Trends in Body Mass Index Before and After Diagnosis of Hidradenitis Suppurativa

S. Wright; A. Strunk; A. Garg

Disclosures

The British Journal of Dermatology. 2021;185(1):74-79. 

In This Article

Discussion

In this study, we observed that baseline BMI and rate of BMI change prior to diagnosis was higher for patients with HS than controls. While the magnitude of difference in baseline BMI was larger (approximately 3 kg m−2), the magnitude of difference in rate of BMI change was smaller (difference of 0·07 kg m−2 per year). In addition, there was no significant change in BMI among patients with HS overall following diagnosis. Subgroup analysis revealed that BMI continued to increase after diagnosis for patients with HS diagnosed before age 40 years, but the rate of increase had slowed and was comparable with that of controls during the same period. Taken together, these results suggest that increased BMI, and to a lesser extent, rate of increase in BMI, is linked to the development of HS rather than being a consequence of disease. The difference in baseline BMI between patients with HS and controls was larger for women than men, and for patients with HS diagnosed before age 40 years than those diagnosed after age 40 years. As such, BMI may have greater influence in the development of HS among women and younger individuals, both of whom are most commonly afflicted with HS.[24,25] Further studies are required to fully elucidate the relationship between baseline BMI, age, sex and the development of HS.

Several studies have observed an association between HS and obesity,[4,10–12,14] although there is conflicting evidence regarding the relationship between obesity and disease severity.[5–9,12,26,27] Data from four European cross-sectional studies show a significant positive association between obesity and disease severity,[5,7,8,27] and some case reports have reported improvement in disease activity with weight loss.[28,29] To our knowledge, this is the first population-based analysis to establish a temporal relationship between HS and obesity, and the first to describe the influence of both baseline BMI and the rate of BMI change on the development of HS.

There are limitations that warrant consideration when interpreting the results of our study. There is potential for misclassification of HS status in clinical databases. To mitigate this possible influence, we used a validated case definition to identify patients with HS. Data on potentially relevant covariates, such as socioeconomic status, that are not typically collected during the course of care are generally unavailable in clinical databases. This analysis may have selected for patients with high healthcare utilization, given the need to track BMI longitudinally. Accordingly, control patients may have been in worse overall health than the general population. As a result, we may have underestimated association between HS and rate of BMI change. Patients with HS may experience delays in diagnosis,[2] and as a result, the timepoint of official HS diagnosis may not accurately reflect the timepoint of the development of symptoms. However, BMI measurements were tracked 7 years prior to diagnosis to account for diagnosis delay. Additionally, our data show a change in BMI trend for patients with HS around the time of diagnosis, which suggests that this timepoint is not arbitrary. Despite potential limitations, this population-based analysis reports important data on the temporal relationship between HS and obesity. Given the size and demographic heterogeneity of our cohort, we believe that these results may be generalized to the US healthcare-seeking population.

In conclusion, baseline BMI and, to a lesser extent, rate of BMI change appear to be risk factors for developing HS. Average BMI does not appear to increase substantially after diagnosis among patients with HS, suggesting that high BMI may not be a disease consequence. Influence of baseline BMI may play a larger role in the development of HS in women and younger patients. Patients with HS are already subject to numerous disease-related stigmatizations.[30,31] The authors underscore herein that findings in this study should not further stigmatize patients who are afflicted with HS. Given the negative impact of the condition on physical activity, we acknowledge that HS may contribute to weight gain in individual cases. There are also other risk factors, both known, such as tobacco smoking,[32] and unknown, which are also likely to contribute to the development of HS. Indeed, there are numerous nonobese patients who also develop disease. Accordingly, it is essential that clinicians do not ascribe development of HS to obesity alone. Moreover, we suggest approaching the topic of obesity in HS with the utmost sensitivity, only after a patient–doctor relationship based on principles of empathy, trust and overall health advocacy has been well established.

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