Anabolic agents (oxandrolone, growth hormone, IGF-1, testosterone) in burn recovery

Overview¶

Severe burns drive the most sustained catabolic state of any survivable injury, and much of the morbidity and mortality of severely burned patients is tied to that hypermetabolism and catabolism with their accompanying impairment of wound healing and increased infection risk ^[47]. Patients with burns over 40% TBSA always experience catabolism, which causes metabolic derangements that persist for at least one year after injury; patients below 40% TBSA generally do not become catabolic unless sepsis develops ^[4]. The damage is structural: lean body mass is consumed, linear growth is arrested in children, and muscle strength and function decline. Nutrition is foundational but insufficient on its own to halt and reverse the damage done by the catabolic pathways activated after severe burn injury ^[24], which is the rationale for adding pharmacologic anabolic agents.

The injury also collapses the body's own anabolic hormone axis. Burned men show profound, persistent depression of serum testosterone, and the growth hormone–IGF-1 axis becomes uncoupled, with low circulating IGF-1 despite the stress of injury ^[1,3,6]. Pharmacotherapy therefore aims either to replace a deficient anabolic signal (testosterone, IGF-1) or to supply a supraphysiologic one (growth hormone), or to deliver a synthetic anabolic steroid that drives protein synthesis (oxandrolone). Among proposed agents, data support testosterone, oxandrolone, recombinant human growth hormone, insulin, metformin, and propranolol in improving skeletal-muscle protein net balance in severe burns ^[5]. This page covers the four anabolic agent classes named in its title; insulin and propranolol are addressed on their own pages. Of these, oxandrolone is the agent with the deepest and most consistent clinical evidence base ^[43].

Pathophysiology of the catabolic state and the anabolic axis¶

The endocrine signature of a major burn is a fall in anabolic drive layered on a catabolic surge. Testosterone collapses early and stays low: levels decline very rapidly after the burn, remain low for weeks, and rise toward the end of hospitalization but usually have not normalized at discharge, and the more severe the burn, the lower the testosterone ^[1]. The defect is central; pulsatile luteinizing-hormone release is absent or diminished in burned patients with low testosterone, pointing to hypothalamic dysfunction rather than primary testicular failure ^[2]. Cortisol and catecholamine output rise at the same time, completing the catabolic hormonal picture.

The growth hormone–IGF-1 axis is also disturbed. Serum growth hormone and IGF-1 are low in the first weeks despite injury stress and more than adequate nutrition, so burn patients have inappropriately low growth-hormone secretion and IGF-1 production ^[3]. IGF-1 is markedly suppressed after severe burn; this suppression correlates with low serum albumin ^[49] and parallels a reduction in its major binding protein, IGFBP-3 ^[50]. This uncoupling, together with elevated glucagon and the loss of insulin's normal restraint on IGFBP-1, drives the reduction in IGF-1 availability after burn ^[6].

These derangements explain the mechanistic targets of each agent. IGF-1 itself changes the metabolic response after thermal injury and is a plausible treatment target, decreasing oxygen consumption and increasing body weight in burned animals ^[8]. Testosterone and androgen-receptor agonists have long been known to prevent or reverse burn muscle wasting, although the exact molecular mechanisms remain incompletely defined ^[34]. Oxandrolone, a synthetic testosterone analog, acts on this same anabolic axis to drive protein synthesis without the catabolic load of the native hormones.

Management by agent¶

Anabolic pharmacotherapy is an adjunct layered on early excision, wound closure, and aggressive nutrition; the addition of anabolic agents decreases the degree of lean-mass loss and increases the rate of restoration ^[46]. Attenuation of the hypermetabolic response by pharmacologic means has emerged as an essential component of severe-burn management ^[7]. Agent selection in current practice favors the synthetic testosterone analog oxandrolone, with growth hormone, IGF-1, and testosterone occupying narrower or more investigational roles ^[4].

Oxandrolone¶

Oxandrolone is the most-used and best-evidenced agent, and has been characterized as having proven benefits in thermal burn injury that have made it a standard of care in many centers ^[43]. The standard regimen is 0.1 mg/kg by mouth twice daily ^[17]. In a controlled study, muscle protein net balance decreased in controls but improved in the oxandrolone group, with the gain driven by increased protein-synthesis efficiency while breakdown was unchanged ^[9]. A subsequent trial confirmed that oxandrolone improves protein net balance and lean mass in the severely burned ^[10]. Early studies established that an anabolic steroid combined with increased protein intake significantly increases the rate of post-burn weight restoration ^[11], and that oxandrolone significantly decreases weight and nitrogen loss and accelerates donor-site healing compared with placebo ^[12]. Lean mass regained on oxandrolone is durable: in a rehabilitation cohort, patients regained weight and lean mass two to three times faster than with nutrition alone, and the regained mass was maintained six months after stopping the drug ^[13].

The pivotal adult trial was a multicenter, prospective, randomized, double-blind study showing that length of stay was shorter in the oxandrolone group than in placebo (31.6 versus 43.3 days), a difference that strengthened when deaths were excluded and stay was indexed to burn size ^[14]. A separate analysis of severely burned adults found early oxandrolone treatment to be safe and possibly associated with improved survival ^[15]. In adults, oxandrolone 10 mg orally twice daily has been used to improve wound healing, restore lean body mass, and accelerate weight gain ^[16].

Recombinant human growth hormone¶

Recombinant human growth hormone (rhGH) is a potent anabolic agent whose burn evidence centers on wound and donor-site healing in children, typically at 0.2 mg/kg/day subcutaneously. In severely burned children, rhGH at 0.2 mg/kg/day produced significantly higher serum IGF-1 levels and a significant decrease in donor-site healing times compared with placebo, shortening length of stay indexed to burn size ^[25]. A double-blind randomized study in children with large burns found both forms of rhGH effective in reducing donor-site healing time, with total length of stay reduced by more than 25% ^[26]. The healing effect is structural; donor sites in rhGH-treated patients showed increased basal-lamina coverage of the dermal–epidermal junction, with significantly decreased healing times versus placebo ^[27]. A prospective multicenter trial in adults with severe burns reported a mortality rate of 0.89% with rhGH versus 5.26% in controls, a difference that did not reach significance, and concluded that rhGH in appropriate dosage could be safe with blood-glucose monitoring ^[28].

IGF-1 and IGF-1/IGFBP-3¶

IGF-1 has been studied as a way to deliver the anabolic signal that growth hormone normally produces, often complexed with its binding protein IGFBP-3 to improve tolerability. In severely burned children, IGF-1/IGFBP-3 at 1 to 4 mg/kg/day improved net protein balance and increased muscle protein fractional synthetic rates, with the effect more pronounced in catabolic children and with negligible clinical side effects ^[31]. In severely burned adults, IGF-1/IGFBP-3 improved leg protein balance and net protein synthesis without development of glucose abnormalities, and patients remained euglycemic without electrolyte imbalances ^[32]. IGF-1 therapy has remained largely investigational and has not entered routine burn practice.

Testosterone¶

Restoring the testosterone that the burn suppresses is a physiologically direct strategy. In severely burned men, testosterone enanthate 200 mg intramuscularly weekly raised total testosterone to the normal range, decreased protein breakdown nearly two-fold, and improved net amino-acid balance to approximately zero, so that restoration of blood testosterone can ameliorate the muscle catabolism of severe burn injury with normal feedings ^[33]. Testosterone has gained renewed practical importance: after oxandrolone was removed from the US market in June 2023, at least one institution implemented testosterone as the alternative anabolic agent ^[36].

Outcomes¶

Across body-composition, wound-healing, and length-of-stay endpoints, the anabolic agents share a consistent anabolic signal that does not extend to a survival benefit.

Body composition, muscle, and protein kinetics¶

The anticatabolic effect is the most robust and best-replicated outcome, strongest for oxandrolone. Long-term oxandrolone safely improves lean body mass, bone mineral content, and bone mineral density in severely burned children ^[19]; over a 12-month course it improves body composition and muscle strength ^[20]. A five-year randomized trial found that oxandrolone improves long-term recovery in height, bone mineral content, cardiac work, and muscle strength, with the bone gain likely mediated by IGF-1 ^[21]. Oxandrolone also increases constitutive proteins such as albumin and prealbumin while reducing acute-phase proteins, shifting hepatic protein synthesis toward recovery ^[18,17]. For growth hormone, rhGH at 0.2 mg/kg/day raises serum IGF-1 several-fold above placebo in severely burned children ^[25]. IGF-1/IGFBP-3 attenuates catabolism by improving net protein balance and raising muscle protein fractional synthetic rates ^[31].

Wound and donor-site healing¶

Accelerated wound closure is the headline growth-hormone outcome and a secondary oxandrolone effect. rhGH reduces donor-site healing time in burned children and adults ^[26,25], and a Cochrane review found some evidence that rhGH in people with burns over 40% TBSA could produce more rapid healing of burn wounds and donor sites in adults and children and reduce length of stay, with adult burns healing roughly 9 days faster than placebo ^[37,38]. Oxandrolone also accelerated burn-wound and donor-site healing in early trials ^[12], though the most recent meta-analysis found no significant difference in donor-site healing time for oxandrolone ^[41].

Length of stay and mortality¶

Length of stay is reduced by both oxandrolone and rhGH in several trials and pooled analyses. The 2006 multicenter oxandrolone trial showed shorter stay indexed to burn size ^[14], and 2025 meta-analyses confirm oxandrolone reduces operative procedures and shortens hospitalization normalized to TBSA ^[40]. Survival, however, does not improve: the largest 2025 meta-analysis found no mortality benefit for oxandrolone, and an earlier pooled analysis likewise found oxandrolone did not affect mortality or infection ^[39,40]. The single positive adult survival signal came from an observational analysis suggesting early oxandrolone may be associated with improved survival, not from a randomized mortality trial ^[15].

Complications¶

Each agent carries a characteristic toxicity, and the safety profile diverges sharply between oxandrolone and growth hormone, and between children and adults.

Oxandrolone — transaminitis. Transaminitis is the most frequent side effect of oxandrolone, occurring in 128 of 309 adults (41.4%) after a median of 13 days ^[43]. A separate cohort found transaminitis in 42% of patients, occurring significantly more frequently than previously reported ^[44]. Younger age and concurrent vasopressor or amiodarone use are independent predictors of oxandrolone-induced transaminitis, and these patients warrant close monitoring ^[43]. Importantly, the enzyme elevation is usually clinically benign: it was not significantly associated with length of stay or mortality after adjusting for age and TBSA ^[43], and a comparative analysis found no significant increase in clinically meaningful hepatic dysfunction in patients who received oxandrolone versus those who did not ^[45], and a meta-analysis concluded oxandrolone does not increase the risk of progressive or transient liver injury, though monitoring liver enzymes is still recommended ^[42]. Pediatric long-term trials reported hepatic transaminases remaining within normal levels and no deleterious side effects attributed to long-term administration ^[17,21]. Mild liver-transaminase increases and reversible sexual changes have also been observed during oxandrolone therapy, which is otherwise reported safe when given at 0.1 mg/kg twice daily for up to 12 months ^[48].

Growth hormone — hyperglycemia and the mortality concern. rhGH reliably provokes hyperglycemia: in a head-to-head comparison, hyperglycemia occurred in 100% of rhGH patients versus 55% of controls and 50% of oxandrolone patients, and growth hormone caused significant complications of hyperglycemia and accentuated hypermetabolism while oxandrolone caused none ^[35]. The Cochrane review found the incidence of hyperglycemia significantly higher in adults during rhGH treatment (risk ratio 2.43) but not in children ^[37,38]. The larger safety question is mortality: treatment with rhGH increases the mortality of critical illness ^[29], and rhGH has been shown to increase mortality in adult trauma patients, a signal that prompted careful study of its side effects in children ^[30]. Pediatric burn series have not reproduced this, reporting no difference in mortality between rhGH and placebo ^[30].

IGF-1 and testosterone. IGF-1/IGFBP-3 has been notably well tolerated, with patients remaining euglycemic and without electrolyte imbalance ^[32]. Testosterone's burn-specific complication data are sparse in this evidence base.

Special considerations¶

The pediatric–adult divide dominates agent selection and dosing. The deepest long-term evidence for oxandrolone and growth hormone is pediatric, where multi-year randomized trials document sustained gains in growth, bone, and strength ^[21,20]. Adults tolerate lower doses and carry a heavier toxicity burden: the adult growth-hormone mortality signal and the high adult oxandrolone transaminitis rate both argue for caution and monitoring outside the pediatric population ^[29,43].

Combination and sequencing matter. Combined oxandrolone and propranolol given for one year shortened the period of growth arrest by 84 days and increased growth rate in severely burned children ^[22], and the same combination was associated with reduced post-burn hypertrophic scarring and improved physical recovery ^[23]. Anabolic therapy also extends into rehabilitation: oxandrolone's effect on muscle protein kinetics is one of the few that persists after hospital discharge, where most agents' effects are largely unknown ^[5].

Controversies and Evidence Gaps¶

The central tension is a robust anabolic signal without a survival signal. Meta-analyses consistently show oxandrolone reduces weight loss in the catabolic phase, operative procedures, and length of stay while increasing weight gain and lean body mass ^[39,40]. They just as consistently show no mortality benefit, and the 2025 analyses report extreme statistical heterogeneity (I² ≥ 95%) that mandates cautious interpretation ^[39,40]. The evidence supports an adjunctive role in metabolic rehabilitation but calls for risk-stratified implementation rather than blanket use ^[40].

The growth-hormone evidence is genuinely split by age. The adult critical-illness mortality signal ^[29] sits against pediatric burn trials showing benefit without excess death ^[30], leaving rhGH a pediatric-leaning agent whose adult use remains contested. Oxandrolone's own adult evidence has historically been criticized: most data derive from single-center studies, many with small samples and some with poor design, prompting repeated calls for multicenter randomized trials to define optimal dosing and confirm efficacy and safety in adults ^[16]. Direct agent-to-agent comparison is thin; one early study found growth hormone and oxandrolone gave nearly identical anabolic benefits, but growth hormone caused hyperglycemia that oxandrolone did not ^[35].

The practice landscape shifted with oxandrolone's 2023 withdrawal from the US market, forcing centers toward testosterone as a substitute; preliminary data show a trend toward higher transaminitis with oxandrolone than testosterone without reaching statistical significance, and higher early drug discontinuation with oxandrolone ^[36]. Whether testosterone fully replicates oxandrolone's outcome profile is an open question. For IGF-1 the gap is even wider: outside of oxandrolone, the effects of these drugs on muscle protein kinetics after hospital discharge are largely unknown ^[5], and IGF-1 has not progressed beyond investigational use.

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