Other forms of pain inhibition have included stress-induced analgesia (SIA), in which a laboratory stressor is used to reduce experimental pain, and exercise-induced analgesia. Assuming that basal pain sensitivity may reflect the activity of endogenous pain modulatory systems, it would be expected that females and males may also differ in endogenous pain modulation. The results from 7 studies that examined sex differences in experimental ischemic pain are presented in the lower portion of Table 5. Studies used several variations of the submaximal effort tourniquet test to induce ischemic pain. Overall, a majority of the studies reported no sex differences in threshold (6 studies), tolerance (5 studies), or pain ratings (2 studies) to ischemic pain.
- Unfortunately, there is little standardization in the pain measures used or the time frame for assessing postoperative pain.
- For example, the effects of estrogens on bone deposition and cartilage homeostasis could influence the development of articular pathology and pain.400 Of more direct relevance to pain are the hormonal contributions to inflammation.
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Most of the studies reviewed above address quantitative differences, which refers to whether females and males display different amounts of pain or analgesia. In contrast, qualitative sex differences are present when a given variable influences pain or analgesia differently in women versus men. Because qualitative differences may indicate sex-specific pain mechanisms they represent the most compelling rationale for the development of sex-specific pain treatments. Thus, even in the absence of quantitative sex differences, researchers should conduct analyses to uncover potential qualitative sex differences, which simply involves including sex as a moderator in the statistical model. Responses to the TRPV1 agonist capsaicin have been compared across sexes, and three of these five studies reveal significant sex-related differences in subjective pain ratings, suggesting higher sensitivity in females (Table 8).
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Furthermore, duplications of the SOX3 locus were detected in three cases of 46,XX testicular DSD10). SOX3 analysis can be considered the next step for the diagnosis of 46,XX SRY-negative testicular DSD with normal copies of SOX9. A family study recently reported that 46,XY persons with a 178 kb duplication in a region about 500 kb upstream of SOX9 were completely normal fertile males, whereas 46,XX SRY-negative persons in the same family with duplications were clinically infertile males6). In this report, two of the three paternal cousins of their probands are known as infertile and the two probands share the same paternal haplotype for the SOX9 region, confirming the possibility that the father was indeed the carrier of the same triplication. Therefore, we should investigate family members of 46,XX male patients caused by SOX9 duplication. The 46,XX testicular disorder of sex development (DSD), also known as 46,XX male syndrome, is a rare condition with an estimated prevalence of one in 20,000 males1).
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