American Association of Clinical Endocrinologists Medical Guidelines for Clinical Practice for the Evaluation and Treatment of Hypogonadism in Adult Male Patients—2002 Update

Petak, Steven M.; Nankin, Howard R.; Spark, Richard F.; Swerdloff, Ronald S.; Rodriguez‐Rigau, Luis J.; Anderson, Robert J.; Bergman, Donald A.; Garber, Jeffrey R.; Hamilton, Carlos R.; Hershon, Kenneth S.; Jovanovič, Lois; Kleerekoper, Michael; Mechanick, Jeffrey I.; Palumbo, Pasquale; Peters, Anne L.; Rettinger, Herbert I.; Rodbard, Helena W.; Rubenstein, Harvey A.; Seibel, John A.; Tourtelot, John B.

doi:10.4158/ep.8.6.439

Cited by 281 publications

(56 citation statements)

References 70 publications

(63 reference statements)

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“…These clinics are staffed by board certified physicians in various specialties as well as physician assistants. The protocols for determining treatment are specific to Low T Centers, modified from established guidelines from both the Endocrine Society and the American Association of Clinical Endocrinologists [4, 5]. Patients are selected for treatment if deemed hypogonadal, defined as total testosterone <350 ng/dL or free testosterone <10 ng/mL.…”

Section: Introductionmentioning

confidence: 99%

Myocardial Infarction and Stroke Risk in Young Healthy Men Treated with Injectable Testosterone

Tan

Cook²,

Reilly³

2015

International Journal of Endocrinology

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This study was conducted to examine the association between testosterone therapy and new myocardial infarction (MI) and stroke events in a series of patients treated at Low T Centers across the United States, consisting of mainly young (mean age = 46), otherwise, healthy men. Electronic medical records were queried between the years 2009 and 2014 to identify patients diagnosed with hypogonadism, MI, and stroke, as indicated by ICD-9 codes. The incidence of MI and stroke events was compared to community-based registries. 39,936 patients recruited from 40 Low T Centers across the United States were treated and 19,968 met eligibility criteria for receiving testosterone treatment. The incidence rate ratio (IRR) for MI in testosterone- (T-) treated versus nontreated patients was 0.14 (C.I. = 0.08 to 0.18, P < 0.0001) whereas the IRR for stroke for T-treated versus nontreated patients was 0.11 (C.I. = 0.02 to 0.13, P < 0.0001). There was no evidence of worsening preexisting MI or stroke in patients treated with testosterone. The experience in Low T Centers shows that, in an injectable testosterone patient registry, testosterone is generally safe for younger men who do not have significant risk factors. Of patients that developed MI with testosterone, there was no association with testosterone or hematocrit levels.

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Section: Introductionmentioning

confidence: 99%

Myocardial Infarction and Stroke Risk in Young Healthy Men Treated with Injectable Testosterone

Tan

Cook²,

Reilly³

2015

International Journal of Endocrinology

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“…ACE converts angiotensin (Ang)- [1][2][3][4][5][6][7][8][9][10] into Ang- [1][2][3][4][5][6][7][8], which can promote vasoconstriction by acting on the angiotensin type 1 receptor (AT 1 ) or vasodilation via the angiotensin type 2 receptor (AT 2 ). ACE2 is a monocarboxypeptidase that catabolizes the conversion of Ang- [1][2][3][4][5][6][7][8] to the heptapeptide Ang- [1][2][3][4][5][6][7], which is described to have vasodilatory effects by binding MAS or MAS-related G protein-coupled receptors. ACE2 also converts Ang- [1][2][3][4][5][6][7][8][9][10] into the nonopeptide Ang- [1][2][3][4][5][6]…”

mentioning

confidence: 99%

“…ACE2 is a monocarboxypeptidase that catabolizes the conversion of Ang- [1][2][3][4][5][6][7][8] to the heptapeptide Ang- [1][2][3][4][5][6][7], which is described to have vasodilatory effects by binding MAS or MAS-related G protein-coupled receptors. ACE2 also converts Ang- [1][2][3][4][5][6][7][8][9][10] into the nonopeptide Ang- [1][2][3][4][5][6][7][8][9], also described to have vasodilatory effects by binding to AT 2 (15). ACE2 has been identified as an important reninangiotensin system (RAS) regulator, which is a peptidergic system that regulates extracellular fluid volume and controls homeostasis of the cardiovascular and renal systems (10,15,31).…”

mentioning

confidence: 99%

“…Likewise, supplementation with E2 caused a downregulation of ACE2 mRNA expression in the mouse kidney, but not in the lung, showing that sex hormones can also regulate ACE2 in a tissue-specific manner (30). However, under pathological conditions, several studies have found that Ang- [1][2][3][4][5][6][7] levels are higher in women than in men, particularly in those with hypertension (45), indicating a higher ACE2 activity. Thus, increased levels of this vasodilator could also contribute to female protection from Ang-[1-8]-induced hypertension (45).…”

mentioning

confidence: 99%

“…In this regard, a recent study in mice showed that ACE2 plays a larger role in protecting females than males from Ang- [1][2][3][4][5][6][7][8]-induced hypertension by increasing catabolism of Ang- [1][2][3][4][5][6][7][8] and by downregulating AT 1 (19). Hypertension is a recognized major risk factor for COVID-19 morbidity and mortality (26).…”

mentioning

confidence: 99%

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Let’s talk about sex in the context of COVID-19

Gargaglioni

Marques

2020

Journal of Applied Physiology

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In recent months, the coronavirus disease 2019 (COVID-19) pandemic has sent many countries into crisis. Studies have shown that this virus causes worse outcomes and a higher mortality in men than in women. It has been recognized that sex can affect the immune response to a pathogenic agent, as well as the susceptibility for some respiratory diseases. These different responses in males and females may be related to the actions of sex hormones. Angiotensin-converting enzyme 2 (ACE2) acts as the receptor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes COVID-19. The expression of ACE2 is influenced by sex hormones; therefore, we discuss in this article that this could be one of the reasons why COVID-19 is more prevalent in men than in women.

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