Testosterone therapy increases muscle mass in men with cirrhosis and low testosterone: A randomised controlled trial

Sinclair, Marie; Grossmann, Mathis; Hoermann, Rudolf; Angus, Peter W; Gow, Paul J

doi:10.1016/j.jhep.2016.06.007

Cited by 213 publications

(187 citation statements)

References 53 publications

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“…These findings are congruent with data reported by Svartberg et al [52] in which T therapy demonstrated significant improvement in LBM by approximately 4.2 kg and reduced fat mass with concomitant reduction in total body mass. In severely ill patients with liver cirrhosis and sarcopenia, T therapy resulted in an increase in LBM by 4.7 kg after one year of T therapy [78]. Additional evidence is surmised from studies in which T therapy in men with medically induced TD results in a dose-dependent increase in muscle mass and reduction in FM in young and elderly men [79].…”

Section: Benefits Of T Therapy In Men With Tdmentioning

confidence: 99%

Testosterone therapy in men with testosterone deficiency: Are we beyond the point of no return?

Traish

2016

Investig Clin Urol

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Although testosterone therapy in men with testosterone deficiency was introduced in the early 1940s, utilization of this effective treatment approach in hypogonadal men is met with considerable skepticism and resistance. Indeed, for decades, the fear that testosterone may cause prostate cancer has hampered clinical progress in this field. Nevertheless, even after considerable knowledge was acquired that this fear is unsubstantiated, many in the medical community remain hesitant to utilize this therapeutic approach to treat men with hypogonadism. As the fears concerning prostate cancer have subsided, a new controversy regarding use of testosterone therapy and increase in cardiovascular disease was introduced. Although the new controversy was based on one ill-fated clinical trial, one meta-analysis with studies that utilized unapproved formulation in men with liver cirrhosis, and two retrospective studies with suspect or nonvalidated statistical methodologies and database contaminations, the flames of such controversy were fanned by the lay press and academics alike. In this review we discuss the adverse effect of testosterone deficiency and highlight the numerous proven benefits of testosterone therapy on men's health and debunk the myth that testosterone therapy increases cardiovascular risk. Ultimately, we believe that there is considerable scientific and clinical evidence to suggest that testosterone therapy is safe and effective with restoration of physiological levels in men with testosterone deficiency, irrespective of its etiology.

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Section: Benefits Of T Therapy In Men With Tdmentioning

confidence: 99%

Testosterone therapy in men with testosterone deficiency: Are we beyond the point of no return?

Traish

2016

Investig Clin Urol

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“…Testosterone was the focus of many early trials because it was found to be significantly decreased in men with cirrhosis. Recently, a 1‐year controlled clinical trial of intramuscular testosterone in male ESLD patients with low serum testosterone demonstrated that testosterone safely increased muscle mass . This finding was supported by a second trial using a transdermal approach .…”

Section: Interventions Targeting Sarcopenia and Physical Fitnessmentioning

confidence: 91%

Exercise and physical activity for patients with end‐stage liver disease: Improving functional status and sarcopenia while on the transplant waiting list

Duarte‐Rojo¹,

et al. 2017

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and physical deconditioning are frequent complications in patients with cirrhosis and end-stage liver disease (ESLD). They are the end result of impaired dietary intake, chronic inflammation, altered macronutrient and micronutrient metabolism, and low physical activity. Frailty is the end result of prolonged sarcopenia and physical deconditioning. It severely affects a patient's functional status and presents in approximately 1 in 5 patients on the liver transplantation waiting list. Sarcopenia, poor physical fitness/cardiopulmonary endurance (CPE), and frailty are all associated with increased mortality in ESLD. Clinical trials addressing the usefulness of exercise in patients with cirrhosis have shown that it improves the metabolic syndrome, sarcopenia, CPE, health-related quality of life, and hepatic venous pressure gradient. Although evidence on the benefits of exercise on clinical outcomes derived from large clinical trials is still missing, based on existing literature from multiple medical subspecialties, we believe that an exercise program coupled to a tailored nutritional intervention benefits both cardiopulmonary and musculoskeletal functions, ultimately translating into improved functional status, sense of well-being, and possibly less complications from portal hypertension. In conclusion, although supervised exercise training is the prevailing approach to manage ESLD patients, such intervention is not sustainable or feasible for most patients. Innovative home-based physical activity interventions may be able to effectively reach a larger number of patients.Liver Transplantation 24 122-139 2018 AASLD.

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“…Both growth hormone and testosterone are known to inhibit myostatin expression and signaling responses [101, 102] but it is not known if these hormonal alterations of cirrhosis also contribute to the impaired protein synthesis and increased myostatin expression in cirrhosis. A recent randomized trial showed that testosterone supplementation in male cirrhotics did result in an increase in lean body mass but not survival [103]. …”

Section: Mechanisms Of Skeletal Muscle Loss In Cirrhosismentioning

confidence: 99%

Sarcopenia from mechanism to diagnosis and treatment in liver disease

Dasarathy

Merli

2016

Journal of Hepatology

480

578

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Sarcopenia or loss of skeletal muscle mass is the major component of malnutrition and is a frequent complication in cirrhosis that adversely affects clinical outcomes including survival, quality of life, development of other complications and post liver transplantation survival. Radiological image analysis is currently used to diagnose sarcopenia in cirrhosis. Nutrient supplementation and physical activity are used to counter sarcopenia but have not been consistently effective because the underlying molecular and metabolic abnormalities persist or are not influenced by these treatments. Even though alterations in food intake, hypermetabolism, alterations in amino acid profiles, endotoxemia, accelerated starvation and decreased mobility may all contribute to sarcopenia in cirrhosis, hyperammonemia as a possible mediator of the liver-muscle axis has recently gained attention Increased muscle ammonia causes: cataplerosis of α-ketoglutarate, increased transport of leucine in exchange for glutamine, impaired signaling by leucine, increased expression of myostatin, a TGFβ superfamily member and an increased phosphorylation of eukaryotic initiation factor 2α, mitochondrial dysfunction, increased reactive oxygen species that decrease protein synthesis and increased autophagy mediated proteolysis. These molecular and metabolic alterations may contribute to the anabolic resistance and inadequate response to nutrient supplementation in cirrhosis. Central and skeletal muscle fatigue contributes to impaired exercise capacity and responses. Use of proteins with low ammoniagenic potential, leucine enriched amino acid supplementation, long term ammonia lowering strategies and a combination of resistance and endurance exercise to increase muscle mass and function may target the molecular abnormalities in the muscle. Strategies targeting endotoxemia and the gut microbiome need further evaluation.

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Testosterone therapy increases muscle mass in men with cirrhosis and low testosterone: A randomised controlled trial

Cited by 213 publications

References 53 publications

Testosterone therapy in men with testosterone deficiency: Are we beyond the point of no return?

Testosterone therapy in men with testosterone deficiency: Are we beyond the point of no return?

Exercise and physical activity for patients with end‐stage liver disease: Improving functional status and sarcopenia while on the transplant waiting list

Sarcopenia from mechanism to diagnosis and treatment in liver disease

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