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)

The therapeutic efficacy of cyclosporine (CsA) as an immunosuppressive agent was complemented by a modest, long-term incidence of toxic complications in 402 renal allograft recipients engrafted one to five years prior to analysis. The overall patient and graft survivals at one year were 97% and 84% (actual), and at five years 92% and 67% (actuarial). The immunosuppressive therapeutic index was excellent: only 12% of allografts were lost from rejection, with 5% of patients succumbing to infection. While infections were common, tending to emanate in the urinary tract or to be viral in etiology, they were generally mild and readily controlled. Only four patients displayed malignancies; none succumbed to this cause. The most common toxic complication was hypertrichosis, which was accentuated in pediatric patients. While tremors occurred in 20% of patients, primarily during the first three months, other neuroectodermal complications of parethesias, depression, somnolence, and seizures were rare. Hepatotoxicity, which was noted in 50% of patients, particularly recipients of cadaveric grafts, generally was first seen as a transaminase elevation, at least partially reversible by dose-reduction and abating by the third year. Associated disturbances of cholelithiasis and pancreatitis were occasionally observed. Nephrotoxicity was the only persistent, long-term complication. Hypertension occurred in 72% of patients during the first month, 36% in the second year, and about 15% thereafter. Hyperuricemia, which occurred in about 30% of recipients during the first two years, was occasionally associated with symptomatic gout. The mean serum creatinine level remained elevated throughout the follow-up period at 1.8-1.9 mg/dl, suggesting persistent, but nonprogressive, drug-induced renal injury. The present analysis documents the relative safety of CsA for long-term therapy, and highlights the need for new approaches to ameliorate drug-induced nephrotoxicity.
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PMID:Complications of cyclosporine-prednisone immunosuppression in 402 renal allograft recipients exclusively followed at a single center for from one to five years. 354 76

We present the case of a 17-year-old male who was diagnosed at birth with hereditary fructose intolerance (HFI). The patient complained of morning-time asthenia and post-prandial drowsiness despite a correct sleep pattern. The physical examination and biological check-up only showed severe vitamin C deficiency (<10 mol/l; normal range: 26-84). The patient's tiredness was attributed to this vitamin C deficiency, which is a frequent side-affect of the fructose-free diet. A change in diet associated with a supplementation in vitamin C was advised, with an increase in vegetable intake, principally avoiding carrots, onions, leaks and tinned sweet-corn. This case offers the opportunity for a review of this rare disease. Two kinds of fructose metabolism disorders (both autosomal recessive) are recognized: 1) essential fructosuria caused by a deficiency of fructokinase, which has no clinical consequence and requires no dietary treatment; 2) HFI, linked to three main mutations identified in aldolase B gene that may be confirmed by fructose breath test, intravenous fructose tolerance test, and genetic testing. In HFI, fructose ingestion generally induces gastro-intestinal (nausea and vomiting, abdominal pain, meteorism) and hypoglycemic symptoms. Fasting is well tolerated. If the condition remains undiagnosed, it leads to liver disease with hepatomegaly, proximal tubular dysfunction, and slow growth and weight gain. In conclusion, endocrinologists should be aware of this rare metabolic disease in order to provide careful follow-up, particularly important when the patient reaches adulthood. Moreover, hypoglycemia induced by fructose absorption, unexplained liver disease, irritable bowel syndrome or familial gout in an adult is suggestive of the diagnosis.
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PMID:Doctor, my son is so tired... about a case of hereditary fructose intolerance. 1803 30

The objective of the present study was to investigate the toxico-pathological effects of diclofenac in different avian species including broiler chicks (Gallus gallus, 15 days old), pigeons (Columba livia, 3 months old), Japanese quail (Coturnix japonica, 4 weeks old) and mynah (Acridotheres tristis, independent young). For each species, five groups each containing 10 birds were maintained and administered diclofenac sodium orally at dose rates of 0, 0.25, 2.5, 10 and 20 mg/kg body weight, respectively, for seven consecutive days. Clinical signs in all species included depression, somnolence, decreased body weight and mortality. Severity of clinical disease increased in a dose-related manner and was most severe in broiler chicks, followed by pigeons, Japanese quail, and was least severe in mynah. Serum creatinine levels were elevated in all species. Serum urea levels varied non-significantly in broiler birds, significantly decreased in pigeons and significantly elevated in Japanese quail and mynah. Broiler chicks and pigeons administered 10 and 20 mg diclofenac/kg had visceral gout; however, this was not observed in Japanese quail and mynah. The kidneys and liver were enlarged in all species. Histologically, the kidneys of all species showed acute renal necrosis and the livers had fatty change and necrosis of hepatocytes. The kidneys and liver of broiler chicks and pigeons given 10 and 20 mg/kg diclofenac also exhibited uric acid crystal aggregates (tophi) and associated lesions in the parenchyma.
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PMID:Toxicological effects of diclofenac in four avian species. 1856 59

Herod the Great was appointed "king of Jews," to govern Judea, by the Roman Emperor and Senate. He lived from 73/74 BCE to 4 CE. He died with an illness and symptoms that have been the source of considerable speculation. Richard Strauss depicted Herod in his classic opera, "Salome." That opera was derived from a play of the same name by Oscar Wilde, which was based on an 1876 painting, "Salome Dancing Before Herod," by Gustave Moreau. The operatic Herod was afflicted with an illness characterized by dementia, hallucinations, paranoia, alcoholism (from drinking the Emperor's wine), violence, twitches, and sterility; different interpretations showed him also with falls, chills, shaking, thirst, forgetfulness, and sleepiness, for which we suggest the novel diagnosis of chronic lead intoxication (which can manifest to rheumatologists as saturnine gout). He had compatible symptoms (encephalopathy and neuromuscular abnormalities) and consumed excessive quantities of imperial wine, known to be highly contaminated with lead and likely associated with similar symptoms among Roman aristocracy. Herod's demented cruelties-an oppressive reign which including the beheading of John the Baptist-exacerbated the political climate and may have contributed to the subsequent violent 7-year revolt culminating in the destruction of the second temple. How different might history have been if Herod the Great had been abstemious?
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PMID:Did King Herod suffer from a rheumatic disease? 2873 92