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The Effect of Gender-Affirming Hormone Therapy on the Risk of Subclinical Atherosclerosis in the Transgender Population: A Systematic Review
Institution:1. Department of Social Medicine, School of Medicine, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina;2. Department of Biostatistics, Gillings School of Global Public Health, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina;3. Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland;4. Callen-Lorde Community Health Center, New York, New York;5. Department of Medicine, Harvard Medical School, Boston, Massachusetts;6. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts;7. The Fenway Institute, Fenway Health, Boston, Massachusetts;8. Research Department, Whitman-Walker Institute, Washington, District of Columbia;9. Department of Health Behavior, Gillings School of Global Public Health, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina;10. Infectious Diseases Division, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts;11. Section of General Internal Medicine, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts;12. Center for Transgender Medicine and Surgery, Boston Medical Center, Boston, Massachusetts
Abstract:ObjectiveThe impact of gender-affirming hormone therapy (GAHT) on cardiovascular (CV) health is still not entirely established. A systematic review was conducted to summarize the evidence on the risk of subclinical atherosclerosis in transgender people receiving GAHT.MethodsA systematic review was performed following Preferred Reporting Items for Systematic Reviews and Meta-analyses guidelines, and data were searched in PubMed, LILACS, EMBASE, and Scopus databases for cohort, case-control, and cross-sectional studies or randomized clinical trials, including transgender people receiving GAHT. Transgender men and women before and during/after GAHT for at least 2 months, compared with cisgender men and women or hormonally untreated transgender persons. Studies reporting changes in variables related to endothelial function, arterial stiffness, autonomic function, and blood markers of inflammation/coagulation associated with CV risk were included.ResultsFrom 159 potentially eligible studies initially identified, 12 were included in the systematic review (8 cross-sectional and 4 cohort studies). Studies of trans men receiving GAHT reported increased carotid thickness, brachial-ankle pulse wave velocity, and decreased vasodilation. Studies of trans women receiving GAHT reported decreased interleukin 6, plasminogen activator inhibitor-1, and tissue plasminogen activator levels and brachial-ankle pulse wave velocity, with variations in flow-mediated dilation and arterial stiffness depending on the type of treatment and route of administration.ConclusionsThe results suggest that GAHT is associated with an increased risk of subclinical atherosclerosis in transgender men but may have either neutral or beneficial effects in transgender women. The evidence produced is not entirely conclusive, suggesting that additional studies are warranted in the context of primary prevention of CV disease in the transgender population receiving GAHT.Systematic Review RegistrationPROSPERO, identifier CRD42022323757.
Keywords:transgender people  gonadal steroids  testosterone  estrogens  cardiovascular risk  atherosclerosis  ABI"}  {"#name":"keyword"  "$":{"id":"kwrd0045"}  "$$":[{"#name":"text"  "_":"ankle-brachial index  baPWV"}  {"#name":"keyword"  "$":{"id":"kwrd0055"}  "$$":[{"#name":"text"  "_":"brachial-ankle pulse wave velocity  BMI"}  {"#name":"keyword"  "$":{"id":"kwrd0065"}  "$$":[{"#name":"text"  "_":"body mass index  cAI"}  {"#name":"keyword"  "$":{"id":"kwrd0075"}  "$$":[{"#name":"text"  "_":"carotid augmentation  CC"}  {"#name":"keyword"  "$":{"id":"kwrd0085"}  "$$":[{"#name":"text"  "_":"compliance coefficient  CEE"}  {"#name":"keyword"  "$":{"id":"kwrd0095"}  "$$":[{"#name":"text"  "_":"conjugated equine estrogen  CIMT"}  {"#name":"keyword"  "$":{"id":"kwrd0105"}  "$$":[{"#name":"text"  "_":"carotid intima-media thickness  CPA"}  {"#name":"keyword"  "$":{"id":"kwrd0115"}  "$$":[{"#name":"text"  "_":"cyproterone  CV"}  {"#name":"keyword"  "$":{"id":"kwrd0125"}  "$$":[{"#name":"text"  "_":"cardiovascular  CVD"}  {"#name":"keyword"  "$":{"id":"kwrd0135"}  "$$":[{"#name":"text"  "_":"cardiovascular disease  DC"}  {"#name":"keyword"  "$":{"id":"kwrd0145"}  "$$":[{"#name":"text"  "_":"distensibility coefficient  EE"}  {"#name":"keyword"  "$":{"id":"kwrd0155"}  "$$":[{"#name":"text"  "_":"ethinyl estradiol  EV"}  {"#name":"keyword"  "$":{"id":"kwrd0165"}  "$$":[{"#name":"text"  "_":"estradiol valerate  FMD"}  {"#name":"keyword"  "$":{"id":"kwrd0175"}  "$$":[{"#name":"text"  "_":"flow-mediated dilation  FMD-NTG"}  {"#name":"keyword"  "$":{"id":"kwrd0185"}  "$$":[{"#name":"text"  "_":"nitroglycerin-induced flow-mediated dilation  GAHT"}  {"#name":"keyword"  "$":{"id":"kwrd0195"}  "$$":[{"#name":"text"  "_":"gender-affirming hormone therapy  GSH"}  {"#name":"keyword"  "$":{"id":"kwrd0205"}  "$$":[{"#name":"text"  "_":"glutathione  IL"}  {"#name":"keyword"  "$":{"id":"kwrd0215"}  "$$":[{"#name":"text"  "_":"interleukin  IM"}  {"#name":"keyword"  "$":{"id":"kwrd0225"}  "$$":[{"#name":"text"  "_":"intramuscular  NO"}  {"#name":"keyword"  "$":{"id":"kwrd0235"}  "$$":[{"#name":"text"  "_":"nitric oxide  PAI-1"}  {"#name":"keyword"  "$":{"id":"kwrd0245"}  "$$":[{"#name":"text"  "_":"plasminogen activator inhibitor-1  SOD"}  {"#name":"keyword"  "$":{"id":"kwrd0255"}  "$$":[{"#name":"text"  "_":"superoxide dismutase  TD"}  {"#name":"keyword"  "$":{"id":"kwrd0265"}  "$$":[{"#name":"text"  "_":"transdermal  tPA"}  {"#name":"keyword"  "$":{"id":"kwrd0275"}  "$$":[{"#name":"text"  "_":"tissue plasminogen activator
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