1. On exposure of synovial fluid to superoxide and hydrogen peroxide, generated enzymically or by activated polymorphonuclear leucocytes, hyaluronic acid is depolymerized and the fluid loses its lubricating properties. The ability of synovial fluid from rheumatoid patients to scavenge superoxide and hydrogen peroxide was therefore examined. 2. Synovial fluid from a range of rheumatoid patients contained no superoxide dismutase activity, insufficient caeruloplasmin to scavenge any superoxide radical and little, if any, catalase activity. 3. Total ascorbate (reduced ascorbate + dehydroascorbate) concentrations in the plasma and synovial fluid of rheumatoid patients were similar in each case. The values are at the low end of the normal range. 4. These results are discussed in relation to the role of oxygen radicals in inflammatory joint disease.

The metabolic consequences of thiazide diuretics are well known. The elderly to whom these agents are widely prescribed may be particularly susceptible. To quantify this metabolic risk, plasma and intracellular electrolytes and plasma glucose were measured in the elderly population of a Somerset village. Highly significant reductions in both plasma and cellular magnesium and potassium were found in the 47 thiazide-treated people. Forty-eight per cent of the thiazide-treated group were hypomagnesaemic and 28% were hypokalaemic. Thus, magnesium and potassium depletion are commonly associated with thiazide therapy in the elderly. These metabolic effects should be considered carefully prior to the use of these agents.

SummaryFourteen men aged 73-94 showed a fall in leucocyte ascorbic acid levels during five days' treatment with 1 g of tetracycline daily. A control group of nine men aged [74][75][76][77][78][79][80][81][82][83][84][85][86][87][88][89][90] showed no fail in leucocyte ascorbic acid levels. Of the control group, three were treated with phenobarbitone 60 mg thrice daily, three with phenylbutazone 200 mg thrice daily, and three with aloxiprin 1,200 mg four times a day. A further two men aged 87 and 90 showed increased urinary excretion of ascorbic acid while receiving 1 g of tetracycline daily.

Twenty-seven elderly men aged 69-94 years had tyrosine tolerance tests measured before and after receiving ascorbic acid 1 g daily for four days. There was a significant rise in the fasting and half-hourly mean plasma tyrosine levels after ascorbic acid administration in those subjects with an initial leucocyte ascorbic-acid level (LAA) below 15 micrograms/10(8) w.c.c. The peak of the tyrosine tolerance curve was also advanced following administration of ascorbic acid in those subjects with an initial LAA below 15 micrograms/10(8) w.c.c. A further ten elderly men aged 73-89 years had simultaneous measurements of the circadian rhythms of LAA, plasma cortisol and plasma tyrosine levels before and after receiving ascorbic acid 1 g daily for four days. All ten subjects showed a peak LAA level at 5 p.m. when saturated with vitamin C but there was no significant correlation between plasma cortisol changes and plasma tyrosine changes. Possible explanations for the results are discussed.

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