to 18 h, included: congestion of the major organs, fatty degeneration of the liver, and extensive parenchymal degeneration of the kidney, particularly the proximal tubular epithelial cells. Progressive late effect developed in rooks and pheasants at 2.2 to 5.0 and 16.0 to 120.0 mg/kg doses, respectively, which died in coma between 32 to 80 h. It was characterized by a grayish white, frost-like material of uric acid overlaying the serosal surfaces of the various organs, accompanied by sterile inflammation and necrosis in the affected and adjacent tissues. Few urate deposition was also seen in some of the kidneys. Infrequently, interstitial pneumonia did also occur. The lesions produced by the toxic effect of the test compound seemed to be analogous to that of avian visceral gout.
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PMID:Pathological features of 3-chloro-4-methyl benzamine HCl toxicity in rooks (Corvus frugilegus L.) and pheasants (Phasianus colchicus L.). 715 25

We report a 62-year-old man who developed coma and died in a fulminant course. The patient was well until May 1, 1996 when he noted chillness, tenderness in his shoulders, and he went to bed without having his lunch and dinner. In the early morning of May 2, his families found him unresponsive and snoring; he was brought into the ER of our hospital. He had histories of hypertension, gout, and hyperlipidemia since 42 years of the age. On admission, his blood pressure was 120/70, heart rate 102 and regular, and body temperature 36.3 degrees C. His respiration was regular and he was not cyanotic. Low pitch rhonchi was heard in his right lower lung field. Otherwise general physical examination was unremarkable. Neurologic examination revealed that he was somnolent and he was only able to respond to simple questions such as opening eyes and grasping the examiner's hand, but he was unable to respond verbally. The optic discs were flat; the right pupil was slightly larger than the left, but both reacted to light. He showed ptosis on the left side, conjugate deviation of eyes to the left, and right facial paresis. The oculocephalic response and the corneal reflex were present. His right extremities were paralyzed and did not respond to pain Deep tendon reflexes were exaggerated on the right side and the plantar response was extensor on the right. No meningeal signs were present. Laboratory examination revealed the following abnormalities; WBC 18,400/ml, GOT 131 IU/l GPT 50 IU/l, CK616 IU/l, BUN 30 mg/dl, Cr 2.1 mg/ dl, glucose 339 mg/dl, and CRP 27.4 mg/dl. ECG showed sinus tachycardia and ST elevation in II, III and a VF leads and abnormal q waves in I, V5, and V6 leads. Chest X-ray revealed cardiac enlargement but the lung fields were clear. Cranial CT scan revealed low density areas in the left middle cerebral and left posterior cerebral artery territories. The patient was treated with intravenous glycerol infusion and other supportive measures. At 2: 10 AM on May 3, he developed sudden hypotension and cardiopulmonary arrest. He was pronounced dead at 3:45 AM. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had acute myocardial infarction involving the inferior and the true posterior walls and left internal carotid embolism from a mural thrombus. Post mortem examination revealed occlusion of the circumflex branch of the left coronary artery due to atherom plaque rupture and myocardial infarction involving the posterior and the lateral wall with a rupture in the postero-lateral wall. Marked atheromatous changes were seen in the left internal carotid, the middle cerebral and the basilar arteries; the left internal carotid and the middle cerebral arteries were almost occluded by thrombi and blood coagulate. The territories of the left middle cerebral and the occipital arteries were infarcted; but the left thalamic area was spared. The neuropathologist concluded that the infarction was thrombotic origin not an embolic one as the atherosclerotic changes were severe. Cardiac rupture appeared to be the cause of terminal sudden hypotension and cardiopulmonary arrest. It appears likely that a vegetation which had been attached to the aortic valve induced thromboembolic occlusion of the left internal carotid artery which had already been markedly sclerotic by atherosclerosis. It is also possible that the vegetations in the aortic valve came from mural thrombi at the site of acute myocardial infarction, as no bacteria were found in those vegetations.
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PMID:[A 62-year-old man with an acute onset of consciousness disturbances]. 945 48

About the 'Omnipotence' of the Chelation Therapy In the eighties the 'method of treatment proven in many thousands of cases over 20 years' was transferred from the USA to Germany (enjoys a priori considerable faith) using very dubious promises. It was Clarke et al. who introduced this 'therapy' in 1955. The dubious promise was to maintain that the chelation therapy eliminates or alleviates symptoms in the case of the following illnesses: Alzheimer's disease, senility, schizophrenia, rheumatoid arthritis, osteoarthritis, gout, renal calculus, apoplectic coma, gallstones, multiple sclerosis, osteoporosis, chronic fatigue syndrome, varicose veins, hypertension, failure of memory, scleroderma, Raynaud's disease, digitalis intoxication, intermittent claudication, diabetic ulcer, disturbance of the blood supply, ulcer on the legs, snake poison, impotence, emotional difficulties, defective hearing, vision disorder. There is not the slightest proof of effectiveness for any of the listed indications. The burden of proof lies with the supplier. Even in the case of the relatively often examined peripheral atherosclerotic changes (claudicatio intermittens) there is no proof that EDTA has a greater effect than placebo. For coronary heart disease too there is no evidence for any usefulness of the chelation therapy beyond that of a placebo effect. Only controlled studies can help to improve the therapy in the sense of 'Evidence-based medicine'. Retrospective investigations on thousands of patients cannot 'prove' anything, although this is maintained again andagain.
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PMID:ber die laquo;Omnipotenz>> der Chelattherapie. 997 59