Testosterone Undecanoate Injection (Aveed) - Medical Clinical Policy Bulletins (2022)


Table Of Contents

Applicable CPT / HCPCS / ICD-10 Codes

Brand Selection for Medically Necessary Indications

As defined in Aetna commercial policies, health care services are not medically necessary when they are more costly than alternative services that are at least as likely to produce equivalent therapeutic or diagnostic results. Aveed (testosterone undecanoate) long-acting injectable anabolic-androgenic steroid is more costly to Aetna than other long-acting anabolic-androgenic steroids. There is a lack of reliable evidence that Aveed (testosterone undecanoate) is superior to the lower cost long-acting injectable anabolic-androgenic steroids, Delatestryl (testosterone enanthate) and Depo-Testosterone (testosterone cypionate) for medically necessary indications. Therefore, Aetna considers Aveed (testosterone undecanoate) to be medically necessary only for members who have a contraindication, intolerance or ineffective response to the available equivalent alternative long-acting injectable anabolic-androgenic steroids: Delatestryl (testosterone enanthate) and Depo-Testosterone (testosterone cypionate).


Note: Requires Precertification:

Precertification of testosterone undecanoate injection (Aveed) is required of all Aetna participating providers and members in applicable plan designs. For precertification of testosterone undecanoate injection (Aveed), call (866) 752-7021, or fax (888) 267-3277.

Note: Most policies specifically exclude coverage of steroids for performance enhancement. For plans without this exclusion, androgens and anabolic steroids as well as other medical interventions for performance enhancement are not covered because performance enhancement of non-diseased individuals is not considered treatment of disease or injury. Please check benefit plan descriptions for details.

  1. Criteria for Initial Approval

    Aetna considers testosterone undecanoate injection (Aveed) medically necessaryfor the following indications:

    1. Primary hypogonadism or hypogonadotropic hypogonadism when all of the following criteria are met:

      1. Member is a biological male or a person that self identifies as male; and
      2. Member is at least 18 years of age; and
      3. Member has at least two confirmed low morning serum total testosterone concentrations based on the reference laboratory range or current practice guidelines.
    2. Gender dysphoria when all of the following are met:

      1. The member is able to make an informed decision to engage in hormone therapy; and
      2. The member has a diagnosis of gender dysphoria; and
      3. The member's comorbid conditions are reasonably controlled; and
      4. The member has been educated on any contraindications and side effects to therapy; and
      5. The member has been informed of fertility preservation options; and
      6. This medication will be prescribed by or in consultation with a pediatric endocrinologist that has collaborated care with a mental health care provider for members less than 18 years of age.

    Aetna considers all other indications as experimental and investigational (for additional information, see Experimental and Investigational and Background sections).

  2. Continuation of Therapy

    Aetna considerscontinuation of testosterone undecanoate injection (Aveed) therapy medically necessary for the following indications:

    1. Primary hypogonadism or hypogonadotropic hypogonadism - For members who are not currently receiving Aveed therapy through samples or a manufacturer’s assistance program, andmember is at least 18 years of age.All other members (including new members) must meet all inital authorization criteria.
    2. Gender dysphoria for all members (including new members) who meet all initial authorization criteria.
  3. Related Policies

    For testosterone enanthate injection (Delatestryl) and testosterone enanthate injection (Xyosted), see Pharmacy Clinical Policy Bulletin:Testosterone - Testosterone Enanthate TGC PA Policy 1368-A.

    For testosterone cypionate injection (Depo-Testosterone), see Pharmacy Clinical Policy Bulletin: Testosterone - Depo-Testosterone TGC PA Policy 976-A.

    For oral / buccal, topical or nasalandrogen and anabolic steroid products, refer to pharmacy benefit plan.

    See also:

    1. CPB 0345 - Implantable Hormone Pellets
    2. CPB 0501 - Gonadotropin-Releasing Hormone Analogs and Antagonists
    3. CPB 0574 - Female Sexual Dysfunction (FSD).

Dosage and Administration

Aveedis availablefor injectionas 750 mg/3 mL (250 mg/mL) testosterone undecanoate sterile injectable solution, single use vial. Aveed is for intramuscular use only. Dosage titration is not necessary.

Primary Hypogonadism (Congenital or Acquired) orHypogonadotropic Hypogonadism (Congenital or Acquired)

For adult males, the recommended dose of Aveed is 3 mL (750 mg) injected intramuscularly, followed by 3 mL (750 mg) injected after 4 weeks, then 3 mL (750 mg) injected every 10 weeks thereafter.


  1. Safety and efficacy of Aveed in men with “age-related hypogonadism” (also referred to as “late-onset hypogonadism”) have not been established.
  2. Safety and efficacy of Aveed in males less than 18 years old have not been established.

Source: Endo Pharmaceuticals, 2021

Experimental and Investigational

Aetna considers testosterone undecanoate injections experimental and investigational forthe following indications (not an all-inclusive list)because of insufficient evidence in the peer-reviewed literature:

  1. age-related hypogonadism or late-onset hypogonadism
  2. female sexual dysfunction/hypoactive sexual desire disorder
  3. heart failure
  4. improvement of cognitive function in aging men
  5. males less than 18 years of age
  6. menopause (female or male)
  7. treatment of amyotrophic lateral sclerosis.

CPT Codes / HCPCS Codes / ICD-10 Codes

Information in the [brackets] below has been added for clarification purposes.&nbspCodes requiring a 7th character are represented by"+":

Other CPT codes related to the CPB:

80414Chorionic gonadotropin stimulation panel; testosterone response
84270Sex hormone binding globulin (SHBG)
84402Testosterone; free
84410Testosterone; bioavailable, direct measurement (eg, differential precipitation)
96372Therapeutic prophylactic or diagnostic injection (specify substance or drug); subcutaneous or intramuscular
99506Home visit for intramuscular injection

HCPCS codes covered if selection criteria are met:

J1071Injection, testosterone cypionate, 1 mg
J2320Injection, nandrolone decanoate, up to 50 mg
J3121Injection, testosterone enanthate, 1 mg
J3145Injection, testosterone undecanoate, 1 mg
S0179Megestrol acetate, oral, 20mg

Other HCPCS codes related to the CPB:

J0702Injection, betamethasone acetate 3mg and betamethasone sodium phosphate 3mg
J1020Injection, methylprednisolone acetate, 20 mg
J1030Injection, methylprednisolone acetate, 40 mg
J1040Injection, methylprednisolone acetate, 80 mg
J1094Injection, dexamethasone acetate, 1 mg
J1100Injection, dexamethasone sodium phosphate, 1mg
J1720Injection, hydrocortisone sodium succinate, up to 100 mg
J3300Injection, triamcinolone acetonide, preservative free, 1 mg
J3301Injection, triamcinolone acetonide, not otherwise specified, 10 mg
J3302Injection, triamcinolone diacetate, per 5mg
J3303Injection, triamcinolone hexacetonide, per 5mg

ICD-10 codes covered if selection criteria are met:

B20 Human immunodeficiency virus [HIV] disease
C50.011 - C50.929Malignant neoplasm of breast
C54.1Malignant neoplasm of endometrium
D25.0 - D25.9Leiomyoma of uterus
D46.0 - D46.9
D47.01 - D47.09
Neoplasm of uncertain behavior of other lymphatic and hematopoietic tissues (e.g., myelosclerosis with myeloid metaplasia)
D60.0 - D61.9Aplastic anemias
D63.0 Anemia in neoplastic disease
D63.1Anemia in chronic kidney disease
D68.2 Hereditary deficiency of other clotting factors
D68.59Other primary thrombophilia [antithrombin III deficiency]
D84.1 Defects in the complement system
D89.1 Cryoglobulinemia
E23.0Hypopituitarism [hypogonadotropic hypogonadism]
E23.6Other disorders of pituitary gland [covered for hypothalamic hypogonadism; not covered for idiopathic hypogonadism (not due to disorders of the testicles, pituitary gland or brain)]
E29.1 Testicular hypofunction
E30.0 Delayed puberty
F64.0 - F64.9Gender identity disorders
E89.5 Postprocedural testicular hypofunction
I73.00 - I73.01Raynaud's syndrome
I77.6Arteritis, unspecified
I82.0 - I82.91Other venous embolism and thrombosis
L90.0Lichen sclerosus et atrophicus
L94.0Localized scleroderma [morphea]
L94.1Linear scleroderma
M35.2 Behcet's disease
N60.11 - N60.19Diffuse cystic mastopathy
N64.4Mastodynia [mastalgia]
N80.0 - N80.9Endometriosis
Q54.0 - Q54.9Hypospadias
Q55.62 Hypoplasia of penis
Q98.0 - Q98.4Klinefelter's syndrome
R62.0 - R62.59Lack of expected normal physiological development in childhood and adults
R63.4Abnormal weight loss
T86.00 - T86.09Complications of bone marrow transplant (e.g., graft-versus-host disease (acute) (chronic))
Z17.0Estrogen receptor positive status [ER+]
Z79.52Long term (current) use of systemic steroids
Numerous optionsThird degree burns [Codes not listed due to expanded specificity]

ICD-10 codes not covered for indications listed in the CPB:

E28.310 - E28.319Premature menopause
F52.0 - F52.9Sexual dysfunction not due to a substance or known physiological condition
G12.21Amyotrophic lateral sclerosis
J40 - J47.9Chronic lower respiratory diseases
L89.000 - L89.95Pressure ulcer of skin
N46.0 - N46.9Male infertility
N50.9Disorder of male genital organs, unspecified [male menopause]
N95.0 - N95.9Menopausal and other perimenopausal disorders
N97.0 - N97.9Female Infertility
R37Sexual dysfunction, unspecified
R41.81Age-related cognitive decline [improvement of cognitive function in aging men]
S72.001S - S72.26XSFracture of femur, sequela
Z78.0Asymptomatic menopausal state
Z79.890 Hormone replacement therapy (postmenopausal)

Symptoms and Signs Suggestive of Androgen Deficiency in Men (See appendix Table 1A):

ICD-10 codes covered if selection criteria are met:

D64.9Anemia, unspecified
E29.1Testicular hypofunction [eunuchoidism] [shrinking testes]
E66.0 - E66.9 Overweight and Obesity
F32.9Major depressive disorder, single episode, unspecified
F34.1Dysthymic disorder
F52.21Male erectile disorder
G47.9Sleep disorder, unspecified
L63.0 - L65.9Nonscarring hair loss, unspecified [loss of body (axillary and pubic) hair] [reduced shaving]
M62.81Muscle weakness (generalized) [reduced muscle bulk and strength]
M62.89Other specified disorders of muscle [reduced muscle bulk and strength]
M81.0 - M81.8Osteoporosis
M84.30x+ - M84.38x+Stress fracture [low trauma]
M84.40 x+ - M84.68x+Pathological fracture [low trauma]
M85.80 - M85.9Other specified disorders of bone density and structure
N46.0 - N46.9Male infertility
N52.9Male erectile dysfunction, unspecified
N62Hypertrophy of breast
Numerous OptionsFractures [low trauma]
Q55.0Absence and aplasia of testis
Q55.1Hypoplasia of testis and scrotum [very small testes]
R29.890Loss of height
R41.3Other amnesia
R41.840Attention and concentration deficit
R53.83Other fatigue [decreased energy] [sleepiness]
R61Generalized hyperhidrosis [sweats]
R63.5Abnormal weight gain
R68.82Decreased libido
R86.8Other abnormal finding in specimens from male genital organs [low sperm count]
Z87.81Personal history of (healed) traumatic fracture [low trauma]
Z87.311Personal history of (healed) other pathological fracture [low trauma]
Z87.312Personal history of (healed) stress fracture [low trauma]


U.S. Food and Drug Administration (FDA)-Approved Indications

Aveed is indicated for testosterone replacement therapy in adult males for conditions associated with a deficiency or absence of endogenous testosterone.

  • Primary hypogonadism (congenital or acquired): testicular failure due to cryptorchidism, bilateral torsion, orchitis, vanishing testis syndrome, orchiectomy, Klinefelter’s syndrome, chemotherapy, or toxic damage from alcohol or heavy metals. These men usually have low serum testosterone concentrations and gonadotropins (follicle-stimulating hormone [FSH], luteinizing hormone [LH]) above the normal range
  • Hypogonadotropic hypogonadism (congenital or acquired): gonadotropin or luteinizing hormone-releasing hormone (LHRH) deficiency, or pituitary-hypothalamic injury from tumors, trauma, or radiation. These men have low testosterone serum concentrations but have gonadotropins in the normal or low range.
  • Aveed should only be used in patients who require testosterone replacement therapy and in whom the benefits of the product outweigh the serious risks of pulmonary oil microembolism and anaphylaxis.

Limitations of use:

  • Safety and efficacy of Aveed in men with “age-related hypogonadism” (also referred to as “late-onset hypogonadism”) have not been established
  • Safety and efficacy of Aveed in males less than 18 years old have not been established.

Compendial Use

  • Gender dysphoria (also known as gender non-conforming or transgender persons)

Testosterone undecanoate injection is available as Aveed (Endo Pharmaceuticals Inc).Testosterone undecanoate is metabolized to testosterone.

Testosterone is an endogenous androgen that is responsible for normal growth and development of male sex organs and sexual characteristics. These effects include the growth and maturation of prostate, seminal vesicles,penis, and scrotum; the development of male hair distribution; laryngeal enlargement; vocal cord thickening; and alterations in body musculatureand fat distribution. Low serum testosterone concentrations due to inadequate secretion of testosterone is associated with male hypogonadism. Symptoms include decreased sexual desire with or without impotence, fatigue, and mood disturbances. Male hypogonadism has 2 main etiologies, primaryhypogonadism, which is caused by defects of the gonads, such asKlinefelter’s syndrome or Leydig cell aplasia, and secondary hypogonadism, which is the failure ofthe hypothalamus (or pituitary) to produce sufficient gonadotropins (FSH, LH) (Endo Pharmaceuticals, 2021).

On March 6, 2014, the FDA approved testosterone undecanoate injectable (Aveed, Endo Pharmaceuticals) for the treatment of men with hypogonadism.The approval follows 3 previous rejections of Aveed by the FDA for safety and risk/benefit concerns and comes just a month after the FDA announced that it is investigating cardiovascular safety data for all testosterone preparations. The FDA is requiring that Aveed's label contain a boxed warning regarding the risks of serious pulmonary oil micro-embolism (POME) and anaphylaxis and is making the product available only through a restricted distribution scheme known as a risk evaluation and mitigation strategy (REMS) to ensure that it is used only in men for whom the benefits out-weigh the risks.

Aveed is contraindicated in menwith carcinoma of the breast or known or suspected carcinoma of the prostate, women who are pregnant, and known hypersensitivity to Aveed or its ingredients (testosterone undecanoate, refined castor oil, benzyl benzoate).

Labeled warnings and precautions include monitoring patients for worsening signs and symptoms of benign prostatic hyperplasia (BPH); venous thromboembolism (VTE) (including deep vein thrombosis (DVT)and pulmonary embolism (PE));increased risk of myocardialinfarction and stroke associated with use of testosterone replacementtherapy; azoospermia; edema with or without congestive heart failure in patients with preexisting cardiac, renal, or hepatic disease; sleep apnea in those with risk factors; and monitoring prostatic specific antigen (PSA), hemoglobin, hematocrit, andlipid concentrations periodically.

There are insufficient long-term safety data to assess thepotential risks of cardiovascular disease and prostate cancer in the geriatric population.

Aveed contains testosterone, a Schedule III controlled substance as defined by the Anabolic Steroids Control Act. Aveed is administered via deep intramuscular injection.

The most commonly reported adverse reactions (2% or more) are acne, injection sitepain, prostatic specific antigen (PSA) increased, estradiol increased,hypogonadism, fatigue, irritability, hemoglobin increased, insomnia, andmood swings.

Measurement of the serum testosterone concentration is usually the most important single diagnostic test for male hypogonadism because a low value usually indicates hypogonadism. Measurement of the serum total (free plus protein-bound) testosterone concentration is usually an accurate reflection of testosterone secretion. Interpretation of serum testosterone measurements should take into consideration its diurnal fluctuation, which reaches a maximum at about 8 AM and a minimum, approximately 70 percent of the maximum, at about 8 PM. It is easier to distinguish subnormal from normal when normal is higher, so the measurements should always be made at 8 AM. If a single 8 AM value is well within the normal range, testosterone production can be assumed to be normal. If a single 8 AM value is low or borderline low or does not fit with the clinical findings, the measurement should be repeated once or twice before making the diagnosis of hypogonadism.

Testing during acute illness or during a time of decompensation of chronic illness is not advised since testosterone levels may be temporarily depressed during such times (Hayes, 2015). Relevant chronic illnesses include coronary artery disease, heart failure, and diabetes. The recommended target of testosterone therapy is the middle of a normal range for healthy young men.Food, especially glucose ingestion, also decreases the serum testosterone concentration, so the blood should also be drawn fasting (Snyder, 2013).

Guidelines recommend that free or bioavailable testosterone be measured when total testosterone levels are close to the lower limit of the normal range (less than 400 ng/dL)and when altered SHBG levels are suspected, as may be the case in older men and men with obesity, diabetes mellitus, cachexia, malnutrition, advanced cirrhosis, acromegaly, hypothyroidism, or nephrotic syndrome (Hayes, 2015; ASRM, 2006).

Following a determination of abnormally low serum testosterone, best practice requires measurement of serum LH and FSH levels to distinguish between primary (testicular) and secondary (pituitaryhypothalamic) hypogonadism, as well as other tests for possible causes of primary or secondary hypogonadism (Hayes, 2015).Additional laboratory tests and/or imaging are recommended for cases of secondary hypogonadism in order to evaluate etiology and exclude diagnoses such as pituitary neoplasia, hyperprolactinemia, hemochromatosis, obstructive sleep apnea, and genetic disorders. A karyotype is recommended for cases of primary hypogonadism of unknown etiology to rule out Klinefelter's syndrome.

In symptomatic men, regardless of age, testosterone levels are assessed by comparing them with the normal range for young men, based on the known gradual decline of testosterone levels with aging, starting at approximately age 30 years (Hayes, 2015). The lower limit of normal for healthy young men is 280 to 300 ng/dL (9.7 to 10.4 nmol/L). The panel assembled for the current Endocrine Society guidelines was divided between 2 options for symptomatic older men (Bhasin et al., 2010; Hayes, 2015):

  • Treat only when levels of total testosterone are less than 300 ng/dL (10.4 nmol/L) because of the association between testosterone at those levels and typical symptoms of androgen deficiency;
  • Treatment only when levels of total testosterone are less than 200 ng/dL (6.9 nmol/L) because randomized trials have suggested that testosterone therapy is ineffective in men with pretreatment values of 300 ng/dL.

Free and bioavailable testosterone can be calculated by various formulas on the basis of total testosterone and SHBG assays (Hayes, 2015).There is no consensus regarding cutoff values for free or bioavailable testosterone, but a level of greater than 225 picomoles per liter (pmol/L) (6 ng/dL) is generally considered normal.

Measurement of salivary testosterone has been proposed as an alternative to serum testosterone, but measurement of salivary testosterone is not a standard practice (Hayes, 2015).

Age-Related Hypogonadism / Late-Onset Hypogonadism

Makinen and Huhtaniemi (2011) stated that normal testicular function is essential for the maintenance of male physical strength and behavior irrespective of age. A new term of late-onset hypogonadism (LOH) has been coined for the condition of decreased testosterone and hypogonadal symptoms in aging men. The most important testicular hormone, testosterone, is responsible for the gender-specific androgenic-anabolic effects in men. Testicular production of testosteroneremains stable until around the age of 40 years after which it declines by 1 to 2 % annually. Despite this age-related decline, serum testosterone levels in most older men remain within the reference range of younger men. The decreasing androgen levels are paralleled by well-defined objective biological and non-specific subjective signs and symptoms of aging. Because these symptoms are similar to those observed in young men with documented hypogonadism, androgen replacement therapy (ART) has been considered a logical way to treat them.These researchers conducted athorough review of the existing literature to evaluate the current concepts and controversies related to aging men and ART. Although it is intuitively logical that the symptoms of LOH are due to the aging-related deficiency of testosterone, and that they can be reversed by ART, the evidence for this is still variable and often weak. In particular, evidence-based information about long-term benefits and risks of ART in aging men is largely missing. The authors concluded that despite widespread use, evidence-based proof for the objective benefits and side effects of ART of elderly men is still scanty, and such treatments should be considered experimental.

Shelton and Rajfer (2012) noted that androgen deficiency in aging men is common, and the potential sequelae are numerous. In addition to low libido, erectile dysfunction, decreased bone density, depressed mood, and decline in cognition, studies suggest strong correlations between low testosterone, obesity, and the metabolic syndrome. Because causation and its directionality remain uncertain, the functional and cardiovascular risks associated with androgen deficiency have led to intense investigation of testosterone replacement therapy in older men. Although promising, evidence for definitive benefit or detriment is not conclusive, and treatment of LOH is complicated.

Androgens forFemale Sexual Desire Disorders

Reis and Abdo (2014) evaluated the use of androgens in the treatment of a lack of libido in women, comparing 2 periods, i.e., before and after the advent of the phosphodiesterase type 5 inhibitors. These researchers also analyzed the risks and benefits of androgen administration. They searched the Latin-American and Caribbean Health Sciences Literature, Cochrane Library, Excerpta Medica, Scientific Electronic Library Online, and Medline (PubMed) databases using the search terms disfunção sexual feminina/female sexual dysfunction, desejo sexual hipoativo/female hypoactive sexual desire disorder, testosterona/testosterone, terapia androgênica em mulheres/androgen therapy in women, and sexualidade/sexuality as well as combinations thereof. They selected articles written in English, Portuguese, or Spanish. After the advent of phosphodiesterase type 5 inhibitors, there was a significant increase in the number of studies aimed at evaluating the use of testosterone in women with hypoactive sexual desire disorder. However, the risks and benefits of testosterone administration have yet to be clarified.

Cappelletti and Wallen (2016) noted that both estradiol and testosterone have been implicated as the steroid critical for modulating women's sexual desire. By contrast, in all other female mammals only estradiol has been shown to be critical for female sexual motivation and behavior. Pharmaceutical companies have invested heavily in the development of androgen therapies for female sexual desire disorders (FSDDs), but today there are still no FDA-approved androgen therapies for women. Nonetheless, testosterone is currently, and frequently, prescribed off-label for the treatment of low sexual desire in women, and the idea of testosterone as a possible cure-all for female sexual dysfunction remains popular. These researchers placed the ongoing debate concerning the hormonal modulation of women's sexual desire within a historical context, and reviewed controlled trials of estrogen and/or androgen therapies for low sexual desire in post-menopausal women. They noted that available studies demonstrated that estrogen-only therapies that produce peri-ovulatory levels of circulating estradiol increase sexual desire in post-menopausal women. Testosterone at supra-physiological, but not at physiological, levels enhances the effectiveness of low-dose estrogen therapies at increasing women's sexual desire; however, the mechanism by which supra-physiological testosterone increases women's sexual desire in combination with an estrogen remains unknown. Because effective therapies require supra-physiological amounts of testosterone, it remains unclear whether endogenous testosterone contributes to the modulation of women's sexual desire. The authors concluded that the likelihood that an androgen-only clinical treatment will meaningfully increase women's sexual desire is minimal, and the focus of pharmaceutical companies on the development of androgen therapies for the treatment of FSDDs is likely misplaced.

Androgens for the Treatment for Female Menopause

Cappelletti and Wallen (2016) stated that both estradiol and testosterone have been implicated as the steroid critical for modulating women's sexual desire. By contrast, in all other female mammals only estradiol has been shown to be critical for female sexual motivation and behavior. Pharmaceutical companies have invested heavily in the development of androgen therapies for female sexual desire disorders, but today there are still no FDA approved androgen therapies for women. Nonetheless, testosterone is currently, and frequently, prescribed off-label for the treatment of low sexual desire in women, and the idea of testosterone as a possible cure-all for female sexual dysfunction remains popular. These investigators placed the ongoing debate concerning the hormonal modulation of women's sexual desire within a historical context, and reviewed controlled trials of estrogen and/or androgen therapies for low sexual desire in post-menopausal women. These studies demonstrated that estrogen-only therapies that produce peri-ovulatory levels of circulating estradiol increase sexual desire in post-menopausal women. Testosterone at supra-physiological, but not at physiological, levels enhances the effectiveness of low-dose estrogen therapies at increasing women's sexual desire; however, the mechanism by which supra-physiological testosterone increases women's sexual desire in combination with an estrogen remains unknown. Because effective therapies require supra-physiological amounts of testosterone, it remains unclear whether endogenous testosterone contributes to the modulation of women's sexual desire. The authors concluded that the likelihood that an androgen-only clinical treatment would meaningfully increase women's sexual desire is minimal, and the focus of pharmaceutical companies on the development of androgen therapies for the treatment of female sexual desire disorders is likely misplaced.

Zhao and colleagues (2018) noted that higher androgen and lower estrogen levels are associated with cardiovascular disease (CVD) risk factors in women. However, studies on sex hormones and incident CVD events in women have yielded conflicting results. These investigators evaluated the associations of sex hormone levels with incident CVD, coronary heart disease (CHD), and heart failure (HF) events among women without CVD at baseline. These researchers studied 2,834 post-menopausal women participating in the MESA (Multi-Ethnic Study of Atherosclerosis) with testosterone, estradiol, dehydroepiandrosterone, and sex hormone binding globulin (SHBG) levels measured at baseline (2000 to 2002). They used Cox hazard models to evaluate associations of sex hormones with each outcome, adjusting for demographics, CVD risk factors, and hormone therapy use. The mean age was 64.9 ± 8.9 years. During 12.1 years of follow-up, 283 CVD, 171 CHD, and 103 HF incident events occurred. In multivariable-adjusted models, the hazard ratio (HR; 95 % CI) associated with 1 SD greater log-transformed sex hormone level for the respective outcomes of CVD, CHD, and HF were as follows: total testosterone: 1.14 (95 % CI: 1.01 to 1.29), 1.20 (95 % CI: 1.03 to 1.40), 1.09 (95 % CI: 0.90 to 1.34); estradiol: 0.94 (95 % CI: 0.80 to 1.11), 0.77 (95 % CI: 0.63 to 0.95), 0.78 (95 % CI: 0.60 to 1.02); and testosterone/estradiol ratio: 1.19 (95 % CI: 1.02 to 1.40), 1.45 (95 % CI: 1.19 to 1.78), 1.31 (95 % CI: 1.01 to 1.70). Dehydroepiandrosterone and SHBG levels were not associated with these outcomes. The authors concluded that among post-menopausal women, a higher testosterone/estradiol ratio was associated with an elevated risk for incident CVD, CHD, and HF events, higher levels of testosterone associated with increased CVD and CHD, whereas higher estradiol levels were associated with a lower CHD risk. Sex hormone levels after menopause were associated with women's increased CVD risk later in life.

Furthermore, an UpToDate review on “Treatment of menopausal symptoms with hormone therapy” (Martin and Barbieri, 2018) states that “The known decrease in ovarian androgen production rates and serum androgen concentrations has caused concern that menopause might be associated with a decline in libido. An age-associated decline in sexual desire has been observed in both men and women. However, it is unclear whether the decline in libido in women is age or menopause related, since studies in women have not shown a significant correlation between libido and the serum estradiol or testosterone concentration. Clinical trials of exogenous testosterone replacement suggest modest benefits of testosterone therapy in some postmenopausal women. However, there are potential risks associated with androgen replacement, and the use of testosterone is limited by the lack of approved and commercially available products for women. Until the beneficial effects of androgen replacement are better established, it cannot be routinely recommended to postmenopausal women”.

Testosterone for the Improvement of Cognitive Function in Aging Men

Hua and colleagues (2016) stated that endogenous testosterone in the aging man has been scrutinized extensively in regard to its effects on performance in many cognitive domains, especially verbal fluency, visuo-spatial and visuo-perceptual abilities, memory, and executive function. Studies of testosterone supplementation have sought to identify potential cognitive improvements in men with and without baseline cognitive impairment, and have had a wide range of results. The variability in outcomes is likely related, in part, to the lack of consensus on methods for testosterone measurement and supplementation and, in part, to the disparate measures of cognitive function used in RCTs. Despite the limitations imposed by such inconsistent methods, promising associations have been found between cognition and testosterone supplementation in both eugonadal men and men with low testosterone levels, with and without baseline cognitive dysfunction. These investigators highlighted the cognitive measures used in and the outcomes of existing studies of testosterone and cognition in aging men. The authors concluded that that larger studies and a more standardized approach to assessment are needed before one can fully understand and realize sustained benefits from testosterone supplementation in the elderly male population, especially given the substantial increase in testosterone supplementation in clinical practice.

Resnick and associates (2017) examined if testosterone treatment compared with placebo is associated with improved verbal memory and other cognitive functions in older men with low testosterone and age-associated memory impairment (AAMI). The Testosterone Trials (TTrials) were 7 trials to evaluate the effectiveness of testosterone treatment in older men with low testosterone levels. The Cognitive Function Trial evaluated cognitive function in all TTrials participants. In 12 US academic medical centers, a total of 788 men who were 65 years or older with a serum testosterone level less than 275 ng/ml and impaired sexual function, physical function, or vitality were allocated to testosterone treatment (n = 394) or placebo (n = 394). A subgroup of 493 men met criteria for AAMI based on baseline subjective memory complaints and objective memory performance. Enrollment in the TTrials began on June 24, 2010; the final participant completed treatment and assessment in June 2014. Participants received testosterone gel (adjusted to maintain the testosterone level within the normal range for young men) or placebo gel for 1 year. The primary outcome was the mean change from baseline to 6 months and 12 months for delayed paragraph recall (score range of 0 to 50) among men with AAMI. Secondary outcomes were mean changes in visual memory (Benton Visual Retention Test; score range of 0 to -26), executive function (Trail-Making Test B minus A; range of -290 to 290), and spatial ability (Card Rotation Test; score range of -80 to 80) among men with AAMI. Tests were administered at baseline, 6 months, and 12 months. Among the 493 men with AAMI (mean age of 72.3 years [SD, 5.8]; mean baseline testosterone, 234 ng/dL [SD, 65.1]), 247 were assigned to receive testosterone and 246 to receive placebo. Of these groups, 247 men in the testosterone group and 245 men in the placebo completed the memory study. There was no significant mean change from baseline to 6 and 12 months in delayed paragraph recall score among men with AAMI in the testosterone and placebo groups (adjusted estimated difference, -0.07 [95 % CI: -0.92 to 0.79]; p = 0.88). Mean scores for delayed paragraph recall were 14.0 at baseline, 16.0 at 6 months, and 16.2 at 12 months in the testosterone group and 14.4 at baseline, 16.0 at 6 months, and 16.5 at 12 months in the placebo group. Testosterone was also not associated with significant differences in visual memory (-0.28 [95 % CI: -0.76 to 0.19]; p = 0.24), executive function (-5.51 [95 % CI: -12.91 to 1.88]; p = 0.14), or spatial ability (-0.12 [95 % CI: -1.89 to 1.65]; p = 0.89). The authors concluded that among older men with low testosterone and age-associated memory impairment, treatment with testosterone for 1 year compared with placebo was not associated with improved memory or other cognitive functions.

Testosterone Treatment and Amyotrophic Lateral Sclerosis

The European Federation of Neurological Societies’ guidelines on the clinical management of amyotrophic lateral sclerosis (ALS) (Andersen et al, 2012) did not recommend testosterone for the treatment of amyotrophic lateral sclerosis because of insufficient evidence of its effectiveness.

Testosterone Treatment and Heart Failure

Toma et al (2012) stated that low testosterone is an independent predictor of reduced exercise capacity and poor clinical outcomes in patients with heart failure (HF). These investigators examined if testosterone therapy improves exercise capacity in patients with stable chronic HF. They searched Medline, Embase, Web of Science, and Cochrane Central Register of Controlled Trials (1980 to 2010). Eligible studies included randomized controlled trials (RCTs) reporting the effects of testosterone on exercise capacity in patients with HF. Reviewers determined the methodological quality of studies and collected descriptive, quality, and outcome data. A total of 4 trials (n = 198; men, 84 %; mean age of 67 years) were identified that reported the 6-minute walk test (2 RCTs), incremental shuttle walk test (2 RCTs), or peak oxygen consumption (2 RCTs) to assess exercise capacity after up to 52 weeks of treatment. Testosterone therapy was associated with a significant improvement in exercise capacity compared with placebo. The mean increase in the 6-minute walk test, incremental shuttle walk test, and peak oxygen consumption between the testosterone and placebo groups was 54.0 m (95 % confidence interval [CI]: 43.0 to 65.0 m), 46.7 m (95 % CI: 12.6 to 80.9 m), and 2.70 ml/kg per min (95 % CI: 2.68 to 2.72 mL/kg per min), respectively. Testosterone therapy was associated with a significant increase in exercise capacity as measured by units of pooled SDs (net effect, 0.52 SD; 95 % CI: 0.10 to 0.94 SD). No significant adverse cardiovascular events were noted. The authors concluded that given the unmet clinical needs, testosterone appears to be a promising therapy to improve functional capacity in patients with HF. They stated that adequately powered RCTs are required to assess the benefits of testosterone in this high-risk population with regard to quality of life, clinical events, and safety.

Testosterone Treatment and Increases in Cardiovascular Risk

Based on the available evidence from studies and expert input from an FDA Advisory Committee meeting, the FDA has concluded that there is a possible increased cardiovascular risk associated with testosterone use (FDA, 2015). These studies included aging men treated with testosterone. Some studies reported an increased risk of heart attack, stroke, or death associated with testosterone treatment, while others did not (FDA, 2015).

Budoff and colleagues (2017) stated that recent studies have yielded conflicting results as to whether testosterone treatment increases cardiovascular risk. In a double-blinded, placebo-controlled, multi-center trial, these researchers tested the hypothesis that testosterone treatment of older men with low testosterone slows progression of non-calcified coronary artery plaque volume. Participants were 170 of 788 men aged 65 years or older with an average of 2 serum testosterone levels lower than 275 ng/dL (82 men assigned to placebo, 88 to testosterone) and symptoms suggestive of hypogonadism who were enrolled in the Testosterone Trials between June 24, 2010, and June 9, 2014. Testosterone gel, with the dose adjusted to maintain the testosterone level in the normal range for young men, or placebo gel for 12 months. The primary outcome was non-calcified coronary artery plaque volume, as determined by coronary computed tomographic angiography; secondary outcomes included total coronary artery plaque volume and coronary artery calcium score (range of 0 to greater than 400 Agatston units, with higher values indicating more severe atherosclerosis). Of 170 men who were enrolled, 138 (73 receiving testosterone treatment and 65 receiving placebo) completed the study and were available for the primary analysis. Among the 138 men, the mean (SD) age was 71.2 (5.7) years, and 81 % were white. At baseline, 70 men (50.7 %) had a coronary artery calcification score higher than 300 Agatston units, reflecting severe atherosclerosis. For the primary outcome, testosterone treatment compared with placebo was associated with a significantly greater increase in non-calcified plaque volume from baseline to 12 months (from median values of 204 mm3 to 232 mm3 versus 317 mm3 to 325 mm3, respectively; estimated difference, 41 mm3; 95 % CI: 14 to 67 mm3; p = 0.003). For the secondary outcomes, the median total plaque volume increased from baseline to 12 months from 272 mm3 to 318 mm3 in the testosterone group versus from 499 mm3 to 541 mm3 in the placebo group (estimated difference, 47 mm3; 95 % CI: 13 to 80 mm3; p = 0.006), and the median coronary artery calcification score changed from 255 to 244 Agatston units in the testosterone group versus 494 to 503 Agatston units in the placebo group (estimated difference, -27 Agatston units; 95 % CI: -80 to 26 Agatston units). No major adverse cardiovascular events occurred in either group. The authors concluded that among older men with symptomatic hypogonadism, treatment with testosterone gel for 1 year compared with placebo was associated with a significantly greater increase in coronary artery non-calcified plaque volume, as measured by coronary computed tomographic angiography. Moreover, they stated that larger studies are needed to understand the clinical implications of this finding.


The above policy is based on the following references:

  1. AACE Hypogonadism Task Force. American Association of Clinical Endocrinologists Medical Guidelines for Clinical Practice for the Evaluation and Treatment of Hypogonadism in Adult Male Patients – 2002 Update. Endocr Prac. 2002;8:439‐456.
  2. Bhasin S, Brito JP, Cunninghan GR, et al. Testosterone Therapy in Men with Hypogonadism: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2018;103(5):1715-1744.
  3. Bhasin S, Cunningham GR, Hayes FJ, et al.; Endocrine Society Task Force. Testosterone therapy in men with androgen deficiency syndromes: An Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2010;95(6):2536-2559.
  4. Bhasin S, Javanbakht M. Can androgen therapy replete lean body mass and improve muscle function in wasting associated with human immunodeficiency virus infection? JPEN J Parenter Enteral Nutr. 1999;23(6 Suppl):S195-S201.
  5. Bin-Abbas B, Conte FA, Grumbach MM, et al. Congenital hypogonadotropic hypogonadism and micropenis: Effect of testosterone treatment on adult penile size and why sex reversal is not indicated. J Pediatr. 1999;134(5):579-583.
  6. Bojesen A, Gravholt CH. Klinefelter syndrome in clinical practice. Nat Clin Pract Urol. 2007;4(4):192-204.
  7. Borst SE, Mulligan T. Testosterone replacement therapy for older men. Clin Interv Aging. 2007;2(4):561-566.
  8. Budoff MJ, Ellenberg SS, Lewis CE, et al. Testosterone treatment and coronary artery plaque volume in older men with low testosterone. JAMA. 2017;317(7):708-716.
  9. Cameron DR, Braunstein GD. The use of dehydroepiandrosterone therapy in clinical practice. Treat Endocrinol. 2005;4(2):95-114.
  10. Cappelletti M, Wallen K. Increasing women's sexual desire: The comparative effectiveness of estrogens and androgens. Horm Behav. 2016;78:178-193.
  11. Corcoran C, Grinspoon S. Treatments for wasting in patients with the acquired immunodeficiency syndrome. N Engl J Med. 1999;340(22):1740-1750.
  12. EFNS Task Force on Diagnosis and Management of Amyotrophic Lateral Sclerosis, Andersen PM, Abrahams S, Borasio GD, et al. EFNS guidelines on the clinical management of amyotrophic lateral sclerosis (MALS) -- revised report of an EFNS task force. Eur J Neurol. 2012;19(3):360-375.
  13. Endo Pharmaceuticals Solutions Inc. Aveed (testosterone undecanoate) injection, for intramuscular use. Prescribing Information. Malvern, PA: Endo Pharmaceuticals Solutions; revised August 2021.
  14. Gender Identity Research and Education Society. Guidance for GPs and other clinicians on the treatment of gender variant people. London, UK: UK Department of Health; March 10, 2008.
  15. Goldstein I, Alexander JL. Practical aspects in the management of vaginal atrophy and sexual dysfunction in perimenopausal and postmenopausal women. J Sex Med. 2005;2 Suppl 3:154-165.
  16. Graziottin A, Basson R. Sexual dysfunction in women with premature menopause. Menopause. 2004;11(6 Pt 2):766-777.
  17. Hayes, Inc. Testosterone testing.Final Evidence Report. Prepared by Hayes, Inc. for the Washington State Healthcare Authority Health Technology Assessment Program. Olympia, WA: Health Technology Assessment Program, Washington State Healthcare Authority;February 6, 2015.
  18. Hembree WC, Cohen-Kettenis PT, Gooren L, et al. Endocrine Treatment of Gender-Dysphoric/Gender-Incongruent Persons: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2017:102(11):3869–3903.
  19. Hengge UR. Testosterone replacement for hypogonadism: Clinical findings and best practices. AIDS Read. 2003;13(12 Suppl):S15-S21.
  20. Hua JT, Hildreth KL, Pelak VS. Effects of testosterone therapy on cognitive function in aging: A systematic review. Cogn Behav Neurol. 2016;29(3):122-138.
  21. IBM Micromedex, DRUGDEX System [Internet database]. Armonk, NY: IBM Watson Health; Updated periodically.
  22. Makinen JI, Huhtaniemi I. Androgen replacement therapy in late-onset hypogonadism: Current concepts and controversies - a mini-review. Gerontology. 2011;57(3):193-202.
  23. Martin KA, Barbieri RL. Treatment of menopausal symptoms with hormone therapy. UpToDate [online serial]. Waltham, MA: UpToDate; reviewed October 2018.
  24. No authors listed. Replacing testosterone in men. Drug Ther Bull. 1999;37(1):3-6.
  25. North American Menopause Society. The role of testosterone therapy in postmenopausal women: Position statement of The North American Menopause Society. Menopause. 2005;12(5):496-511; quiz 649.
  26. Payne C, Wiffen PJ, Martin S. Interventions for fatigue and weight loss in adults with advanced progressive illness. Cochrane Database Syst Rev. 2012;(1):CD008427.
  27. Petak SM, Nankin HR, Spark RF, et al.; AACE Hypogonadism Task Force. American Association of Clinical Endocrinologists Medical Guidelines for Clinical Practice for the Evalation and Treatment of Hypogonadism in Adult Male Patients - 2002 Update. Jacksonville, FL: AACE; 2002.
  28. Price JF, Leng GC. Steroid sex hormones for lower limb atherosclerosis. Cochrane Database Syst Rev. 2001;(3):CD000188.
  29. Reis SL, Abdo CH. Benefits and risks of testosterone treatment for hypoactive sexual desire disorder in women: A critical review of studies published in the decades preceding and succeeding the advent of phosphodiesterase type 5 inhibitors. Clinics (Sao Paulo). 2014;69(4):294-303.
  30. Resnick SM, Matsumoto AM, Stephens-Shields AJ, et al. Testosterone treatment and cognitive function in older men with low testosterone and age-associated memory impairment. JAMA. 2017;317(7):717-727.
  31. Rhoden EL, Morgentaler A. Risks of testosterone-replacement therapy and recommendations for monitoring. N Engl J Med. 2004;350(5):482-492.
  32. Richmond EJ, Rogol AD. Male pubertal development and the role of androgen therapy. Nat Clin Pract Endocrinol Metab. 2007;3(4):338-344.
  33. Rolf C, Nieschlag E. Potential adverse effects of long-term testosterone therapy. Baillieres Clin Endocrinol Metab. 1998;12(3):521-534.
  34. Shelton JB, Rajfer J. Androgen deficiency in aging and metabolically challenged men. Urol Clin North Am. 2012;39(1):63-75.
  35. Snyder P. Clinical features and diagnosis of male hyogonadism. UpToDate [online serial]. Waltham, MA: UpToDate; updated October 2013.
  36. Snyder P. Testosterone treatment of male hypogonadism. UpToDate [online serial]. Waltham, MA: UpToDate; updated October 2013.
  37. Somboonporn W, Davis SR. Postmenopausal testosterone therapy and breast cancer risk. Maturitas. 2004;49(4):267-275.
  38. Swedish Council on Technology Assessment in Health Care (SBU). Testosterone replacement in men with age-related hormone deficiency - early assessment briefs (ALERT). Stockholm, Sweden: SBU; 2002.
  39. Theodoraki A, Bouloux PM. Testosterone therapy in men. Menopause Int. 2009;15(2):87-92.
  40. Toma M, McAlister FA, Coglianese EE, et al. Testosterone supplementation in heart failure: A meta-analysis. Circ Heart Fail. 2012;5(3):315-321.
  41. U.S. Food and Drug Administration (FDA). FDA cautions about using testosterone products for low testosterone due to aging; Requires labeling change to inform of possible increased risk of heart attack and stroke. Testosterone Products: Drug Safety Communication. Silver Spring, MD: FDA; March 3, 2015.
  42. Wang C, Nieschlag E, Swerdloff R, et al. Investigation, treatment, and monitoring of late‐onset hypogonadism in males: ISA, ISSAM, EAU, EAA, and ASA recommendations. J Androl. 2008;159:507‐514.
  43. Winters SJ. Current status of testosterone replacement therapy in men. Arch Fam Med. 1999;8(3):257-263.
  44. World Professional Association for Transgender Health. Standards of care for the health of transsexual, transgender, and gender-nonconforming people, 7th version. Minneapolis, MN: World Professional Association for Transgender Health; 2012. Available at http://www.wpath.org. Accessed June 6, 2022.
  45. Zhao D, Guallar E, Ouyang P, et al. Endogenous sex hormones and incident cardiovascular disease in post-menopausal women. J Am Coll Cardiol. 2018;71(22):2555-2566.


Can you get AVEED at the pharmacy? ›

AVEED® is only available through your doctor's office, clinic, or hospital, and it is not a medicine you will give yourself at home.

Is AVEED safe? ›

AVEED® can cause a serious lung problem called POME. POME is caused by tiny droplets of oil that have traveled to the lungs. Symptoms of a POME reaction may include: cough or urge to cough.

Is AVEED an anabolic steroid? ›

Aveed is an androgen and anabolic steroid drug used by men as a testosterone replacement.

How long does it take for AVEED to start working? ›

How long does it take Aveed (testosterone undecanoate) to work? Aveed (testosterone undecanoate) should start to raise your testosterone levels after the first injection. Although your body fully absorbs the medication in about 1 week, it can take 3 to 4 months before your testosterone levels are stable.

Is aveed available in the US? ›

There is currently no therapeutically equivalent version of Aveed available in the United States.

Where can I get aveed? ›

You can acquire AVEED® through a Specialty Pharmacy Provider, which bills the patient or patient's health plan directly. The prescription will be sent to a certified healthcare setting, such as your office or hospital pharmacy.

Is testosterone undecanoate safe to take? ›

Testosterone undecanoate appears to be a safe oral androgen. A yearly checkup of the patient on therapy with this androgen seems adequate.

What is the side effects of Aveed? ›

Common side effects of Aveed include acne, injection site pain or other reactions, PSA (prostate-specific antigen) increase, increased estradiol level, low testosterone levels, fatigue, feeling tired, irritability, increased red blood cell count, difficulty sleeping (insomnia), mood swings, aggression, difficulty ...

How much testosterone undecanoate should I take? ›

What is the dosage for testosterone undecanoate capsule? Males over 18 years of age: The recommended dose of testosterone undecanoate is 750 mg (3 ml) intramuscularly; followed by 750 mg (3 ml) intramuscularly after 4 weeks, then 750 mg (3 ml) intramuscularly every 10 weeks thereafter.

How long does testosterone undecanoate stay in your system? ›

Testosterone undecanoate
Clinical data
MetabolitesTestosterone, undecanoic acid, metabolites of testosterone
Elimination half-lifeIn TSO : 20.9 days ( i.m. ) In CO : 33.9 days ( i.m. )
Excretion~90% Urine, 6% feces
35 more rows

What are the side effects of testosterone undecanoate injection? ›

Nausea, vomiting, headache, skin color changes, increased/decreased sexual interest, oily skin, hair loss, and acne may occur. Pain or redness at the injection site may also occur. If any of these effects last or get worse, tell your doctor or pharmacist promptly.

How long does testosterone undecanoate take to work? ›

It is very likely that the positive effects of testosterone on depressive symptoms start as early as after 3–6 weeks, but will most likely take 18–30 weeks to find the patient with a significant improvement. A recent study in hypogonadal men receiving i.m. testosterone undecanoate demonstrated such effects.

What is a dangerously low testosterone level? ›

What is a low testosterone level? The American Urology Association (AUA) considers low blood testosterone to be less than 300 nanograms per deciliter (ng/dL) for adults. However, some researchers and healthcare providers disagree with this and feel that levels below 250 ng/dL are low.

How fast do testosterone levels drop after injection? ›

Levels of circulating testosterone peak within 10 to 12 hours of initial administration, and reach steady state within 24 hours (14). When the product is discontinued, testosterone levels drop below normal within two to 4 hours, allowing for quick reversal if necessary.

What happens after your first testosterone injection? ›

When you inject testosterone, you're putting a depot of oil into muscle tissue which is slowly dispersed into the bloodstream (for several days, or even weeks, depending on the ester). As a side effect of this, you might experience injection site soreness for a few days after the fact.

Who makes Aveed? ›

U.S. FDA Approves AVEED™ (Testosterone Undecanoate) Injectable Testosterone Replacement Therapy For Men Living With Hypogonadism, Or Low-T. DUBLIN , March 6, 2014 /PRNewswire/ -- Endo International plc (NASDAQ: ENDP) (TSX: ENL) announced today that its operating company Endo Pharmaceuticals Inc.

How do you give Aveed? ›

AVEED® should be injected deeply into the gluteus medius muscle, avoiding the superior gluteal arteries and sciatic nerve. Intravascular injection may lead to pulmonary microembolism of the oily solution. Deliver the full dose using steady pressure over a period of 60 to 90 seconds.

What is testosterone undecanoate use for? ›

Uses. This medication is used by men who have low or no testosterone due to certain medical conditions (such as hypogonadism). Testosterone belongs to a class of drugs known as androgens. It helps the body to develop and maintain male sexual characteristics (masculinity), such as a deep voice and body hair.

What does Aveed do? ›

Aveed is a prescription medicine that contains testosterone. Aveed is used to treat adult males who have low or no testosterone due to certain medical conditions.

What is the CPT code for testosterone injection? ›

Group 1
3 more rows

What is the J code for Aveed? ›

Testosterone Undecanoate Injection (Aveed)
Information in the [brackets] below has been added for clarification purposes. Codes requiring a 7th character are represented by "+":
CodeCode Description
J3145Injection, testosterone undecanoate, 1 mg
S0179Megestrol acetate, oral, 20mg
Other HCPCS codes related to the CPB:
112 more rows

Which testosterone therapy is safest? ›

Injection of testosterone may be safer and more effective than transdermal administration for combating loss of muscle and bone in older men.

Does injecting testosterone affect your liver? ›

The testosterone replacement therapy (TRT) testosterone undecanoate oral capsules shows no evidence of liver toxicity, according to data from a two-year, multi-center study presented at ENDO 2021.

Are testosterone injections safe? ›

Testosterone therapy has various risks, including: Worsening sleep apnea — a potentially serious sleep disorder in which breathing repeatedly stops and starts. Causing acne or other skin reactions. Stimulating noncancerous growth of the prostate (benign prostatic hyperplasia) and growth of existing prostate cancer.

How much testosterone should I inject? ›

Adults—At first, 75 milligrams (mg) injected under the skin once a week. Your doctor may adjust your dose as needed. Children—Use and dose must be determined by your doctor.

How long does testosterone stay in your system? ›

If you take an anabolic steroid or undergo testosterone therapy, your body stops making its own testosterone and relies on the steroids you receive. Testosterone would only stay in your system for around three to four weeks if you stopped taking the steroids.

How many mL are in a vial of testosterone? ›

Testosterone Cypionate Injection USP is available in 10 mL multidose vials.

Can you self inject Nebido? ›

- We do not recommend self-administration of Nebido as this is a more difficult to give (due to the high viscosity and preferred site of administration). If you wish to switch from Nebido to Sustanon, so you can self-inject, we will get advice from your GIC - A change to testosterone gel is an option.

What monitoring is required for patient on testosterone replacement? ›

After starting testosterone (T) therapy, patients should be evaluated at 3, 6 and 12 months, then annually thereafter, to monitor: serum testosterone - aim for a therapeutic target in the mid to upper range (15-30nmol/L), for an optimal response. haematocrit - levels should remain <54%.

How can I get a prescription without seeing a doctor? ›

Can I get a prescription without seeing a doctor? Legally, you need to have a consultation with a doctor before you can receive prescription medication. That said, you can get an online prescription without going into the doctor's office by seeing a virtual doctor.

Can pharmacist give antibiotics? ›

If you want to buy an over-the-counter medicine, the pharmacist and their team can help you choose. Antibiotics will not be available over the counter to treat minor conditions.

How do you get an emergency inhaler? ›

If you do not have a prescription. If you run out of prescription medicine and do not have a prescription with you, you can get an emergency supply from a pharmacy without a prescription. Take an old prescription or the medicine's packaging with you, if you have it.

Can pharmacists issue emergency prescriptions? ›

Once you've arrived at the pharmacy, speak to a pharmacist and explain that you're in need of an emergency prescription. The pharmacist will go over a few simple questions with you and you'll be on your way in no time.

Is Pushhealth com legitimate? ›

Is Push Health secure / legitimate? Yes. Push Health is built on modern software with a strong emphasis on protecting personal health data. All payment information processed through Push Health is done via Braintree, a leading web payment vendor, and credit card data is never stored in our system.

Can you get a repeat prescription without seeing a doctor? ›

Doctors on Demand's online prescription service is called QuickScript and allows you to obtain a repeat prescription without a live doctor's consultation. And there is no need to wait in a doctor's waiting room to see a doctor just for your regular prescription.

How can I get my doctor's prescription online? ›

Download FREE Practo app
  1. Find Doctors - Book an appointment.
  2. Video Consult - Consult top doctors.
  3. Medicines - Practo pharmacy.
  4. Lab Tests - Book tests & checkup.
  5. Surgeries - Expert surgical care.
19 Nov 2018

Is a pharmacist a doctor? ›

To become a pharmacist, you will need to complete a Doctor of Pharmacy. You will need to complete your undergraduate program as well as 4-year PharmD program to become licenced.

Will a pharmacist look in my throat? ›

How to get your sore throat tested. A pharmacist will usually test a sore throat with a throat swab and decide whether or not to offer antibiotics. If the sore throat is not bacterial, they can suggest treatments to help you manage your symptoms, like painkillers and lozenges.

Can 111 give me a prescription? ›

111 Online can now automatically book you an appointment with a nearby open Pharmacy for a consultation about providing your emergency prescription. Using 111 Online, there is also no waiting on the phone to speak to 111, and no waiting for a call-back.

Can inhalers damage your lungs? ›

Constant exposure to the inhaler could lead to your lungs to become under-responsive to the medication, and your airways could become hypersensitive to common asthma triggers.

What are silent asthma symptoms? ›

Silent Asthma Symptoms
  • Distress, anxiety, or restlessness.
  • Fatigue.
  • Chest tightness.
  • Feeling short of breath.
  • Difficulty speaking.
6 Jun 2022

Can I get a blue inhaler over the counter? ›

No, you need a prescription to buy Ventolin, which means that you cannot buy it over the counter.

How often can you get an emergency prescription? ›

Most pharmacies ask people to order their repeat prescription at least two days in advance because there are various checks your prescription will have to go through in order for your medication to be dispensed safely.

What do I do if I ran out of medication? ›

The best thing to do when you realize you're going to run out of medication is call your doctor. They may be willing to contact the pharmacy of your choice so you can get a prescription filled there. Even if it's after-hours, call anyway and leave a message explaining the situation.

Can I take a repeat prescription to any pharmacy? ›

Can I get a repeat prescription from any / a different pharmacy? You are able to change your nominated pharmacy at any time. But in some cases, you GP may send your prescriptions to a specific pharmacy / dispensary.

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