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   2018| March-April  | Volume 20 | Issue 2  
    Online since March 1, 2018

 
 
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INVITED REVIEW
Randomized controlled trials – mechanistic studies of testosterone and the cardiovascular system
T Hugh Jones, Daniel M Kelly
March-April 2018, 20(2):120-130
DOI:10.4103/aja.aja_6_18  PMID:29442075
Testosterone deficiency is common in men with cardiovascular disease (CVD), and randomized placebo-controlled trials (RCTs) have reported beneficial effects of testosterone therapy on exercise-induced cardiac ischemia in chronic stable angina, functional exercise capacity, maximum oxygen consumption during exercise (VO2max) and muscle strength in chronic heart failure (CHF), shortening of the Q-T interval, and improvement of some cardiovascular risk factors. Testosterone deficiency is associated with an adverse CV risk profile and mortality. Clinical and scientific studies have provided mechanistic evidence to support and explain the findings of the RCTs. Testosterone is a rapid-onset arterial vasodilator within the coronary circulation and other vascular beds including the pulmonary vasculature and can reduce the overall peripheral systemic vascular resistance. Evidence has demonstrated that testosterone mediates this effect on vascular reactivity through calcium channel blockade (L-calcium channel) and stimulates potassium channel opening by direct nongenomic mechanisms. Testosterone also stimulates repolarization of cardiac myocytes by stimulating the ultra-rapid potassium channel-operated current. Testosterone improves cardiac output, functional exercise capacity, VO2maxand vagally mediated arterial baroreceptor cardiac reflex sensitivity in CHF, and other mechanisms. Independent of the benefit of testosterone on cardiac function, testosterone substitution may also increase skeletal muscle glucose metabolism and enhance muscular strength, both factors that could contribute to the improvement in functional exercise capacity may include improved glucose metabolism and muscle strength. Testosterone improves metabolic CV risk factors including body composition, insulin resistance, and hypercholesterolemia by improving both glucose utilization and lipid metabolism by a combination of genomic and nongenomic actions of glucose uptake and utilization expression of the insulin receptor, glucose transporters, and expression on regulatory enzymes of key metabolic pathways. The effect on high-density lipoprotein-cholesterol (HDL-C) differs between studies in that it has been found to fall, rise, or have no change in levels. Testosterone replacement can suppress the levels of circulating pro-inflammatory cytokines and stimulate the production of interleukin-10 (IL-10) which has anti-inflammatory and anti-atherogenic actions in men with CVD. No effect on C-reactive protein has been detected. No adverse effects on clotting factors have been detected. RCTs have not clearly demonstrated any significant evidence that testosterone improves or adversely affects the surrogate markers of atherosclerosis such as reduction in carotid intima thickness or coronary calcium deposition. Any effect of testosterone on prevention or amelioration of atherosclerosis is likely to occur over years as shown in statin therapy trials and not months as used in testosterone RCTs. The weight of evidence from long-term epidemiological studies supports a protective effect as evidenced by a reduction in major adverse CV events (MACEs) and mortality in studies which have treated men with testosterone deficiency. No RCT where testosterone has been replaced to the normal healthy range has reported a significant benefit or adverse effect on MACE nor has any recent meta-analysis.
  8,490 1,324 31
Trials of testosterone replacement reporting cardiovascular adverse events
Thiago Gagliano-Jucá, Shehzad Basaria
March-April 2018, 20(2):131-137
DOI:10.4103/aja.aja_28_17  PMID:28782738
The numbers of testosterone prescriptions written have increased several-fold worldwide, but the incidence of pathological hypogonadism due to hypothalamic, pituitary, and testicular disease has remained unchanged. Most of these prescriptions are being dispensed to middle-aged and older men who have experienced age-related decline in serum testosterone levels; a subset of the population in which benefits of testosterone replacement is at best, modest. Recently, some randomized controlled trials have reported increased cardiovascular events in men (mainly older men and those with prevalent cardiovascular disease) with testosterone use, and a few recent meta-analyses have confirmed these findings. In this review, we discuss trials of testosterone therapy that have reported higher cardiovascular events, relevant trials that have not reported increased cardiovascular events and large trials that have focused on cardiovascular risk (mainly atherosclerosis progression) as their main outcome. We also review findings from meta-analyses that have evaluated cardiovascular events in various testosterone trials. Finally, we discuss some potential mechanisms by which testosterone use might result in an increased cardiovascular risk. As none of the trials conducted to date were adequately powered to evaluate cardiovascular events, no firm conclusions can be drawn regarding the cardiovascular safety of testosterone therapy at this time. In the interim, we hope that this review will help practitioners make informed decisions regarding the care of their patients.
  8,008 483 2
Testosterone treatment and cardiovascular events in prescription database studies
Molly M Shores
March-April 2018, 20(2):138-144
DOI:10.4103/aja.aja_25_17  PMID:28816202
Over the past decade, there has been a substantial increase in the number of men who are treated with testosterone. Despite this increase in the use of testosterone, the risks of adverse cardiovascular events are unclear as meta-analyses have reported conflicting findings and no clinical studies have been large enough or long enough to adequately assess for cardiovascular risks. The goal of this paper is to review large prescription database studies of testosterone treatment and adverse cardiovascular events and mortality with the aim of providing some guidance for clinicians and researchers in this controversial area.
  4,860 583 6
Testosterone and its metabolites: differential associations with cardiovascular and cerebrovascular events in men
Bu B Yeap
March-April 2018, 20(2):109-114
DOI:10.4103/aja.aja_50_17  PMID:29199649
As men grow older, circulating testosterone declines while the incidence of cardiovascular disease increases. Thus, the role of sex hormones as biomarkers, and possibly contributing factors to clinical manifestations of cardiovascular disease in the increasing demographic of aging men, has attracted considerable interest. This review focuses on observational studies of endogenous androgens, namely circulating testosterone and dihydrotestosterone, which have examined their associations with cardiovascular events such as myocardial infarction and stroke. Studies which have examined the associations of endogenous estrogens, namely circulating estradiol, with these outcomes are also discussed. In large prospective cohort studies of predominantly middle-aged and older men, lower circulating testosterone consistently predicts higher incidence of cardiovascular events. Of note, both lower circulating testosterone and lower dihydrotestosterone are associated with higher incidence of stroke. These associations are less apparent when myocardial infarction is considered as the outcome. Results for estradiol are inconsistent. Lower circulating testosterone has been shown to predict higher cardiovascular disease-related mortality, as has lower circulating dihydrotestosterone. It is possible that the relationship of circulating androgens to cardiovascular events or mortality outcomes may be U-shaped rather than linear, with an optimal range defining men at lowest risk. Epidemiological studies are observational in nature and do not prove causality. Associations observed in studies of endogenous androgens need not necessarily translate into similar effects of exogenous androgens. Rigorous randomized controlled trials are needed to clarify the effects of testosterone treatment on cardiovascular risk in men.
  4,423 720 8
Would male hormonal contraceptives affect cardiovascular risk?
Michael Zitzmann
March-April 2018, 20(2):145-148
DOI:10.4103/aja.aja_2_18  PMID:29384141
The aim of hormonal male contraception is to prevent unintended pregnancies by suppressing spermatogenesis. Hormonal male contraception is based on the principle that exogenous administration of androgens and other hormones such as progestins suppress circulating gonadotropin concentrations, decreasing testicular Leydig cell and Sertoli cell activity and spermatogenesis. In order to achieve more complete suppression of circulating gonadotropins and spermatogenesis, a progestin has been added testosterone to the most recent efficacy trials of hormonal male contraceptives. This review focusses on the potential effects of male hormonal contraceptives on cardiovascular risk factors, lipids and body composition, mainly in the target group of younger to middle-aged men. Present data suggest that hormonal male contraception can be reasonably regarded as safe in terms of cardiovascular risk. However, as all trials have been relatively short (< 3 years), a final statement regarding the cardiovascular safety of hormonal male contraception, especially in long-term use, cannot be made. Older men with at high risk of cardiovascular event might not be good candidates for hormonal male contraception. The potential adverse effects of hormonal contraceptives on cardiovascular risk appear to depend greatly on the choice of the progestin in regimens for hormonal male contraceptives. In the development of prospective hormonal male contraception, data on longer-term cardiovascular safety will be essential.
  4,556 549 2
ORIGINAL ARTICLES
Phosphoglycerate mutase 1 knockdown inhibits prostate cancer cell growth, migration, and invasion
Yao-An Wen, Bo-Wei Zhou, Dao-Jun Lv, Fang-Peng Shu, Xian-Lu Song, Bin Huang, Chong Wang, Shan-Chao Zhao
March-April 2018, 20(2):178-183
DOI:10.4103/aja.aja_57_17  PMID:29271400
Phosphoglycerate mutase 1 (PGAM1) is upregulated in many cancer types and involved in cell proliferation, migration, invasion, and apoptosis. However, the relationship between PGAM1 and prostate cancer is poorly understood. The present study investigated the changes in PGAM1 expression in prostate cancer tissues compared with normal prostate tissues and examined the cellular function of PGAM1 and its relationship with clinicopathological variables. Immunohistochemistry and Western blotting revealed that PGAM1 expression was upregulated in prostate cancer tissues and cell lines. PGAM1 expression was associated with Gleason score (P = 0.01) and T-stage (P = 0.009). Knockdown of PGAM1 by siRNA in PC-3 and 22Rv1 prostate cancer cell lines inhibited cell proliferation, migration, and invasion and enhanced cancer cell apoptosis. In a nude mouse xenograft model, PGAM1 knockdown markedly suppressed tumor growth. Deletion of PGAM1 resulted in decreased expression of Bcl-2, enhanced expression of Bax, caspases-3 and inhibition of MMP-2 and MMP-9 expression. Our results indicate that PGAM1 may play an important role in prostate cancer progression and aggressiveness, and that it might be a valuable marker of poor prognosis and a potential therapeutic target for prostate cancer.
  4,587 486 12
A retrospective review of single-institution outcomes with robotic-assisted microsurgical varicocelectomy
Andrew McCullough, Leon Elebyjian, Joseph Ellen, Clay Mechlin
March-April 2018, 20(2):189-194
DOI:10.4103/aja.aja_45_17  PMID:29086759
We report the largest single-center experience with robotic-assisted microscopic varicocelectomy (RAMV) in male infertility. From August 2012 to February 2015, men with infertility of at least a year and varicoceles underwent RAMV by a single surgeon. Varicocele was diagnosed on physical examination and confirmed by ultrasound by a single ultrasonographer. Preoperative hormone panel, semen analyses, and testicular Doppler ultrasound were obtained from all men and repeated at 3 months. One hundred and forty consecutive men (258 varicocelectomies) were included. Mean age and duration of infertility was 36.4 and 2.8 years, respectively. Median total and free testosterone increased by 145 ng dl−1 and 4.3 pcg ml−1 (44.3%), respectively (P < 0.0001). Median sperm concentration increased by 37.3% (P < 0.03). Median sperm motility and morphology did not significantly change. Median left and right testicular volume increased by 22.3% (P < 0.0001) and 12.6% (P < 0.0006), respectively. Hydroceles occurred 0.8% of procedures. We had no testicular artery injuries. Persistence of varicocele by Doppler ultrasound was 9.6%. Only 37.3% of patients required pain medications postoperatively. We concluded that RAMV is a safe and effective alternative for varicocele repair with outcomes comparable to historical traditional microsurgical approach.
  4,395 529 10
INVITED REVIEW
Endogenous testosterone and mortality risk
Emily J Meyer, Gary Wittert
March-April 2018, 20(2):115-119
DOI:10.4103/aja.aja_70_17  PMID:29384142
In men, obesity and metabolic complications are associated with lower serum testosterone (T) and dihydrotestosterone (DHT) and an increased risk of, and mortality from, multiple chronic diseases in addition to cardiovascular disease (CVD). The causal interrelationships between these factors remain a matter of debate. In men with untreated congenital and lifelong forms of hypogonadotropic hypogonadism, there appears to be no increased risk. Men with Klinefelter's syndrome have an increased risk of various types of cancers, as well as CVD, which persist despite T therapy. In the absence of pathology of the hypothalamic–pituitary–gonadal axis, the effect of modest reductions in serum T in aging men is unclear. The prevalence of low serum T concentrations is high in men with cancer, renal disease, and respiratory disease and is likely to be an indicator of severity of systemic disease, not hypogonadism. Some population-based studies have found low serum T to be associated with a higher risk of deaths attributed to cancer, renal disease, and respiratory disease, while others have not. Although a meta-analysis of longitudinal studies has shown an association between low serum T and all-cause mortality, marked heterogeneity between studies limited a firm conclusion. Therefore, while a decrease in T particularly occurring later in life may be associated with an increase in all-cause and specific types of mortality in men, the differential effects, if any, of T and other sex steroids as compared to health and lifestyle factors are unknown at the current time.
  4,198 636 4
ORIGINAL ARTICLES
PSA time to nadir as a prognostic factor of first-line docetaxel treatment in castration-resistant prostate cancer: evidence from patients in Northwestern China
Kai-Jie Wu, Xin-Qi Pei, Ge Tian, Da-Peng Wu, Jin-Hai Fan, Yu-Mei Jiang, Da-Lin He
March-April 2018, 20(2):173-177
DOI:10.4103/aja.aja_34_17  PMID:28905815
Docetaxel-based chemotherapy remains the first-line treatment for patients with metastatic castration-resistant prostate cancer (mCRPC) in China; however, the prognostic factors associated with effects in these patients are still controversial. In this study, we retrospectively reviewed the data from 71 eligible Chinese patients who received docetaxel chemotherapy from 2009 to 2016 in our hospital and experienced a reduction of prostate-specific antigen (PSA) level ≥50% during the treatment and investigated the potential role of time to nadir (TTN) of PSA. TTN was defined as the time from start of chemotherapy to the nadir of PSA level during the treatment. Multivariable Cox regression models and Kaplan-Meier analysis were used to predict overall survival (OS). In these patients, the median of TTN was 17 weeks. Patients with TTN ≥17 weeks had a longer response time to chemotherapy compared to TTN <17 weeks (42.83 vs 21.50 weeks, P < 0.001). The time to PSA progression in patients with TTN ≥17 weeks was 11.44 weeks compared to 5.63 weeks when TTN was <17 weeks. We found several factors to be associated with OS, including TTN (hazard ratio [HR]: 3.937, 95% confidence interval [CI]: 1.502-10.309, P = 0.005), PSA level at the diagnosis of cancer (HR: 4.337, 95% CI: 1.616-11.645, P = 0.004), duration of initial androgen deprivation therapy (HR: 2.982, 95% CI: 1.104-8.045, P = 0.031), neutrophil-to-lymphocyte ratio (HR: 3.963, 95% CI: 1.380-11.384, P = 0.011), and total PSA response (Class 1 [<0 response] compared to Class 2 [0-50% response], HR: 3.978, 95% CI: 1.278-12.387, P = 0.017). In conclusion, TTN of PSA remains an important prognostic marker in predicting therapeutic outcome in Chinese population who receive chemotherapy for mCRPC and have >50% PSA remission.
  4,168 513 4
External validation and newly development of a nomogram to predict overall survival of abiraterone-treated, castration-resistant patients with metastatic prostate cancer
Yun-Jie Yang, Guo-Wen Lin, Gao-Xiang Li, Bo Dai, Ding-Wei Ye, Jun-Long Wu, Hu-Yang Xie, Yao Zhu
March-April 2018, 20(2):184-188
DOI:10.4103/aja.aja_39_17  PMID:29111539
Abiraterone acetate is approved for the treatment of castration-resistant prostate cancer (CRPC); however, its effects vary. An accurate prediction model to identify patient groups that will benefit from abiraterone treatment is therefore urgently required. The Chi model exhibits a good profile for risk classification, although its utility for the chemotherapy-naive group is unclear. This study aimed to externally validate the Chi model and develop a new nomogram to predict overall survival (OS). We retrospectively analyzed a cohort of 110 patients. Patients were distributed among good-, intermediate-, and poor-risk groups, according to the Chi model. The good-, intermediate-, and poor-risk groups had a sample size of 59 (53.6%), 34 (30.9%), and 17 (15.5%) in our dataset, and a median OS of 48.4, 29.1, and 10.5 months, respectively. The C-index of external validation of Chi model was 0.726. Univariate and multivariate analyses identified low hemoglobin concentrations (<110 g l−1), liver metastasis, and a short time interval from androgen deprivation therapy to abiraterone initiation (<36 months) as predictors of OS. Accordingly, a new nomogram was developed with a C-index equal to 0.757 (95% CI, 0.678–0.836). In conclusion, the Chi model predicted the prognosis of abiraterone-treated, chemotherapy-naive patients with mCRPC, and we developed a new nomogram to predict the overall survival of this group of patients with less parameters.
  3,963 505 4
Andrographolide sensitizes prostate cancer cells to TRAIL-induced apoptosis
Ruo-Jing Wei, Xin-Shi Zhang, Da-Lin He
March-April 2018, 20(2):200-204
DOI:10.4103/aja.aja_30_17  PMID:28869219
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a promising agent for anticancer therapy. The identification of small molecules that can establish the sensitivity of prostate cancer (PCa) cells to TRAIL-induced apoptosis is crucial for the targeted treatment of PCa. PC3, DU145, JAC-1, TsuPr1, and LNCaP cells were treated with Andrographolide (Andro) and TRAIL, and the apoptosis was measured using the Annexin V/PI double staining method. Real time-polymerase chain reaction (PCR) and Western blot analysis were performed to measure the expression levels of target molecules. RNA interference technique was used to down-regulate the expression of the target protein. We established a nude mouse xenograft model of PCa, which was used to measure the caspase-3 activity in the tumor cells using flow cytometry. In this research study, our results demonstrated that Andro preferentially increased the sensitivity of PCa cells to TRAIL-induced apoptosis at subtoxic concentrations, and the regulation mechanism was related to the up-regulation of DR4. In addition, it also increased the p53 expression and led to the generation of reactive oxygen species (ROS) in the cells. Further research revealed that the DR4 inhibition, p53 expression, and ROS generation can significantly reduce the apoptosis induced by the combination of TRAIL and Andro in PCa cells. In conclusion, Andro increases the sensitivity of PCa cells to TRAIL-induced apoptosis through the generation of ROS and up-regulation of p53 and then promotes PCa cell apoptosis associated with the activation of DR4.
  3,951 502 16
An in vitro prototype of a porcine biomimetic testis-like cell culture system: a novel tool for the study of reassembled Sertoli and Leydig cells
Iva Arato, Giovanni Luca, Francesca Mancuso, Catia Bellucci, Cinzia Lilli, Mario Calvitti, Barbara C Hansen, Domenico Milardi, Giuseppe Grande, Riccardo Calafiore
March-April 2018, 20(2):160-165
DOI:10.4103/aja.ja_47_17  PMID:29148520
At present, there is no reliable in vitro assembled prepubertal testis-like biomimetic organ culture system designed to assess the functional effects of human gonadotropins on Sertoli and Leydig cells. Spermatogenesis is regulated by endocrine, paracrine, and juxtacrine factors (testicular cross-talk), mainly orchestrated by gonadotropins such as luteinizing hormone (LH) and follicle-stimulating hormone (FSH) that play a pivotal role by stimulating Leydig and Sertoli cells, respectively. The aim of our study was to set up an in vitro prepubertal porcine bioengineered construct as a new model for experimental studies on reassembled Sertoli and Leydig cells. We have evaluated Sertoli and Leydig cells obtained from 15- to 20-day-old neonatal pig testes in terms of purity and function. Subsequently, purified Sertoli and enriched Leydig cells were subjected to coincubation to obtain an in vitro prepubertal porcine testis-like culture system. We performed enzyme-linked immunosorbent assay (ELISA) for anti-Müllerian hormone (AMH), inhibin B, and testosterone secretion in the medium, and Real-Time PCR analysis of AMH, inhibin B, FSH-r, aromatase, LHr, and 3β-HSD mRNA expression levels. This in vitro testis-like system was highly responsive to the effects of human gonadotropins and testosterone. AMH mRNA expression and secretion declined, and inhibin-B increased, while FSH-receptor expression was downregulated upon FSH/LH exposure/treatment. Finally, the production of testosterone was increased selectively upon LH treatment. In summary, our proposed model could help to better determine the action of human gonadotropins on Sertoli and Leydig cells. The potential usefulness of the system for shedding light into male infertility-related issues is evident.
  3,915 481 12
LETTERS TO THE EDITOR
Diagnosis of a Chinese man with 45,X/46,X,i(Y)(q10)/47,X,i(Y) (q10) ×2 mosaic Turner syndrome
Yan-Wei Sha, Lu Ding, Zhi-Yong Ji, Yun-Sheng Ge, Hui Kong, Qing Zhang, Yu-Lin Zhou, Ping Li
March-April 2018, 20(2):205-207
DOI:10.4103/1008-682X.193162  PMID:28091398
  4,010 371 -
ORIGINAL ARTICLES
Lipoxin A4 improves erectile dysfunction in rats with type I diabetes by inhibiting oxidative stress and corporal fibrosis
Kai Cui, Zhe Tang, Chuan-Chang Li, Tao Wang, Ke Rao, Shao-Gang Wang, Ji-Hong Liu, Zhong Chen
March-April 2018, 20(2):166-172
DOI:10.4103/aja.aja_49_17  PMID:29111541
Previous studies have shown that oxidative stress and corporal fibrosis in penile tissues of rats were key pathological factors of erectile dysfunction induced by diabetic mellitus (DMED). Lipoxin A4 (LXA4) was reported to inhibit oxidative stress and fibrosis diseases, while whether it could exert a protective role on erectile function was not clear. Type I diabetic mellitus (DM) was induced in thirty male 10-week-old Sprague-Dawley rats using streptozotocin. Ten weeks later, twenty-two rats with DMED confirmed by an apomorphine test were divided into two groups: the DMED group (n = 11) and the DMED + LXA4 group (n = 11; LXA4 injection daily for 4 weeks). In addition, another ten age-matched rats formed the Control group. We found that erectile function was significantly impaired in the DMED group compared with the Control group, but was improved in the DMED + LXA4 group. Similarly, the over-activated oxidative stress and impaired endothelial function in the DMED group were both improved in the DMED + LXA4 group. Moreover, the DMED group showed serious corporal fibrosis, which was also inhibited by the treatment of LXA4 in the DMED + LXA4 group. Taken together, LXA4 could exert an inhibition role on oxidative stress and fibrosis to improve DMED effectively.
  3,719 457 15
INVITED EDITORIAL
Why is understanding the relationship of testosterone to cardiovascular risk so important?
Bu B Yeap, Bradley D Anawalt
March-April 2018, 20(2):107-108
DOI:10.4103/aja.aja_71_17  PMID:29405170
  3,543 585 1
ORIGINAL ARTICLES
The expression of the new epididymal luminal protein of PDZ domain containing 1 is decreased in asthenozoospermia
A-Juan Liang, Gui-Shuan Wang, Ping Ping, Shuang-Gang Hu, Yu Lin, Yi Ma, Zheng-Zheng Duan, Han-Shu Wang, Fei Sun
March-April 2018, 20(2):154-159
DOI:10.4103/aja.aja_65_17  PMID:29405165
Spermatozoa are not mature until they transit the epididymis where they acquire motility and the ability to fertilize an egg through sequential modifications. The epididymis has three functional regions, caput, corpus, and cauda, and the luminal proteins of the epididymis play important roles in the above modifications. However, the proteins with differential enrichment between the caput and cauda are still largely unknown. To reveal the functions of the caput and cauda during sperm maturation, luminal proteins from caput and cauda of mice were analyzed by isobaric tag for relative and absolute quantitation (iTRAQ). Overall, 128 differentially enriched proteins were found, of which 46 were caput enriched and 82 were cauda enriched. Bioinformatic analysis showed that lipid metabolism was active in the caput; while anion- and cation-binding activity and phosphorus and organophosphate metabolism were active in the cauda. A new epididymal luminal protein, the caput-enriched PDZ domain containing 1 (Pdzk1), also named Na+/H+ exchange regulatory cofactor 3 (NHERF3), which plays a critical role in cholesterol metabolism and carnitine transport, was found in the lipid metabolism. Western blotting and immunofluorescence analyses showed that Pdzk1 was expressed in the epididymis but not in the testis, and localized at the middle piece of the sperm tail. Pdzk1 protein level was also reduced in the spermatozoa in case of asthenozoospermic patients compared with that in normozoospermic men, suggesting that Pdzk1 may participate in sperm maturation regulation and may be associated with male infertility. These results may provide new insights into the mechanisms of sperm maturation and male infertility.
  3,505 569 1
Association of subcutaneous testosterone pellet therapy with developing secondary polycythemia
Katherine Lang Rotker, Michael Alavian, Bethany Nelson, Grayson L Baird, Martin M Miner, Mark Sigman, Kathleen Hwang
March-April 2018, 20(2):195-199
DOI:10.4103/aja.aja_51_17  PMID:29205178
A variety of methods for testosterone replacement therapy (TRT) exist, and the major potential risks of TRT have been well established. The risk of developing polycythemia secondary to exogenous testosterone (T) has been reported to range from 0.4% to 40%. Implantable T pellets have been used since 1972, and secondary polycythemia has been reported to be as low as 0.4% with this administration modality. However, our experience has suggested a higher rate. We conducted an institutional review board-approved, single-institution, retrospective chart review (2009–2013) to determine the rate of secondary polycythemia in 228 men treated with subcutaneously implanted testosterone pellets. Kaplan–Meyer failure curves were used to estimate time until the development of polycythemia (hematocrit >50%). The mean number of pellets administered was 12 (range: 6–16). The mean follow-up was 566 days. The median time to development of polycythemia whereby 50% of patients developed polycythemia was 50 months. The estimated rate of polycythemia at 6 months was 10.4%, 12 months was 17.3%, and 24 months was 30.2%. We concluded that the incidence of secondary polycythemia while on T pellet therapy may be higher than previously established.
  3,388 439 4
INVITED COMMENTARY
Testosterone replacement therapy: Dilemmas and challenges in China and Asia
Qi An, Yi-Qun Gu
March-April 2018, 20(2):149-151
DOI:10.4103/aja.aja_16_17  PMID:29405166
  3,233 372 1
LETTERS TO THE EDITOR
Fertility achieved through in vitro fertilization in a male patient with 48,XXYY syndrome
De-Feng Liu, Lian-Ming Zhao, Kai Hong, Jia-Ming Mao, Yu-Zhuo Yang, Zhe Zhang, Hui Jiang
March-April 2018, 20(2):208-209
DOI:10.4103/aja.aja_44_17  PMID:28980534
  3,218 335 1
INVITED EDITORIAL
Conclusions about testosterone therapy and cardiovascular risk
Bradley D Anawalt, Bu B Yeap
March-April 2018, 20(2):152-153
DOI:10.4103/aja.aja_7_18  PMID:29457599
  3,089 434 3
LETTERS TO THE EDITOR
Globozoospermic infertility associated with balanced DPY19L2 translocation/gene deletion at the chromosomal breakpoint
Yan-Wei Sha, Li-Bin Mei, Liang-Kai Zheng, Rui-Hua Tian, Lu Ding, Zhi-Yong Ji, Qing Zhang, Ping Li
March-April 2018, 20(2):210-211
DOI:10.4103/1008-682X.196314  PMID:28272055
  3,144 324 1
INVITED COMMENTARY
Commentary on “Nondegloving technique for Peyronie's disease with penile prosthesis implantation and double dorsal-ventral patch graft”
Gerard D Henry, Kavina Jani
March-April 2018, 20(2):212-212
DOI:10.4103/aja.aja_53_17  PMID:29205179
  2,780 350 -
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