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Query: UMLS:C0018099 (gout)
5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The therapy of gout is discussed taking into consideration the concomitant diseases occurring significantly frequently in patients with gout: Hypertension, uric acid-nephrolithiasis, hyperlipoproteinaemia, obesity, premature arteriosclerosis as well as diabetes mellitus. In contrast to other opinions the authors are of the opinion that the dietetic treatment is furthermore of essential importance. It is referred to the still allowed sufficiently great number in the supply of nourishment, in which cases, however, the limitations in the supply of calories, protein or purin bodies, respectively, lipid and carbohydrate do not remain unmentioned. The propositions for the medicamentous treatment essentially correspond to the central therapeutic recommendations. For the acute attack of gout, however, following to the international experiences, the colchicine therapy is more emphasized again. The medicamentous therapy of the asymptomatic hyperuricaemia is to be included into the considerations after full exhaustion of all dietetic and other possibilities in constant increase of the serum-uric acid-level more than 8 mg/dl.
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PMID:[Therapy of gout]. 33 84

A now 45-year-old man with marked chronic tophous gout and recurrent nephrolithiasis has been followed for 12 years. First gouty symptoms appeared at age 18. Uric-acid reducing treatment freed the patient of symptoms, and bony and soft-tissue tophi in part regressed. The early onset and high urinary uric-acid excretion indicated increased uric-acid production. Decreased activity of the enzyme hypo-xanthine-guanine-phosphoribosyl transferase was demonstrated to be the cause of the hyperuricaemia, which led to an excessive purine synthesis. An almost complete loss of activity of this enzyme is the basis of the Lesch-Nyhan syndrome. In the described patient all of the neurological and behavioural disorders of the Lesch-Nyhan syndrome were absent. A pheochromocytoma was found to be the cause of malignant hypertension, which had been present for many years.
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PMID:[Juvenile gout with decreased activity of hypoxanthine-guanine-phosphoribosyl transferase and pheochromocytoma: partial persistence of tophi despite uric-acid reducing treatment for 12 years (author's transl)]. 66 12

In 60 patients (48 cases were evaluated) with primary gout a longterm therapy (5--10 years) with Allopurinol was performed. Without treatment 4.4 sudden onsets of gout per patient and year were registrated; under Allopurinol only 0.062 (p less than 0.001) onsets were observed. This resulted in a large decrease in hospitalisation time from 44 days to 0.62 days per patient and year. In the majority of cases involution or diminuation of the tophi was found. In 7 cases of nephrolithiasis no further renal colic took place. In 8.3% a skin rasch and in 12.5% a slight gastrointestinal side effect was observed. Together with the clinical results the socio-medical aspects are discussed and the importance of gout in respect to the socioeconomic point of view is pointed out.
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PMID:[Clinical and socio-medical aspects of long term uricostatic treatment of primary gout (a 5-10 year study)]. 68 12

Frequency of gout in French Polynesia has induced us to define a type of "hyperuricemia Polynesian" from a population of patients admitted in a general Medicine Ward. Each admitted patient gets immediately a blood check-up. A figure higher than 70 mg/l in male and 60 mg/l in female is considered as pathological. In such a case, uricemia and uraturia are tested every 24 h for three days and we consider the mean value of these three tests. On the other side, some admitted patients non-hyperuricemic, are examined according to the same protocol. So, we have two groups: 31 hyperuricemics and 20 non-hyperuricemics, secondarily grouped according to age, sex, ethnic. We did not consider some secondary causes of hyperuricemia (chronic renal insufficiency diuretic treatment, psoriasis etc.). 1. Within the hyperuricemic population, mean uricemia is 85.35 mg/l versus 52.65 mg/l in the second sample. In the hyperuricemic group (21 males and 10 females) 48% are gouty and 13% of them are females. Articular manifestations are acute arthritis, affecting mainly inferior limbs, ankles, knees). We did not notice any significant divergence between uricemia and uraturia of gouty and non gouty people. Within the group of gouty people, percentage of individual hyper excretion is 53% (uraturia greater than 600 mg/24 h) with no significant divergence with the non-gouty group: Nephrolithiasis is rare (3%). There is no significant divergence between urinary pH of gouty and non-gouty people. Associated metabolic troubles are: diabetes (26%) high triglyceridemia (43%) three syndromes associated together (hyperuricemia + diabetes + hypertriglyceridemia) in 19.5%, total cholesterol is normal (2.07 g/l) but a low cholesterol (0.30 g/l).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Study of hyperuricemia in Tahiti. 31 cases hospitalized at the Territorial Hospital Center in Papeete (Tahiti)]. 160 55

Today hyperuricaemia and gout are likewise seen in every population of the western industrial world and have been increasing since the fifties. As known from number of studies hyperuricaemia often occurs in connection with hyperlipoproteinaemia, obesity, diabetes mellitus, arterial hypertension and atherosclerosis. Up to now it was not clear whether one disease caused the other. In 1988 Abbot could prove that among men, those afflicted by gout as compared to those without gout experienced a 60% excess of coronary heart disease. Therefore, patients with gout should receive a regular thorough cardiovascular evaluation. Furthermore risk factor levels which predispose to coronary heart disease, arterial hypertension and gout should be reduced. There is a significant positive correlation between the plasma uric acid levels and the prevalence of attacks of gouty arthritis and nephrolithiasis. It is possible to avoid gouty arthritis, tophi and nephrolithiasis with a consequent diet and medical treatment. Unfortunately, many patients interrupt therapy during intervals free of pain. The consequence is that even today the complications of hyperuricaemia cause days of inability to work and to earn one's living, despite of modern therapy. Hyperuricaemia not sufficiently treated reduces the quality of life through attacks of gout, chronic gout and nephrolithiasis as well as life expectancy caused by nephropathy, arterial hypertension and atherosclerosis. This is of special importance because of the frequency of gout and hyperuricaemia in our population. An early diagnosis, a consistent therapy and a thorough monitoring could stop an increase of this disease and prolong life expectancy for those who have gout and the other attendant diseases.
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PMID:[Hyperuricemia--does modern therapy improve life expectancy?]. 227 73

The authors have established that to higher calciuria in patients with calcium nephrolithiasis correspond higher vales of uric acid serum concentrations and urine excretion than in the controls. In the oral calcium tolerance test a significant correlation was found between the changes in the uric acid urine excretion and those in the diuresis. The following conclusions are put forward. I. In the patients with recurrent calcium nephrolithiasis and hypercalcinosis one should look for active impairment of uric acid metabolism which should be kept in mind when an antirecurrence treatment is planned. 2. The established parallel increase of uricosuria and calciuria in the oral calcium tolerance test means that to patients with recurrent calcium nephrolithiasis and gout a rich calcium diet should not be prescribed since it increases the risk of formation of calcium oxalate stones.
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PMID:[The effect of oral calcium loading on the serum concentrations and urinary excretion of uric acid in patients with recurrent calcium nephrolithiasis and hypercalciuria]. 228 2

Since 1962 our group has performed four studies on uric acid values in blood donors in southern Germany (Bavaria). Uric acid levels in men have increased over the years, from 4.86 mg/dl in 1962 to 6.00 mg/dl in 1971, 5.60 mg/dl in 1984, and 5.90 mg/dl in 1989. Levels in women have increased slightly, from 4.05 mg/dl in 1962 to 4.35 mg/dl in 1971, 4.10 mg/dl in 1984, and 4.16 mg/dl in 1989. Women aged 51 to 60 years had significantly higher uric acid levels than those in the fourth decade. In women treated with oral contraceptives uric acid levels were significantly lower than in other women of the same age. Hypouricemia (uric acid levels less than or equal to 2.0 mg/dl) was observed in three women, none of whom had a history of medication. Hyperuricemia exists when uric acid levels are greater than or equal to 6.5 mg/dl. In 1989 2.6% of the female blood donors and 28.6% of the males were hyperuricemic, with an increased risk of gout, nephrolithiasis, and nephropathy.
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PMID:Uric acid levels in southern Germany in 1989. A comparison with studies from 1962, 1971, and 1984. 229 Mar 9

Gout is a clinical syndrome encompassing a group of metabolic diseases that are all characterized by abnormal uric acid metabolism. In its fullest form, gout is defined by: an increase in the serum urate concentration; characteristic, recurrent, acute arthritic attacks, with monosodium urate monohydrate crystals demonstrable in synovial fluid leukocytes; tophi, usually in and around joints of the extremities, composed of monosodium urate monohydrate deposits; renal disease, often accompanied by hypertension with glomerular, tubular, interstitial, and vascular involvement; and uric acid nephrolithiasis. Any combination of these manifestations may occur, although tophi and urate nephropathy rarely antedate gouty arthritis.
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PMID:Hyperuricemia and gout. 351 32

An appreciation of the physiology of fasting is essential to the understanding of therapeutic dietary interventions and the effect of food deprivation in various diseases. The practice of prolonged fasting for political or religious purposes is increasing, and a physician is likely to encounter such circumstances. Early in fasting weight loss is rapid, averaging 0.9 kg per day during the first week and slowing to 0.3 kg per day by the third week; early rapid weight loss is primarily due to negative sodium balance. Metabolically, early fasting is characterized by a high rate of gluconeogenesis with amino acids as the primary substrates. As fasting continues, progressive ketosis develops due to the mobilization and oxidation of fatty acids. As ketone levels rise they replace glucose as the primary energy source in the central nervous system, thereby decreasing the need for gluconeogenesis and sparing protein catabolism. Several hormonal changes occur during fasting, including a fall in insulin and T(3) levels and a rise in glucagon and reverse T(3) levels. Most studies of fasting have used obese persons and results may not always apply to lean persons. Medical complications seen in fasting include gout and urate nephrolithiasis, postural hypotension and cardiac arrhythmias.
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PMID:Fasting: the history, pathophysiology and complications. 675 55

Using the Princeton School Family Study, our specific aim was to estimate the prevalence of familial hyper- and hypouricemia, to estimate the proportion of probands' first-degree relatives who were similarly affected, and to evaluate the contribution of diseases, drugs, and alcohol intake (if any) to uric acid levels. We studied 379 probands and a total of 1928 subjects, 125 and 52 black probands from a randomly recalled group, 147 white and 55 black probands from a hyperlipidemic recall (top decile cholesterol and/or triglyceride) group. Familial hyper- and hypouricemias were arbitrarily identified in those kindreds having at least two first-degree relatives in the same decile as the proband, top or bottom respectively, for serum uric acid. No probands had symptomatic gout. Diseases, drugs, and alcohol intake were not consistently associated with aggregations of high and/or low uric acid levels in families, and had little relationship to uric acid levels in individuals. Of the 177 randomly recalled probands, and of the 55 black probands in hyperlipidemic recall familial hyperuricemia, with concurrent primary hyperlipoproteinemia and hypertension. Familial hypouricemia was present in 1 of 125 white and in 1 of 52 randomly recalled black kindreds, and in 3 of 147 white and 3 of 55 hyperlipidemic recall black kindreds. While familial clustering of hyperuricemia was limited, clustering of hypouricemia was much more marked. Seventy-four and 84% respectively of first-degree relatives of hypouricemic white and black probands had uric acid less than the 50th percentile. In randomly recalled probands and their first-degree relatives there were significant inverse partial correlations between uric acid and high density lipoprotein cholesterol. Inverse associations of uric acid with high density lipoprotein cholesterol and the concurrence of hyperlipoproteinemia and hypertension in hyperuricemic families points to the importance of lipoprotein and blood pressure screening in families with asymptomatic hyperuricemia. The potential ramifications of within-family clustering of hypouricemia need to be further assessed in populations, particularly in regards to uric acid nephrolithiasis.
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PMID:Familial hyper- and hypouricemias in random and hyperlipidemic recall cohorts: the Princeton School District Family Study. 682 94


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