Aetna considers the following established methods medically necessary for the treatment of vitiligo:
Excimer laser (e.g., XTRAC, PhotoMedex, Radnor, PA; EX-308, Ra Medical Systems, Inc., Carlsbad, CA)
Narrow-band ultraviolet B (UVB)
Topical and oral psoralen photochemotherapy (PUVA)
Topical and systemic corticosteroids
Aetna considers continued PUVA or narrow-band UVB therapy not medically necessary unless there is significant follicular pigmentation after 6 months of therapy (8 to 10 treatments per month).
Aetna considers home phototherapy experimental and investigational for the treatment of vitiligo because there is a lack of evidence regarding the safety and effectiveness of home phototherapy for this condition.
Aetna considers treatments for vitiligo cosmetic if they do not affect the underlying condition and do not result in improved protection against skin cancer; specifically micropigmentation (tattooing) and depigmentation (with monobenzylether of hydroquinone/monobenzone) are considered cosmetic.
Aetna considers melanocyte transplantation for the treatment of vitiligo experimental and investigational because its effectiveness has not been established.
Aetna considers vitamin D analogs (e.g., calcitriol and paricalcitol) experimental and investigational for the treatment of vitiligo because their effectiveness for this indication has not been established.
Aetna considers tumor necrosis factor-alpha agents (e.g., adalimumab, etanercept, and infliximab) experimental and investigational for the treatment of vitiligo because their effectiveness for this indication has not been established.
Vitiligo is an acquired pigmentary disorder of skin and mucous membranes, manifesting itself by expanding depigmented lesions. While the cause is not well understood, the observed variation in clinical manifestations of the condition has suggested several possible etiologies, including association with other medical conditions. The 3 prevailing theories of the pathogenesis of vitiligo include an immune hypothesis, a neural-mediated hypothesis, and a “self-destruct” hypothesis. These 3, plus newer hypotheses suggesting that vitiligo may be due to a melanocyte growth factor deficiency or to an abnormal melatonin receptor on melanocytes, have not been definitively proven, and it is likely that the loss of epidermal and follicular melanocytes in vitiligo may be the result of several different pathogenic mechanisms.
Psoralen photochemotherapy (psoralen and ultraviolet light A or PUVA) is appropriate for properly selected patients with vitiligo. The treatment involves taking oral psoralen or applying it topically followed by carefully timed exposure to UVA. Repigmentation may begin after 15 to 25 treatments. Approximately 50 % of patients will develop repigmentation after 150 to 200 PUVA treatments over 12 to 24 months. The response is slow and repigmentation may not be complete. Response to PUVA is unlikely to occur if follicular pigmentation has not appeared after 3 months of PUVA therapy. Dark-skinned patients respond better than fair skin patients do; the latter are unlikely to benefit from PUVA unless there is marked disfigurement. Most patients who respond do not develop new areas of pigment loss; furthermore, maintenance with PUVA therapy is not necessary.
Children under age 10 are generally not treated with oral phototherapy; instead, a mild topical corticosteroid cream is often prescribed. A stronger topical corticosteroid cream can be prescribed for adults. Patients must apply the cream (e.g., triamcinolone 0.1 %, desonide 0.05 %) once-daily to the white patches on their skin for at least 3 to 4 months before seeing any results. Systemic corticosteroids can stop the progression of vitiligo for some patients, but may also produce unacceptable side effects. Oral mini-pulse therapy with 5 mg betamethasone/dexamethasone may stop the progression and induce spontaneous repigmentation in some vitiligo patients.
A number of recently published studies have demonstrated that narrow-band UVB is an effective treatment for vitiligo, and compares favorably to UVA and psoralens (e.g., Westerhof, 1997; Njoo et al, 2000; Scherschun et al, 2001). Unlike PUVA, narrow-band UVB does not involve the use of sensitizing agents. Narrow-band UVB is typically administered 2 to 3 times per week for several months. However, there is a lack of evidence regarding the safety and effectiveness of home narrow-band UVB phototherapy for the treatment of vitiligo.
In a randomized controlled study, Ada et al (2005) concluded that narrow-band UVB phototherapy is effective in treating vitiligo, and the addition of topical calcipotriol does not improve treatment outcome.
In a double-blind randomized study, Yones et al (2007) compared the effectiveness of oral PUVA with that of narrowband-UVB (NB-UVB) phototherapy in patients with non-segmental vitiligo. A total of 56 patients received twice-weekly therapy with PUVA or NB-UVB. The change in body surface area affected by vitiligo and the color match of repigmented skin compared with unaffected skin were assessed after 48 sessions of therapy, at the end of the therapy course, and 12 months after the end of therapy. The results in the 25 patients each in the PUVA and NB-UVB groups who began therapy were analyzed. The median number of treatments was 47 in the PUVA-treated group and 97 in the NB-UVB-treated group (p = 0.03); this difference was probably due to differences in effectiveness and adverse effects between the 2 modalities, such that patients in the NB-UVB group wanted a longer course of treatment. At the end of therapy, 16 (64 %) of 25 patients in the NB-UVB group showed greater than 50 % improvement in body surface area affected compared with 9 (36 %) of 25 patients in the PUVA group. The color match of the repigmented skin was excellent in all patients in the NB-UVB group but in only 11 (44 %) of those in the PUVA group (p < 0.001). In patients who completed 48 sessions, the improvement in body surface area affected by vitiligo was greater with NB-UVB therapy than with PUVA therapy (p = 0.007). Twelve months after the cessation of therapy, the superiority of NB-UVB tended to be maintained. The authors concluded that in the treatment of non-segmental vitiligo, NB-UVB therapy is superior to oral PUVA therapy.
In a randomized, investigator-blinded and half-side comparison study, Casacci and colleagues (2007) compared the effectiveness of NB-UVB phototherapy and 308-nm monochromatic excimer light (MEL) in patients with vitiligo. A total of 21 subjects with symmetrical vitiligo lesions were enrolled in this study. Vitiligo lesions on one body side were treated twice-weekly for 6 months with 308-nm MEL, while NB-UVB phototherapy was used to treat lesions on the opposite side. At the end of the study, 6 lesions (37.5 %) treated with 308-nm MEL and only 1 lesion (6 %) treated with NB-UVB achieved an excellent repigmentation (score 4) while 4 lesions (25 %) treated with 308-nm MEL and 5 lesions (31 %) treated with NB-UVB showed a good repigmentation (score 3). The authors concluded that it appears that 308-nm MEL is more effective than NB-UVB in treating vitiligo lesions and it induces repigmentation more rapidly.
Several clinical studies have demonstrated that the Xenon-Chloride excimer laser is effective in repigmentation of vitiligo patches (Hadi et al, 2004; Choi et al, 2004; Esposito et al, 2004; Kawalek et al, 2004; Taneja et al, 2003; Spencer et al, 2002). The excimer laser may be especially useful in treatment of localized vitiligo that is refractory to topical corticosteroids. Treatments are typically administered twice weekly and up to 60 treatments may generally be medically necessary. Recent studies have also suggested that combination treatment with excimer laser and topical methoxypsoralen resulted in better repigmentation than excimer laser alone. However, due to the small sample sizes in these studies, their findings need to be validated by additional studies (Grimes, 2005).
Transplantation of autologous pigment cells is considered experimental and investigational for the treatment of vitiligo because of a lack of adequate clinical evidence of effectiveness from randomized controlled clinical trials.
van Geel and colleagues (2006) investigated the the effectiveness of non-cultured epidermal cell transplantation in treating stabilized vitiligo using objective and subjective evaluation methods. Non-cultured autologous melanocytes and keratinocytes were grafted in a hyaluronic-acid-enriched suspension on superficially laser-abraded vitiligo lesions in 40 patients with refractory stable vitiligo (30 with generalized and 10 with localized vitiligo). The repigmentation was evaluated 3 to 12 months after grafting using a digital image analysis system. Furthermore, the treatment was evaluated from patients' point of view with the DLQI (Dermatology Life Quality Index) and a global assessment. The mean percentage of repigmentation, evaluated at the last follow-up visit, was 72 % (median of 84 %), and a repigmentation of greater than or equal to 70 % was observed in 62 % of patients. The best results were achieved in the neck and the pre-sternal region. A subjective evaluation was performed in 50 % of the subjects. The mean DLQI score at inclusion (6.95, SD = 6.68, n = 20) was significantly lowered after treatment (p = 0.013, mean 3.85, SD = 4.13, n = 20). The patients were satisfied with the achieved result, and they found it worthwhile to undergo the treatment and would choose it again. The authors concluded that according to both subjective and objective evaluation methods, non-cultured epidermal cell transplantation is promising in patients with stable vitiligo.
In a randomized, double-blind clinical trial, Rodríguez-Martín and colleagues (2009) assessed the safety and effectiveness of tacalcitol (a vitamin D analog) ointment plus sunlight exposure in the treatment of non-segmental vitiligo. A total of 80 patients participated in this study. Effectiveness was assessed by quantification of the lesional re-pigmentation area at the end of the study compared with the baseline. Tacalcitol (n = 40) or matching placebo ointment (n = 40) was applied once-daily at night. Daily exposure to sunlight for 30 mins was performed. Treatment was continued for 4 months. The response of the lesions was clinically verified every 2 weeks by a "blinded" medical investigator. All adverse effects were recorded. Over 16 weeks, 64 patients completed the study requirements. There was no significant difference in the re-pigmentation response at the 16-week time point between the vehicle plus sunlight exposure and the tacalcitol plus sunlight exposure groups. No reduction in the size of the lesions greater than 25 % was observed in the tacalcitol-treated patients. No serious adverse effects were observed. The authors concluded that the combination of tacalcitol with heliotherapy has no additional advantages compared with heliotherapy alone.
In a Cochrane review on interventions for vitiligo, Whitton et al (2010) stated that new interventions include MEL, polypodium leucotomos, melanocyte transplantation, oral anti-oxidants, Chinese zengse pill, and pimecrolimus. These investigators analyzed the data from 28 studies that met their outcome criteria of improvement in quality of life and greater than 75 % repigmentation. A total of 15 analyses from studies comparing various interventions showed a statistically significant difference between the proportions of participants achieving more than 75 % repigmentation. The majority of analyses showing statistically significant differences were from studies that assessed combination interventions that generally included some form of light treatment. Topical preparations, in particular corticosteroids, reported most adverse effects. However, in the combination studies it was difficult to ascertain which treatment caused these effects. None of the studies was able to demonstrate long-term benefits. Very few studies were conducted on children or included segmental vitiligo. These researchers found 1 study of psychological interventions and none evaluating micropigmentation, depigmentation, or cosmetic camouflage. The authors concluded that this review has found some evidence from individual studies to support existing therapies for vitiligo, but the usefulness of the findings is limited by the different designs and outcome measurements and lack of quality of life measures. There is a need for follow-up studies to assess permanence of repigmentation as well as high quality randomized trials using standardized measures and which also address quality of life.
Alghamdi and colleagues (2012) stated that although the exact pathogenesis of vitiligo is not fully understood, it appears to be an autoimmune disease. It is hypothesized that tumor necrosis factor-alpha (TNF-alpha) plays an important role in vitiligo. Tumor necrosis factor-alpha can destroy melanocytes through the induction of various apoptotic pathways. In addition, TNF-alpha can inhibit melanocyte stem cell differentiation. These researchers evaluated the safety and effectiveness of treating vitiligo patients with anti-TNF-alpha agents. A total of 6 patients were recruited. All patients had widespread non-segmental vitiligo. Biologics, including infliximab, etanercept, and adalimumab, were given according to treatment regimens used for psoriasis. Photographs were taken at the initial visit, every 2 months during the therapy and then 6 months after therapy completion. All patients completed the treatment; 2 patients were treated with infliximab, 2 with etanercept, and 2 with adalimumab. All of the biologics were well- tolerated throughout the treatment period, and none of the patients reported any significant adverse events. Digital images were compared before, during and after treatment. Repigmentation of the vitiliginous areas was not observed in any of the patients. Vitiligo worsened in 1 patient who was treated with infliximab and developed a psoriasiform rash. However, the remaining patients did not develop any new depigmented patches during treatment or at the 6-month follow-up; vitiligo was considered stable in these 5 patients. The authors concluded that although the anti-TNF-alpha agents were well-tolerated in all 6 vitiligo patients, efficacy was not observed. They stated that further evaluation with larger studies may be required.
CPT Codes / HCPCS Codes / ICD-9 Codes
CPT codes covered if selection criteria are met:
96920 - 96922
CPT codes not covered for indications listed in the CPB:
11920 - 11922
HCPCS codes covered if selection criteria are met:
Injection, betamethasone acetate 3mg and betamethasone sodium phosphate, 3 mg
Injection, methylprednisolone acetate, 20 mg
Injection, methylprednisolone acetate, 40 mg
Injection, methylprednisolone acetate, 80 mg
Injection, dexamethasone acetate, 1 mg
Injection, dexamethasone sodium phosphate, 1mg
Injection, hydrocortisone acetate, up to 25 mg (i. e., Hydrocortone acetate)
Injection, hydrocortisone sodium phosphate, up to 50 mg (i.e., Hydrocortone phosphate)
Injection, hydrocortisone sodium succinate, up to 100 mg (i.e., Solu-Cortef)
Injection, prednisolone acetate, up to 1 ml (i.e., Key-Pred 25, Key-Pred 50, Predcor-25, Predcor-50, Predoject 50, Predalone-50, Predicort-50)
Injection, methylprednisolone sodium succinate, up to 40 mg (i.e., Solu-Medrol)
Injection, methylprednisolone sodium succinate, up to 125 mg (i.e., Solu-Medrol)
Injection, triamcinolone acetonide, per 10 mg (i.e., Kenalog)
Injection, triamcinolone diacetate, per 5 mg (i.e., Aristocort)
Injection, triamcinolone hexacetonide, per 5 mg (i.e., Aristospan)
Prednisone, oral, per 5 mg
Methylprednisolone, oral, per 4 mg
Prednisolone, oral, per 5 mg
Dexamethasone, oral, 0.25 mg
HCPCS codes not covered for indications listed in the CPB:
Replacement bulb/lamp for ultraviolet light therapy system, each
Ultraviolet light therapy system, includes bulbs/lamps, timer, and eye protection; treatment area 2 square feet or less
Ultraviolet light therapy system panel, includes bulbs/lamps, timer, and eye protection, four foot panel
Ultraviolet light therapy system panel, includes bulbs/lamps, timer, and eye protection, six foot panel
Ultraviolet multidirectional light therapy system in 6 foot cabinet, includes bulbs/lamps, timer, and eye protection
Injections, adalimumab, 20 mg
Injection, calcitriol, 0.1 mcg
Injection, etanercept, 25 mg (code may be used for Medicare when drug administered under the direct supervision of a physician, not for use when drug is self-administered)
Injection, infliximab, 10 mg
Injection, paricalcitol, 1 mcg
Calcitrol, 0.25 mcg
ICD-9 codes covered if selection criteria are met:
The above policy is based on the following references:
Grimes PE. Diseases of hypopigmentation. In: Principles and Practice of Dermatology. WM Sams Jr, PJ Lynch, eds. 2nd ed. New York, NY: Churchill Livingstone; 1996:843-859.
Lorton DA. Pigmentary disorders. In: Conn's Current Therapy. RE Rakel, ed. Philadelphia, PA: W.B. Saunders Co.; 1999:875-876.
Kim SM, Lee HS, Hann SK. The efficacy of low-dose oral corticosteroids in the treatment of vitiligo patients. Int J Dermatol. 1999;38(7):546-550.
Jimbow K. Vitiligo. Therapeutic advances. Dermatol Clin. 1998;16(2):399-407.
Grimes PE. Vitiligo. An overview of therapeutic approaches. Dermatol Clin. 1993;11(2):325-338.
National Institutes of Health (NIH), National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS). Questions and answers about vitiligo. Health Topics. NIH Publication No. 01-4909. Bethesda, MD: NIH; updated May 2001. Available at: http://www.niams.nih.gov/hi/topics/vitiligo/vitiligo.htm. Accessed June 29, 2005.
Arnold HL, Odom RB, James WD. Andrews' Diseases of the Skin: Clinical Dermatology. 8th Ed. Philadelphia, PA: W.B. Saunders Co.; 1990.
Njoo MD, Spuls PI, Bos JD, et al. Nonsurgical repigmentation therapies in vitiligo: Meta-analysis of the literature. Arch Dermatol. 1998;134(12):1532-1540.
Njoo MD, Westerhof W, Bos JD, et al. The development of guidelines for the treatment of vitiligo. Arch Dermatol. 1999;135:1514-1521.
Halder RM. New and emerging therapies for vitiligo. Dermatol Clin. 2000;18(1):79-89, ix.
Scherschun L, Kim JJ, Lim HW. Narrow-band ultraviolet B is a useful and well-tolerated treatment for vitiligo. J Am Acad Dermatol. 2001;44(6):999-1003.
Njoo MD, Bos JD, Westerhof W. Treatment of generalized vitiligo in children with narrow-band (TL-01) UVB radiation therapy. J Am Acad Dermatol; 2000;42(2 Pt 1):245-253.
Njoo MD, Westerhof W, Bos JD, Bossuyt PM. The development of guidelines for the treatment of vitiligo. Clinical Epidemiology Unit of the Istituto Dermopatico dell'Immacolata-Istituto di Recovero e Cura a Carattere Scientifico (IDI-IRCCS) and the Archives of Dermatology. Arch Dermatol. 1999;135(12):1514-1521.
Westerhof W, Nieuweboer-Krobotova L. Treatment of vitiligo with UV-B radiation vs topical psoralen plus UV-A. Arch Dermatol. 1997;133(12):1525-1528.
Chen YF, Chang JS, Yang PY, et al. Transplant of cultured autologous pure melanocytes after laser-abrasion for the treatment of segmental vitiligo. J Dermatol. 2000;27(7):434-439.
Phillips J, Gawkrodger DJ, Caddy CM, et al. Keratinocytes suppress TRP-1 expression and reduce cell number of co-cultured melanocytes - implications for grafting of patients with vitiligo. Pigment Cell Res. 2001;14(2):116-125.
Sachdev M, Shankar DS. Dermatologic surgery: Pulsed erbium:YAG laser-assisted autologous epidermal punch grafting in vitiligo. Int J Dermatol. 2000;39(11):868-871.
Kim HY, Kang KY. Epidermal grafts for treatment of stable and progressive vitiligo. J Am Acad Dermatol. 1999;40(3):412-417.
Olsson MJ, Juhlin L. Epidermal sheet grafts for repigmentation of vitiligo and piebaldism, with a review of surgical techniques. Acta Derm Venereol. 1997;77(6):463-466.
Roelandts R. Photo(chemo) therapy for vitiligo. Photodermatol Photoimmunol Photomed. 2003;19(1):1-4.
Hadi SM, Spencer JM, Lebwohl M. The use of the 308-nm excimer laser for the treatment of vitiligo. Dermatol Surg. 2004;30(7):983-986.
Choi KH, Park JH, Ro YS. Treatment of vitiligo with 308-nm xenon-chloride excimer laser: Therapeutic efficacy of different initial doses according to treatment areas. J Dermatol. 2004;31(4):284-292.
Esposito M, Soda R, Costanzo A, Chimenti S. Treatment of vitiligo with the 308 nm excimer laser. Clin Exp Dermatol. 2004;29(2):133-137.
Kawalek AZ, Spencer JM, Phelps RG. Combined excimer laser and topical tacrolimus for the treatment of vitiligo: A pilot study. Dermatol Surg. 2004;30(2 Pt 1):130-135.
Taneja A, Trehan M, Taylor CR. 308-nm excimer laser for the treatment of localized vitiligo. Int J Dermatol. 2003;42(8):658-662.
Spencer JM, Nossa R, Ajmeri J. Treatment of vitiligo with the 308-nm excimer laser: A pilot study. J Am Acad Dermatol. 2002;46(5):727-731.
Baltás E, Nagy P, Bónis B, et al. Repigmentation of localized vitiligo with the xenon chloride laser. Br J Dermatol. 2001;144:1266-1267.
Kostovic K, Nola I, Bucan Z, Situm M. Treatment of vitiligo: Current methods and new approaches. Acta Dermatovenerol Croat. 2003;11(3):163-170.
Hartmann A, Brocker EB, Becker JC. Hypopigmentary skin disorders: Current treatment options and future directions. Drugs. 2004;64(1):89-107.
Sarkany RP, Anstey A, Diffey BL, et al. Home phototherapy: Report on a workshop of the British Photodermatology Group, December 1996. Br J Dermatol. 1999;140(2):145-149.
Passeron T, Ostovari N, Zakaria W, et al. Topical tacrolimus and the 308-nm excimer laser: A synergistic combination for the treatment of vitiligo. Arch Dermatol. 2004 Sep;140(9):1065-1069.
Ada S, Sahin S, Boztepe G, et al. No additional effect of topical calcipotriol on narrow-band UVB phototherapy in patients with generalized vitiligo. Photodermatol Photoimmunol Photomed. 2005;21(2):79-83.
Grimes PE. New insights and new therapies in vitiligo. JAMA. 2005;293(6):730-735.
Hartmann A, Lurz C, Hamm H, et al. Narrow-band UVB311 nm vs. broad-band UVB therapy in combination with topical calcipotriol vs. placebo in vitiligo. Int J Dermatol. 2005;44(9):736-742.
Rusfianti M, Wirohadidjodjo YW. Dermatosurgical techniques for repigmentation of vitiligo. Int J Dermatol. 2006;45(4):411-417.
van Geel N, Ongenae K, Vander Haeghen Y, et al. Subjective and objective evaluation of noncultured epidermal cellular grafting for repigmenting vitiligo. Dermatology. 2006;213(1):23-29.
Yones SS, Palmer RA, Garibaldinos TM, Hawk JL. Randomized double-blind trial of treatment of vitiligo: Efficacy of psoralen–UV-A therapy vs narrowband–UV-B therapy. Arch Dermatol 2007;143(5):578-584.
Casacci M, Thomas P, Pacifico A, et al. Comparison between 308-nm monochromatic excimer light and narrowband UVB phototherapy (311-313 nm) in the treatment of vitiligo -- a multicentre controlled study. J Eur Acad Dermatol Venereol. 2007;21(7):956-963.
Mulekar SV, Ghwish B, Al Issa A, Al Eisa A. Treatment of vitiligo lesions by ReCell vs. conventional melanocyte-keratinocyte transplantation: A pilot study. Br J Dermatol. 2008;158(1):45-49.
Szczurko O, Boon HS. A systematic review of natural health product treatment for vitiligo. BMC Dermatol. 2008;8:2.
Gawkrodger DJ, Ormerod AD, Shaw L, et al; Therapy Guidelines and Audit Subcommittee, British Association of Dermatologists; Clinical Standards Department, Royal College of Physicians of London; Cochrane Skin Group; Vitiligo Society. Guideline for the diagnosis and management of vitiligo. Br J Dermatol. 2008;159(5):1051-1076.
Rodríguez-Martín M, García Bustínduy M, Sáez Rodríguez M, Noda Cabrera A. Randomized, double-blind clinical trial to evaluate the efficacy of topical tacalcitol and sunlight exposure in the treatment of adult nonsegmental vitiligo. Br J Dermatol. 2009;160(2):409-414.
Matin R. Vitiligo in adults and children. In: BMJ Clinical Evidence. London, UK: BMJ Publishing Group; March 2010.
Birlea SA, Costin GE, Norris DA. New insights on therapy with vitamin D analogs targeting the intracellular pathways that control repigmentation in human vitiligo. Med Res Rev. 2009;29(3):514-546.
Whitton ME, Pinart M, Batchelor J, et al. Interventions for vitiligo. Cochrane Database Syst Rev. 2010;(1):CD003263.
Le Duff F, Fontas E, Giacchero D, et al. 308-nm excimer lamp vs. 308-nm excimer laser for treating vitiligo: A randomized study. Br J Dermatol. 2010;163(1):188-192.
Gawkrodger DJ, Ormerod AD, Shaw L, et al. Vitiligo: Concise evidence based guidelines on diagnosis and management. Postgrad Med J. 2010;86(1018):466-471.
Alghamdi KM, Khurrum H, Taieb A, Ezzedine K. Treatment of generalized vitiligo with anti-TNF-alpha agents. J Drugs Dermatol. 2012;11(4):534-539.
Bacigalupi RM, Postolova A, Davis RS. Evidence-based, non-surgical treatments for vitiligo: A review. Am J Clin Dermatol. 2012 Mar 16. [Epub ahead of print]
Copyright Aetna Inc. All rights reserved. Clinical Policy Bulletins are developed by Aetna to assist in administering plan benefits and constitute neither offers of coverage nor medical advice. This Clinical Policy Bulletin contains only a partial, general description of plan or program benefits and does not constitute a contract. Aetna does not provide health care services and, therefore, cannot guarantee any results or outcomes. Participating providers are independent contractors in private practice and are neither employees nor agents of Aetna or its affiliates. Treating providers are solely responsible for medical advice and treatment of members. This Clinical Policy Bulletin may be updated and therefore is subject to change.