Abstract

To the editor:
We have read the articles by Dominguez C, et al. (1), published online first in Cephalalgia with great interest. The authors performed a cross-sectional study of a total of 135 subjects (111 patients, 24 healthy controls) to relate serum adipocytokine levels to clinical and biochemical parameters associated with migraine. The authors concluded that leptin and adiponectin are increased in migraineurs and there is a correlation between adipocytokine levels and other inflammation-related molecules. We think the major strength of this study is that they suggest a potential role of adipocytokines in migraine pathophysiology and chronification as the authors described in the conclusion. However, we would like to make some comments about this study for the benefit of the readers.
First of all, we want to point out two minor authors’ mistakes. 1) The authors described that “One hundred and eleven patients (mean age 39.7 years, 93% female) and 24 healthy controls (mean age 35.9 years, 90% female) were included” in the abstract and the results. However, the mean age of both groups and female’s rate of control group described in Table 1 were different. 2) hs-CRP was incorrectly described as hs-PCR in some sentences (page 5, the second sentence and page 7, Clinical implications) or PCRus in Table 2.
Second, there was no difference between patients suffering migraine with or without aura for both leptin serum levels and adiponectin serum levels in this study. However, we suggest the authors should consider the effect of plasma hemodilution, since there was a positive correlation between serum levels of leptin and BMI and a negative correlation between serum levels of adiponectin and BMI. Recent studies demonstrated that a lower concentration of tumor markers was measured in obese people due to their larger plasma volume than non-obese people (2–5). Although adipocytokines are not a tumor marker and all patients’ BMIs were higher than two standard deviations, an increased plasma volume secondary to overweight and obesity could dilute the actual adipocytokine levels. Therefore, we think the author performed the statistical analysis after calibration of adipocytokine levels according to individual BMI.
Last, there are parts of the results that we do not understand. In the results, adiponectin serum level of the patients’ group was described as 72.3 ± 38.5 µg/mL and adiponectin serum level of the control group was described as 37.7 ± 16.9 µg/mL. On the other hand, adiponectin serum level of chronic migraine patients was described as 65.8 ± 42.9 µg/mL and adiponectin serum level of episodic migraine patients was described as 33.2 ± 31.0 µg/mL. Based on these data, we would like to ask two questions about the data. 1) Why are the mean values of patients different? (72.3 ± 38.5 µg/mL vs. 65.8 ± 42.9 µg/mL and 33.2 ± 31.0 µg/mL). 2) Is the mean value of adiponectin serum levels of episodic migraine patients lower than that of the healthy control group? (33.2 ± 31.0 µg/mL vs. 37.7 ± 16.9 µg/mL).
Footnotes
Declaration of conflicting interests
The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding
The authors received no financial support for the research, authorship, and/or publication of this article.
