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The paper “Mortality in rheumatoid arthritis patients with disease onset in the 1980s” is of considerable interest.1 A decrease in mortality risk for rheumatoid arthritis (RA) patients in more recent years would be important, even if only in the first 10 years of RA. However, this inception cohort differs from those previously published so that no direct comparison is possible. As earlier (and older and larger) studies have shown standardised mortality ratios of two to three, a finding of “normal” mortality might imply that more recently used treatment strategies are reversing the excessive mortality in RA previously observed.
Yet, even at first perusal, there are a lot of deaths in this series of relatively young people. In the 10 years after a mean age of 51, 18 patients (10%) had died. Over 20 deaths were said to have been “expected”. However, using US mortality rates for a population mean aged the same, projected over 10 years, two thirds women, and white, one would expect only 11 deaths using 1996 mortality rates and 12 deaths using 1985 rates, over the 1710 patients years of follow up. While we did not have the age distribution of this RA cohort to calculate precise expectations, these figures should be conservative. Female mortality rates in the US white female population, at 3.4 per 1000 per year at age 51 and 9.0 per 1000 per year at age 61 are presumably higher than those in long lived Malmöhus County, Sweden.
Of interest, in our own larger study with meticulously computed “expected” values in four different populations we also had an “expected” death rate of about 10% to 15% over 10 years.2 But, these were not inception cohorts and their age at start of follow up was 60.4, 62.6, 59.8, and 69.1 years. Thus, they were much older cohorts. Given the expected doubling of mortality rates each eight years (Gompertz’s law), expected deaths should have been two to three times more in our cohorts than in a cohort beginning at age 51.
Finally, recent studies have not suggested that “rheumatoid” deaths in themselves are the cause of the increased mortality in RA. The observed “excess” deaths are spread around in multiple disease categories, with accelerated atherosclerosis numerically the largest problem and only a slight relative increase in systemic RA complications, gastrointestinal haemorrhage, and infections.2
We were pleased to notice the interest in our paper shown by Drs Fries and Bloch. In reply to their comments we do not consider the death rate of 10% in the cohort as an excessive one compared with the age and sex matched general population. It is not possible to calculate more precise figures of expected deaths knowing the mean age of the cohort only. To clarify this and make comparison possible we enclose a table of the age distribution in our cohort in five year intervals giving the number of observed and expected deaths for each age interval separately.
Women do live longer in Malmöhus County, Sweden than in the US. Female mortality rates in Malmöhus County were 3.76 per 1000 at age 51 and 7.32 per 1000 at age 61 in 1985. In 1996 the corresponding figures were 2.03 per 1000 at age 51 and 3.39 per 1000 at age 61.
We agree that the main cause of death in RA patients very seldom is the rheumatoid disease in itself. This was true also for our study where no certain connection between RA and death was found in any of the cases.
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