Evaluation and Follow-up of a Case Receiving Hormone Replacement Therapy

Author(s):  
Vijay Zutshi ◽  
Nidhi Khera
Maturitas ◽  
1994 ◽  
Vol 20 (2-3) ◽  
pp. 81-89 ◽  
Author(s):  
F.P.M.J. Groeneveld ◽  
F.P. Bareman ◽  
R. Barentsen ◽  
H.J. Dokter ◽  
A.C. Drogendijk ◽  
...  

Author(s):  
Marta Casella ◽  
Samantha Manfredi ◽  
Maria Grazia Andreassi ◽  
Cristina Vassalle ◽  
Concetta Prontera ◽  
...  

Medicina ◽  
2019 ◽  
Vol 55 (9) ◽  
pp. 573 ◽  
Author(s):  
Marta D’Alonzo ◽  
Valentina Elisabetta Bounous ◽  
Michela Villa ◽  
Nicoletta Biglia

Hormone replacement therapy (HRT) remains the most effective treatment for menopausal symptoms and has been shown to prevent bone loss and fracture. The progestogen is added to provide endometrial protection in women with an intact uterus. After the publication of the initial WHI (Women’s Health Initiative) results in 2002 reporting an overall increased risk of breast cancer, many women discontinued HRT. Despite the re-analysis of the results by subgroups of patients and updates with extended follow-up, much controversy remains, which we will analyze later in the text. Different types of estrogen or progestogen, as well as different formulations, doses, and durations, may play a role in HRT’s effects on breast tissue. Evidence states that conjugated equine estrogen (CEE), compared to estro-progestin therapy, shows a better profile risk (HR 0.79, CI 0.65–0.97) and that, among different type of progestins, those structurally related to testosterone show a higher risk (RR 3.35, CI 1.07–10.4). Chronic unopposed endometrial exposure to estrogen increases the risk of endometrial hyperplasia and cancer, whereas the association with progestins, especially in continuous combined regimen, seems to reduce the risk (RR 0.71, CI 0.56–0.90). HRT was also associated with a protective effect on colon cancer risk (HR 0.61, CI 0.42–0.87). Data about ovarian and cervical cancer are still controversial.


2006 ◽  
Vol 154 (1) ◽  
pp. 101-107 ◽  
Author(s):  
Kati Pentti ◽  
Risto Honkanen ◽  
Marjo T Tuppurainen ◽  
Lorenzo Sandini ◽  
Heikki Kröger ◽  
...  

Objectives: To analyze prospectively the association between hormone replacement therapy (HRT) and mortality in women before old age. Design and methods: A group of 11 667 women (91% of the age cohort of the area) aged 52–62 years from the population-based Kuopio Osteoporosis Risk Factor and Prevention Study were followed for 7 years in 1994–2001. Information about HRT use and health events was obtained from two repeated questionnaires in 1989 and 1994. Information about deaths and causes of death from the follow-up period was obtained from the Statistics Finland. Cox’s proportional-hazards models were used to calculate risk of death related to the use of HRT. Results: At the start of follow-up, 2203 women had used HRT >5 years, 3945 women ≤5 years and 5519 women had never used it. During the follow-up, 361 deaths occurred. Compared with non-users of HRT, the adjusted hazard ratio (HR) of death from any cause was 1.05 (95% confidence interval (CI) 0.80–1.36) in women who used HRT ≤5 years and 1.06 (95% CI 0.78–1.46) in women who used HRT >5 years. The adjusted HR for coronary heart disease (CHD) mortality in women who used HRT ≤5 years was 0.79 (95% CI 0.36–1.73), and in women who used HRT >5 years, 2.16 (95% CI 0.93–4.98). For breast cancer mortality the adjusted HR for ≤5 years of HRT use was 0.96 (95% CI 0.32–2.82) and 2.62 (95% CI 0.98–7.00) for >5 years of HRT use. Conclusions: History of HRT use does not affect overall or CHD mortality in women. More than 5 years of HRT use may increase the risk of breast cancer mortality.


2021 ◽  
Vol 12 ◽  
Author(s):  
Enrique Soto-Pedre ◽  
Moneeza K. Siddiqui ◽  
Cyrielle Maroteau ◽  
Adem Y. Dawed ◽  
Alex S. Doney ◽  
...  

AimsAtrial fibrillation (AF) is a risk for patients receiving thyroid hormone replacement therapy. No published work has focused on pharmacogenetics relevant to thyroid dysfunction and AF risk. We aimed to assess the effect of L-thyroxine on AF risk stratified by a variation in a candidate gene.Methods and ResultsA retrospective follow-up study was done among European Caucasian patients from the Genetics of Diabetes Audit and Research in Tayside Scotland cohort (Scotland, United Kingdom). Linked data on biochemistry, prescribing, hospital admissions, demographics, and genetic biobank were used to ascertain patients on L-thyroxine and diagnosis of AF. A GWAS-identified insulin receptor-INSR locus (rs4804416) was the candidate gene. Cox survival models and sensitivity analyses by taking competing risk of death into account were used. Replication was performed in additional sample (The Genetics of Scottish Health Research register, GoSHARE), and meta-analyses across the results of the study and replication cohorts were done. We analyzed 962 exposed to L-thyroxine and 5,840 unexposed patients who were rs4804416 genotyped. The rarer G/G genotype was present in 18% of the study population. The total follow-up was up to 20 years, and there was a significant increased AF risk for patients homozygous carriers of the G allele exposed to L-thyroxine (RHR = 2.35, P = 1.6e–02). The adjusted increased risk was highest within the first 3 years of exposure (RHR = 9.10, P = 8.5e–04). Sensitivity analysis yielded similar results. Effects were replicated in GoSHARE (n = 3,190).ConclusionHomozygous G/G genotype at the INSR locus (rs4804416) is associated with an increased risk of AF in patients on L-thyroxine, independent of serum of free thyroxine and thyroid-stimulating hormone serum concentrations.


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