Prevalence of Low Lean Mass in Patients With Adult Growth Hormone Deficiency With or Without Low-Dose Growth Hormone Therapy

Xiaoya Zheng; Qingfeng Cheng; Jian Long; Yunting Wang; Lilin Gong; Qiang Wei; Rong Luo; Kun Liao; Wei Ren

Disclosures

Clin Endocrinol. 2019;90(6):834-841. 

In This Article

Abstract and Introduction

Abstract

Objective: The importance of muscle mass has been emphasized in various studies, and growth hormone (GH) deficiency is tightly associated with lean mass loss. Therefore, we aimed to investigate the prevalence of low lean mass in patients with adult growth hormone deficiency (AGHD) who received or did not receive GH therapy.

Methods: In this retrospective study, we included patients diagnosed with AGHD by using the insulin tolerance test (ITT) in our hospital. Patients without completed follow-up data were excluded, and data for 56 patients were analysed. Twenty-six patients who had received GH therapy for more than 6 months, based on the medical record, were included in the GH group and received recombinant human growth hormone (rhGH) at a dose of 0.5 IU/d. Thirty patients who had not previously received GH treatment were included in the non-GH group. Many anthropometric and blood biochemical indicators were measured. Body composition was measured on a dual-energy X-ray-absorptiometry (DXA) scanner. Low lean mass was defined as a skeletal muscle index (SMI) <7.0 kg/m2 in males or 5.7 kg/m2 in females. Statistical analyses were performed using GraphPad Prism 5.0.

Results: Compared to the non-GH group, the patients who received GH therapy had significantly lower total cholesterol (TC), low-density lipoprotein cholesterol (LDL-c) and fasting plasma glucose (FPG). The percentage of patients with low lean mass in GH and non-GH groups was 30.77% and 60%, respectively. The percentage of total lean was lower in the GH group than in the non-GH group, but the difference in total lean mass was not statistically significant. Conversely, patients with GH treatment had significantly lower fat mass and percentage than non–GH-treated patients (P < 0.05). The GH group had significantly higher serum levels of both IGF-1 and IGFBP3. Moreover, both IGF-1 and IGFBP3 were significantly correlated with SMI (r 2 = 0.275, P = 0.003, and r 2 = 0.138, P = 0.005, respectively).

Conclusions: Our data showed that AGHD patients who received low-dose GH treatment had a lower prevalence of low lean mass than those who did not receive GH treatment. Patients with GH treatment had significantly lower cardiovascular risk factors, especially the lipid profile.

Introduction

Adult growth hormone deficiency (AGHD) is a clinical syndrome due to the decreased secretion of growth hormones (GH) in adults, and AGHD is characterized by abnormalities in body composition, increased cardiovascular risk factors such as central obesity, insulin resistance and dyslipidaemia, decreased bone mineral density and muscle strength, and a poor perceived quality of life.[1,2] Over the last three decades, various studies have provided relevant information on the efficacy and safety of GH therapy in patients with AGHD. The knowledge acquired during this time has been compiled into different guidelines that offer clinicians an evidence-based, practical approach for the management of AGHD.[3]

In comparison with normal individuals, patients with AGHD have reduced lean body mass and muscle strength.[4] Loss of skeletal muscle mass and consequent loss in muscle function has been associated with negative impacts on the activities of daily living and increases patients' frailty and likelihood to fall. Roh et al[5] found that a low appendicular lean mass might increase the risk of poor functional recovery after surgery. A prospective cohort study[6] found that low lean mass predicted incident fractures independently from the Fracture Risk Assessment Tool (FRAX). Vega et al[7] found that low lean mass was an independent risk factor for mortality in patients with stage 4 or 5 nondialysis chronic kidney disease. The pathophysiology of low lean mass is multifactorial, among which growth hormone deficiency seems an important contributor to decreased muscle mass. Growth hormone and insulin-like growth factor 1 (IGF-1) are key regulators of bone and muscle growth. Reduced efficiency of IGF-1 signalling likely contributes to muscle loss.[8,9] Given that the importance of muscle mass has been emphasized in various studies and GH deficiency is tightly associated with lean mass loss, exploring the prevalence of low lean mass in patients with AGHD is necessary.

Initial studies found that treatment with GH induced a decrease in fat mass and an increase in lean mass.[10] However, a recent systematic review reported that the long-term effects on body mass index seem to be inconclusive, with some studies reporting an increase and other reporting no change.[11] The clinical response to GH therapy is highly variable among patients with AGHD and is influenced by sex, age, body mass index (BMI) and GH dose.[12] A randomized and placebo-controlled study 7 found that GH treatment significantly improved body composition in a dose-responsive manner. A previous study reported that an initial low dose of GH (0.4-0.5 IU/d) was sufficient to restore serum IGF-1 to the upper limit of the reference range in most AGHD patients.[13] Therefore, it was of interest to compare the prevalence of low lean mass in patients with AGHD who did or did not receive a low-fixed dose of GH therapy.

Many methods of measuring skeletal muscle mass have been developed, among which the skeletal muscle index (SMI) is one of the most commonly used indexes.[14] Appendicular skeletal muscle mass (ASM) was assessed using dual-energy X-ray-absorptiometry (DXA) and excluding the bone mass from the calculated mass of the extremities, as fat mass is already excluded. The SMI was determined by dividing the ASM by height in square metres.[14] Low lean mass was defined as an SMI <7.0 kg/m2 in males or 5.7 kg/m2 in females.[15] Here, we conducted a retrospective study to investigate the prevalence of low lean mass in patients with AGHD who did or did not receive a low-fixed dose of GH therapy.

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