Clinical UM Guideline


Subject: Tesamorelin (Egrifta®)
Document #: CG-DRUG-85 Publish Date:    02/27/2019
Status: Reviewed Last Review Date:    01/24/2019


This document addresses Tesamorelin (Egrifta®, Theratechnologies Inc., EMD Serono, Inc., Rockland, MA) a novel growth hormone-releasing factor used to reduce excess central fat accumulation in human immunodeficiency virus (HIV)–associated lipodystrophy.

Note: Please see the following related document for additional information:

Medically Necessary: In this document, procedures are considered medically necessary if there is a significant physical functional impairment AND the procedure can be reasonably expected to improve the physical functional impairment.

Reconstructive: In this document, procedures are considered reconstructive when intended to address a significant variation from normal related to accidental injury, disease, trauma, treatment of a disease or congenital defect.

Note: Not all benefit contracts include benefits for reconstructive services as defined by this document. Benefit language supersedes this document.

Cosmetic: In this document, procedures are considered cosmetic when intended to change a physical appearance that would be considered within normal human anatomic variation.  Cosmetic services are often described as those which are primarily intended to preserve or improve appearance.

Clinical Indications


  1. An initial 6-month course of tesamorelin injections (Egrifta) is considered reconstructive when used for reduction of excess abdominal visceral adipose tissue (VAT) in HIV-infected individuals with lipodystrophy when all of the following criteria are met:
    1. Adults age 18 or older; and
    2. Body mass index (BMI) is greater than 20 kg/m2; and
    3. Waist circumference and a waist-to-hip ratio are both at least 2.5 standard deviations above normal based on age and gender (see Appendix A); and
    4. Fasting blood glucose (FBG) is less than 150 mg/dL (8.33 mmol/L); and
    5. No history of type 1 diabetes or insulin-treated type 2 diabetes; and
    6. No active malignancy (for example, a potential cancer which is being evaluated or a diagnosed cancer which is being treated); and
    7. Not currently pregnant or breast-feeding.
  2. Continuation of tesamorelin injections is considered reconstructive for individuals when there is a clear response in reduction of visceral adipose tissue measured by waist circumference or computed tomography (CT) scan.

Cosmetic and Not Medically Necessary:

Tesamorelin injection is considered cosmetic and not medically necessary when used for HIV-associated abdominal lipodystrophy which does not meet the criteria above.

Not Medically Necessary:

Tesamorelin injection is considered not medically necessary for all of the following indications:

  1. Lipodystrophy of anatomic sites aside from the abdomen.
  2. Lipodystrophy not associated with HIV infection.
  3. Individuals who meet reconstructive criteria above for an initial course, but do not show a clear response as judged by the degree of reduction in visceral adipose tissue measured by waist circumference or CT scan.
  4. Weight loss management.
  5. In individuals with a history of disruption of the hypothalamic-pituitary (HPA) axis due to hypophysectomy, hypopituitarism, pituitary tumor, pituitary surgery, head irradiation, or head trauma.
  6. All other conditions not addressed above.

The following codes for treatments and procedures applicable to this guideline are included below for informational purposes. Inclusion or exclusion of a procedure, diagnosis or device code(s) does not constitute or imply member coverage or provider reimbursement policy. Please refer to the member's contract benefits in effect at the time of service to determine coverage or non-coverage of these services as it applies to an individual member.




Unclassified drugs [when specified as tesamorelin (Egrifta)]



ICD-10 Diagnosis



Human immunodeficiency virus [HIV] disease


Lipodystrophy, not elsewhere classified

Discussion/General Information

Concepts of Medical Necessity, Reconstructive and Cosmetic

The availability of coverage for a given therapy is based on the determination of whether the treatment is considered medically necessary, reconstructive, cosmetic, not medically necessary based on the member’s certificate of coverage.  Benefits may be available for services determined to be reconstructive when the member’s contract states that reconstructive services are covered and the coverage criteria are met.  Generally, reconstructive services are performed to "return the individual to whole" when the individual’s appearance varies significantly from normal as a result of a congenital anomaly, disease or other condition (including post trauma or post therapy).  Cosmetic services differ from reconstructive services in that cosmetic services are performed to improve or alter a physical appearance that would be considered within normal human anatomic variation.  When services are both medically necessary and reconstructive, for example, services intended to correct a leg length discrepancy as a result of trauma which is causing both a significant physical functional impairment and which also represents a significant variation from normal appearance, the services are eligible for coverage based on medical necessity, without the need to determine coverage based on reconstructive services language in the benefit plan, unless some other exclusion applies.  In this example, if there was no significant functional impairment, the services to restore appearance would be considered reconstructive, but not medically necessary.  Reconstructive services may be performed without associated functional impairment to address significant variation from normal appearance arising from, including but not limited to, for example: a) surgery, b) accidental trauma or injury, c) disease, d) congenital anomaly, e) severe anatomic variant, and f) chemotherapy.

Tesamorelin and HIV-Associated Lipodystrophy

Tesamorelin is an analog of growth hormone releasing factor (GRF).  GRF, also known as growth hormone-releasing hormone (GHRH), is a hypothalamic peptide that acts on the pituitary somatotroph cells to stimulate the synthesis and pulsatile release of endogenous growth hormone (GH), which is both anabolic and lipolytic (Product Information [PI] Label, 2015).  GH exerts its effects by interacting with specific receptors on a variety of target cells, including chondrocytes, osteoblasts, myocytes, hepatocytes, and adipocytes, resulting in a host of pharmacodynamic effects.  Some, but not all of these effects are primarily mediated by IGF-1 produced in the liver and in peripheral tissues.  GH secretion is stimulated and subsequently increases IGF-1 and insulin-like growth factor binding protein (IGFBP)-3 levels without clinically significant changes in the levels of other pituitary hormones.  Individuals with HIV-associated lipodystrophy and increased VAT have diminished secretion of GH and IGF-1.

In HIV-infected individuals, restoring GH and IGF-1 levels can favorably impact increased visceral adipose tissue of HIV-associated lipodystrophy.

Lipodystrophy is a disorder of fat metabolism involving a loss of subcutaneous adipose tissue (SAT) from the face, extremities and buttocks as well as an accumulation of fat around the liver, stomach, and other abdominal organs (visceral adipose tissues [VAT]), and the dorsocervical region, the trunk and the breasts.  Lipodystrophy is linked to antiretroviral therapy and is problematic for people with HIV infection (Cofrancesco, 2009).  Lipodystrophy may result from other congenital or acquired conditions.  The accumulation of VAT is associated with insulin resistance and dyslipidemia, increasing the risk of diabetes mellitus and coronary artery disease.  Strategies to reduce visceral fat may decrease the cardiovascular risk in affected individuals.  

Numerous pathophysiologic mechanisms have been implicated in the causation of HIV-associated lipodystrophy, including dysfunction or dysregulation of mitochondria, proteins, hormones and fatty acids.  Among these, remedies to improve impaired growth hormone secretion have had the greatest success.  There is no relationship between specific antiretroviral therapies and lipodystrophy.  Exercise has had inconsistent results on lipodystrophy.

Tesamorelin (Egrifta) was approved by the Food and Drug Administration (FDA) in November 2010 as a daily subcutaneous therapy to reduce lipodystrophy in HIV-infected individuals.  Two multicenter, randomized, double-blind, placebo-controlled studies were conducted in individuals with HIV-associated lipodystrophy and excess abdominal fat.  Study 1 randomized 412 participants and Study 2 included 404 randomized participants.  Both studies (Study 1 and 2) consisted of a 26-week Main Phase and a 26-week Extension Phase.  Primary inclusion criteria were age 18-65 years, a waist circumference ≥ 95 cm (37.4 inches) and a waist-to-hip ratio ≥ 0.94 for men, ≥ 94 cm (37.0 inches) and ≥ 0.88 for women, respectively, and FBG < 150 mg/dL (8.33 mmol/L).  Primary exclusion criteria included BMI ≤ 20 kg/m2, type 1 diabetes, and type 2 diabetes if previously treated with insulin.  At week 26, treatment with tesamorelin resulted in a reduction from baseline in mean abdominal fat of 1.0 kg in Study 1 and 0.8 kg in Study 2, respectively (compared with an increase of 0.4 kg in Study 1 and of 0.2 kg in Study 2, respectively, in individuals receiving placebo).  Treatment with tesamorelin resulted in an increase from baseline in mean lean body mass of 1.3 kg in Study 1 and of 1.2 kg in Study 2, respectively (compared with a decrease of 0.2 kg in Study 1 and of 0.03 kg in Study 2, respectively, in individuals receiving placebo).  Tesamorelin did not adversely alter antiretroviral effectiveness as measured by mean circulating levels of CD4 counts or HIV-1 RNA (viral load) (PI Label, 2015).  In Study 2, the reduction of VAT was approximately 18% (p<0.001) and continued for 12 months.  Those participants who switched from treatment with tesamorelin to placebo lost the initial improvements in VAT.  The decrease in VAT was statistically significant for the treatment group (-10.9%) compared to -0.6% in the placebo group at 6 months (p<0.0001).  There was no change in abdominal or limb subcutaneous fat (Falutz, 2010).  Secondary endpoints were significantly improved for self-rating of belly appearance distress (p=0.02) and physician rating of belly profile (p=0.02) in the treatment groups compared to the placebo groups.  Levels of triglyceride changes from baseline (-51 ± 169 mg/dl, p<0.001 compared to baseline) and total cholesterol (-7 ± 36 mg/dl, p=0.009 compared to baseline) were maintained in the treatment group.  However, there were no significant changes observed in the ratio of total cholesterol to high-density lipoprotein (HDL) cholesterol in the treatment group (Falutz, 2008).  In a 2010 report by Falutz and colleagues, the decrease in triglycerides was not significant in the participants enrolled in the extension study.  However, there was “a trend amounting to a net reduction in triglycerides of 26 mg/dL compared with placebo.”

Stanley and colleagues (2012) performed a post hoc analysis of the combined data from the two pivotal randomized, double-blind, placebo-controlled phase III studies to investigate whether metabolic effects of tesamorelin were associated with changes in VAT.  Participants were deemed to be “responders” when clinically significant decreases of at least 8% of VAT area were achieved.  Metabolic and endocrine responses were compared by responder status at baseline and weeks 26 and 52.  A total of 402 (73%) individuals treated with tesamorelin and 197 (74%) individuals treated with placebo met criteria for the 26-week analysis.  Of these participants, 337 individuals in the tesamorelin treatment group had baseline and 26-week VAT data for analysis.  A total of 152 participants who were randomized to 52 weeks of tesamorelin therapy and had baseline and 52-week VAT data for analysis were included in the 52-week analysis.  The responder rate of 69% was higher in the tesamorelin treatment group compared to 33% in the placebo group (p<0.001).  The responder rate rose to 72% among those who continued treatment with tesamorelin for 52 weeks.  In the 26-week analysis, insulin-like growth factor-1 (IGF-1) was significantly increased in responders versus nonresponders (p<0.001) but the change was not significantly different at the 52-week analysis.  Adiponectin levels increased in the responder cohorts at both 26- and 52-week intervals while the nonresponders did not have significant changes in the adiponectin levels.  The responders also had significantly decreased triglyceride levels compared to nonresponders at 26 weeks (p=0.005) and 52 weeks (p=0.003).  Cholesterol levels at 26 weeks were significantly decreased for responders (p=0.014) versus nonresponders, but at 52 weeks, the difference was not significant between the groups (p=0.205).  C-reactive protein (CRP) and high-density lipoprotein cholesterol levels were not affected by responder status and did not change significantly at both 26- and 52-week analyses.  Hemoglobin A1C (HbA1c) levels increased for both groups at 26 weeks but the change was less in the responder group compared to the nonresponder group (p<0.001).  At the 52-week analysis, the HbA1c levels in responders did not change significantly from baseline, but the nonresponders had a significant increase from baseline.  The authors concluded tesamorelin responders with a decrease in VAT of 8% or more had “greater improvements in levels of triglycerides, adiponectin and preservation of long-term glucose homeostasis over 52 weeks, suggesting metabolic benefits associated with reducing VAT in this population” (Stanley, 2012).  Although the data suggests metabolic benefits of tesamorelin therapy and the corresponding reduction in VAT, this indication is not in accordance with generally accepted standards of medical practice.

The PI Label (2015) includes the following limitations of tesamorelin use:

There are no data indicating that improved body image with tesamorelin improves adherence to antiretroviral treatments.

Tesamorelin Treatment to Improve Cognitive Function

Normal brain function and feedback communications include somatotrophic hormones such as growth hormone-releasing hormone (GHRH), growth hormone (GH) and IGF-1.  Decreased levels of somatotrophic hormones may be associated with advancing age, adverse cognition, poor short-term memory and increased Alzheimer disease in the brain (Baker, 2012).  A phase II randomized, double-blind, placebo-controlled trial investigated the effects of 20 weeks of tesamorelin therapy compared to placebo in healthy adults and adults with mild cognitive impairment.  Cognitive testing, including executive function, verbal and visual episodic memory, was done at baseline, weeks 10, 20 and 30 (washout period 10 weeks after discontinuation of treatment).  IGF-1 levels increased to normal young adult levels with 5 months of tesamorelin therapy.  The tesamorelin group had favorable cognitive function at week 20 compared to baseline (p=0.03).  The treatment group also had comparable beneficial effects for both healthy adults and adults with mild cognitive impairment (p=0.22).  Although the study suggested tesamorelin had a favorable effect on cognition in both healthy and mild cognitive impairment adults, the authors noted “the clinical significance of the findings remain unclear.”  Larger, long-term phase III trials are needed to “firmly establish the therapeutic potential of GHRH administration to promote brain health in normal aging and pathological aging” (Baker, 2012).  Additional studies are also necessary to identify the mechanisms of cognition-enhancing effects tesamorelin therapy may exert on the brain.

Other Conditions for Which Tesamorelin Treatment Has Been Considered

Makimura and colleagues published data from a phase II, randomized, double-blind, placebo-controlled trial that investigated the effects of tesamorelin use on body composition and cardiovascular disease (CVD) indices in adults with generalized abdominal obesity and low GH levels.  A total of 60 participants were enrolled between 2008 and 2010.  Eligibility criteria included waist circumference (WC) of at least 102 cm for men and at least 88 cm for women, with peak stimulated GH levels no higher than 9 µg/liter on a standardized GHRH-arginine stimulation test.  Exclusion criteria included obesity due to a known secondary cause; hormone replacement therapy within 3 months of enrollment; or history of chronic illness, including HIV.  Participants were stratified and randomized by gender to 2 mg of tesamorelin subcutaneously for 1 year, or placebo.  The primary endpoint was the change in VAT from baseline.  In total, 17 participants in the placebo group and 19 participants in the tesamorelin group completed the study.  There was a significant decrease in VAT for the tesamorelin group (-16 ± 9 cm2) versus the placebo control group (19 ± 9 cm2) (95% confidence interval [CI], -35 (-58, -12) cm2; p=0.003).  There was a significant reduction in carotid intima-media thickness with 12 months of tesamorelin therapy compared to placebo (-0.03 ± 0.01 vs. 0.01 ± 0.01 mm; p=0.02).  Participants in the tesamorelin group had overall percent changes in IGF-1 by 90% and 20% decrease in triglycerides compared to placebo.  However, tesamorelin did not have a significant effect on total cholesterol (p=0.69), high-density lipoprotein (HDL, p=0.66), or low-density lipoprotein (LDL, p=0.60).  The authors noted these results in obese subjects with low GH provide initial data to support larger studies to determine “whether these changes can be maintained over longer treatment periods.”

In 2014, Stanley and colleagues published the results of an on-going randomized, double-blind, placebo-controlled efficacy study.  HIV-infection is associated with a high prevalence of nonalcoholic fatty liver disease (NAFLD), which may predispose individuals to cardiovascular-related health decline, and is often presented in the context of increased VAT.  This study aimed to evaluate tesamorelin’s efficacy on ectopic fat depots other than VAT in HIV-positive adults, with an emphasis specifically on the potential benefits of reductions in liver fat.  A total of 50 HIV-positive participants enrolled and were randomized to receive either daily tesamorelin (2 mg) or placebo injections subcutaneously for 6 months.  At the 6-month visit, a total of 23 participants were available for analysis in the tesamorelin group and 20 in the placebo group.  In this small efficacy study, investigators found that tesamorelin administered for 6 months was associated with significant reductions in visceral fat and modest reductions in liver fat. 

Tesamorelin has also been studied in hip fracture recovery, immune responsiveness to influenza vaccine, sleep maintenance, and type 2 diabetes mellitus; none of these studies have demonstrated efficacy in the setting of a randomized, Phase III clinical trial.

Warnings from the FDA PI Label (2015) include the following:

The most commonly reported adverse reactions (> 5% and more frequent than placebo):  Arthralgia, injection site pruritus, pain in extremity, peripheral edema and myalgia.

Egrifta induces the release of endogenous GH, a known growth factor.  Thus, individuals with active malignancy should not be treated with Egrifta.

For individuals with a history of non-malignant neoplasms, Egrifta therapy should be initiated after careful evaluation of the potential benefit of treatment.  For individuals with a history of treated and stable malignancies, Egrifta therapy should be initiated only after careful evaluation of the potential benefit of treatment relative to the risk of re-activation of the underlying malignancy.

Elevated IGF-1
Egrifta stimulates GH production and increases serum IGF-I. Given that IGF-I is a growth factor and the effect of prolonged elevations in IGF-I levels on the development or progression of malignancies is unknown, IGF-I levels should be monitored closely during Egrifta therapy.  Careful consideration should be given to discontinuing Egrifta in individuals with persistent elevations of IGF-1 levels (e.g., greater than 3 standard deviations), particularly if the efficacy response is not robust (e.g., based on VAT changes measured by waist circumference or CT scan).

Fluid Retention
Fluid retention may occur during Egrifta therapy and is thought to be related to the induction of GH secretion.  It manifests as increased tissue turgor and musculoskeletal discomfort resulting in a variety of adverse reactions (e.g. edema, arthralgia, carpal tunnel syndrome) which are either transient or resolve with discontinuation of treatment.

Glucose Intolerance
Egrifta treatment may result in glucose intolerance.  An increased risk of developing diabetes with Egrifta (HbA1c level ≥ 6.5%) relative to placebo was observed (intent-to-treat hazard odds ratio of 3.3 [confidence interval, 1.4, 9.6]).  Therefore, glucose status should be carefully evaluated prior to initiating Egrifta treatment.  In addition, all individuals treated with Egrifta should be monitored periodically for changes in glucose metabolism to diagnose those who develop impaired glucose tolerance or diabetes.

Hypersensitivity Reactions
Hypersensitivity reactions may occur in individuals treated with Egrifta.  These reactions included pruritus, erythema, flushing, urticaria, and other rash.  In cases of suspected hypersensitivity reactions, individuals should be advised to seek prompt medical attention and treatment with Egrifta should be discontinued immediately.

Injection Site Reactions
Egrifta treatment may cause injection site reactions, including injection site erythema, pruritus, pain, irritation, and bruising.  The incidence of injection site reactions was 24.5% in Egrifta-treated individuals and 14.4% in placebo-treated individuals during the first 26 weeks of treatment in the Phase III clinical trials.  In order to reduce the incidence of injection site reactions, it is recommended to rotate the site of injection to different areas of the abdomen.

Acute Critical Illness
Increased mortality in individuals with acute critical illness due to complications following open heart surgery, abdominal surgery or multiple accidental traumas, or those with acute respiratory failure has been reported after treatment with pharmacologic amounts of growth hormone.  Egrifta has not been studied in individuals with acute critical illness.


Functional impairment: Limits on normal physical functioning that may include, but are not limited to, problems with ambulation, mobilization, communication, respiration, eating, swallowing, vision, facial expression, skin integrity, distortion of nearby body parts, or obstruction of an orifice.  The cause of the physical functional impairment can be due to pain, structural, congenital or other means.  Physical functional impairment excludes social, emotional, and psychological impairments or potential impairments.

Waist-to-hip ratio: The waist circumference divided by the circumference of the hips.


Peer Reviewed Publications:

  1. Baker LD, Barsness SM, Borson S, et al. Effects of growth hormone-releasing hormone on cognitive function in adults with mild cognitive impairment and healthy older adults: results of a controlled trial. Arch Neurol. 2012; 69(11):1420-1429.
  2. Braun LR, Feldpausch MN, Czerwonka N, et al. Fibroblast growth factor 21 decreases after liver fat reduction via growth hormone augmentation. Growth Horm IGF Res. 2017; 37:1-6.
  3. Cofrancesco J Jr, Freedland E, McComsey G. Treatment options for HIV-associated central fat accumulation. AIDS Patient Care STDS. 2009; 23(1):5-18.
  4. Falutz J, Allas S, Blot K, et al. Metabolic effects of a growth hormone-releasing factor in patients with HIV. N Engl J Med. 2007; 357(23):2359-2370.
  5. Falutz J, Allas S, Kotler D, et al. A placebo-controlled, dose-ranging study of a growth hormone releasing factor in HIV-infected patients with abdominal fat accumulation. AIDS. 2005; 19(12):1279-1287.
  6. Falutz J, Allas S, Mamputu JC, et al. Long-term safety and effects of tesamorelin, a growth hormone-releasing factor analogue, in HIV patients with abdominal fat accumulation. AIDS. 2008; 22(14):1719-1728.
  7. Falutz J, Mamputu JC, Potvin D, et al. Effects of tesamorelin (TH9507), a growth hormone-releasing factor analog, in human immunodeficiency virus-infected patients with excess abdominal fat: a pooled analysis of two multicenter, double-blind placebo-controlled phase 3 trials with safety extension data. J Clin Endocrinol Metab. 2010; 95(9):4291-4304.
  8. Falutz J, Potvin D, Mamputu JC, et al. Effects of tesamorelin, a growth hormone-releasing factor, in HIV-infected patients with abdominal fat accumulation: a randomized placebo-controlled trial with a safety extension. J Acquir Immune Defic Syndr. 2010; 53(3):311-322.
  9. Fourman LT, Czerwonka N, Feldpausch MN, et al.  Visceral fat reduction with tesamorelin is associated with improved liver enzymes in HIV. AIDS. 2017; 31(16):2253-2259.
  10. Makimura H, Feldpausch MN, Rope AM, et al. Metabolic effects of a growth hormone-releasing factor in obese subjects with reduced growth hormone secretion: a randomized controlled trial. J Clin Endocrinol Metab. 2012; 97(12):4769-4779.
  11. Shields M, Tremblay MS, Laviolette M, et al. Fitness of Canadian adults: results from the 2007-2008 Canadian Health Measures Survey. Health Rep. 2010; 21(1):7-20.
  12. Sivakumar T, Mechanic O, Fehmie DA, Paul B. Growth hormone axis treatments for HIV-associated lipodystrophy: a systematic review of placebo-controlled trials. HIV Med. 2011; 12(8):453-462.
  13. Spooner LM, Olin JL. Tesamorelin: a growth hormone-releasing factor analogue for HIV-associated lipodystrophy. Ann Pharmacother. 2012; 46(2):240-247.
  14. Stanley TL, Falutz J, Mamputu JC, et al. Effects of tesamorelin on inflammatory markers in HIV patients with excess abdominal fat: relationship with visceral adipose reduction. AIDS. 2011; 25(10):1281-1288.
  15. Stanley TL, Falutz J, Marsolais C, et al. Reduction in visceral adiposity is associated with an improved metabolic profile in HIV-infected patients receiving tesamorelin. Clin Infect Dis. 2012; 54(11):1642-1651.
  16. Stanley TL, Feldpausch MN, Oh J, et al. Effect of tesamorelin on visceral fat and liver fat in HIV-infected patients with abdominal fat accumulation: a randomized clinical trial. JAMA. 2014; 312(4):380-389.  
  17. Yusuf S, Hawken S, Ounpuu S, et al.; INTERHEART Study Investigators. Obesity and the risk of myocardial infarction in 27,000 participants from 52 countries: a case-control study. Lancet. 2005; 366(9497):1640-1649.

Government Agency, Medical Society, and Other Authoritative Publications:

  1. Egrifta. In: DrugPoints® System (electronic version). Truven Health Analytics, Greenwood Village, CO. Updated October 31, 2016. Available at: Accessed on December 21, 2018.
  2. Egrifta [Product Information]. Theratechnologies Inc., distributed by EMD Serono, Inc., Rockland, MA. June, 2015. Available at: Accessed on January 02, 2019.
  3. Tesamorelin Monograph. Lexicomp® Online, American Hospital Formulary Service® (AHFS®) Online, Hudson, Ohio, Lexi-Comp., Inc. Last revised March 11, 2016. Accessed on December 21, 2018.
Websites for Additional Information
  1. Centers for Disease Control and Prevention. Body Mass Index. Available at: Accessed on January 2, 2019.
  2. U.S. Department of Health & Human Services HIV/AIDS information. Available at: Accessed on January 2, 2019.
  3. U.S. National Library of Medicine. MedlinePlus: Tesamorelin injection. Last updated on November 15, 2016. Available at: Accessed on January 2, 2019. 


The use of specific product names is illustrative only. It is not intended to be a recommendation of one product over another, and is not intended to represent a complete listing of all products available.







Medical Policy & Technology Assessment Committee (MPTAC) review. Updated Discussion/General Information and References Sections.



MPTAC review. Initial document development. Moved content of DRUG.00045 Tesamorelin (Egrifta®) to new clinical utilization management guideline document with the same title.


Waist Circumference and Waist-to-Hip Ratio



Age 18 - 39 years

Age 40- 59 years

Age 60 years and older

2.5 Standard Deviations above the mean
Waist-to-Hip Ratio (WHR)














2.5 Standard Deviations above the mean
Waist circumference (WC)


123.5 cm or 48.6 in

131.5 cm or 51.7 in

135.5 cm or 53.3 in


115.5 cm or 45.5 in

120.5 cm or 47.4 in

126.5 cm or 49.8 in






Waist-to-Hip Ratio (WHR)














Waist circumference (WC)


91 cm

99 cm

103 cm


83 cm

88 cm

94 cm






Standard Deviation Waist-to-Hip Ratio (WHR)














Standard Deviation Waist circumference (WC)


9 cm

9 cm

9 cm


9 cm

9 cm

9 cm

cm = centimeter
in = inches

Source data used in the table are from:

Shields M, Tremblay MS, Laviolette M, et al. Fitness of Canadian adults: results from the 2007-2008 Canadian Health Measures Survey. Health Rep. 2010; 21(1):7-20.