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PubMed1990

[Hyperuricemia--does modern therapy improve life expectancy?].

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.

Cause of Death↗
PubMed1989

[Pilot study of the action of Doqualast on dietary hyperuricemia in volunteers].

For eight days 8 healthy volunteers were treated with a formula diet and additional 1680 purine base per day. Beginning with day 5, doqualast was administered orally in a dosage of 200 mg t.i.d. Serum uric acid level was lowered by doqualast from 7.84 +/- 0.9 mg/dl to 5.09 +/- 0.8 mg/dl (p less than 0.01). Uric acid clearance increased from 7.6 +/- 2.5 ml/min to 11.5 +/- 2.4 ml/min (p less than 0.05). Excretion of uric acid in urine increased from 622 +/- 231 mg/d to 890 +/- 233 mg/d at the end of therapy. Total cholesterol in serum was lowered from 222 +/- 70 mg/dl to 159 +/- 48 mg/dl (p less than 0.05). The new uric acid lowering drug doqualast was well tolerated clinically. No adverse effects on biochemistry parameters were observed.

Adult↗
PubMed1989

Oxalate crystallization in the kidney in the presence of hyperuricemia.

It has been a long time since uric acid was suggested to be a promoting factor in calcium oxalate stones, and a number of in vitro studies have been carried out on the relationship between uric acid or urate and calcium oxalate. Concerning in vivo studies, urate or calcium oxalate stone-forming diets were given alone in most cases, and diets that induce formation of stones with different composition have not been given in combinations. We administered a low-concentration oxalemic diet, and a mixed diet containing oxalic acid and uric acid, and biochemically and histologically studied the effects of oxalate and uric acid on kidney stone formation. In the kidney of the animals given the mixed diet, formation of crystalloids of uric acid or urate was evident when no crystallization was noted in the kidney of those given the low concentration oxalemic diet alone. The morphological differences in the uric acid and urate crystalloids in the kidney and the process leading to crystallization of calcium oxalate were examined under transmission and scanning electron microscopy. Histological examination indicated that these uric acid crystals and urate crystals serve as seeds and induce formation and epitaxial growth of calcium oxalate crystals. Our in vivo study provides additional evidence that uric acid is a promoting factor in calcium oxalate stone formation.

Animals↗
PubMed1989

Intermittent control of hyperuricemia in the treatment of gout.

Fifty patients with gout were randomly allocated to one of 2 groups receiving allopurinol, either continuously or for 2 months every year. Patients with renal functional impairment or tophacous gout were excluded. Duration of treatment ranged from 2-4 years. Acute gouty arthritis occurred to a similar degree in the 2 groups during the first year, but thereafter attacks occurred with diminishing frequency in the continuous group compared with the intermittent group. We concluded that the intermittent administration of allopurinol as given here is less effective in controlling symptoms of gout than continuous therapy.

Allopurinol↗
PubMed1989

[Changes in uric acid and blood lipids in patients with asymptomatic hyperuricemia treated with diet therapy in a rehabilitation procedure].

More than 300 patients with asymptomatic hyperuricaemia had been included in lipometabolic analysis performed before and after 4 weeks of a special low-cholesterol, low-triglyceride and low-purine dietetic regimen. Remarkable in almost the entire hyperuricaemic population (96.7%) had been the presence of serum cholesterol levels of more than 200 mg/dl. Lipoprotein analysis showed that 87% of the patients had increased LDL- and 69% increased VLDL-levels; HDL-levels were pathologically lowered to below 40mg/dl in 41% of the group. After a four-week rehabilitation programme, all lipometabolic parameters and serum urate concentrations were found to have been significantly reduced by the special diet. The results therefore are impressive proof of the major health benefits of purposive nutritional behaviour.

Adult↗