Changes

April 2025 — reviewed. A literature search was conducted in March 2025 to identify evidence-based guidelines, UK policy, systematic reviews, and key randomized controlled trials published since the last revision of the topic.

Update

Goals

To support primary healthcare professionals to:

• To make a diagnosis of vitiligo.
• Assess for other autoimmune conditions (if appropriate).
• Provide information on sources of advice and support.
• Offer appropriate management of vitiligo and any psychosocial complications in primary care.
• Arrange referral to a skin camouflage service and/or dermatologist if needed.

Outcome measures

Audit criteria

QOF indicators

QIPP - Options for local implementation

NICE quality standards

What is it?

• Vitiligo is an acquired, chronic, depigmentation disorder, characterized by selective loss of functional melanocytes resulting in white patches on the skin and sometimes the hair.
  • It is classified into two subtypes (non-segmental and segmental) according to distribution and extent.
  • Vitiligo can also be used as an umbrella term for all non-segmental vitiligo. 
• Non-segmental vitiligo is more common, accounting for 85–90% of people with vitiligo. It has a symmetrical distribution and has a number of subtypes:
  • Acrofacial vitiligo — involved sites are usually limited to the face, orifices, head, hands and feet. It may subsequently develop into generalized vitiligo.
    • The 'lip-tip' variety describes lesions that are restricted to the cutaneous lips and distal tips of the digits.
  • Generalized vitiligo — bilateral, often symmetrical, depigmented macules or patches occurring in a random distribution over the entire body surface. It often affects areas that tend to experience pressure, friction, and/or trauma. It may begin in childhood or early adulthood. 
  • Universal vitiligo — this is the most extensive form, where there is complete or nearly complete depigmentation of the skin (over 80% of the body surface area). It is usually preceded by generalized vitiligo.
  • Focal vitiligo — a small, isolated, depigmented lesion without an obvious segmental distribution pattern that has not evolved after a period of at least 2 years. 
  • Mucosal vitiligo — lesions are located on more than one mucosal site (oral and/or genital mucosa). 
  • Follicular vitiligo — depigmented body hairs caused by involvement of the melanocyte follicular reservoir, with limited skin involvement.
  • Undetermined/unclassified vitiligo — describes an isolated patch that has not developed into non-segmental vitiligo after a period of at least 2 years. May be focal or mucosal (on one isolated site).  
• Segmental vitiligo is usually unilateral and characterized by rapid stabilization, is less common, typically has an earlier age of onset, and affects 20–30% of children and about 5% of adults with vitiligo.
  • It usually has a dermatomal distribution, is most commonly unilateral, and is limited to one segment. However, it may affect several segments (which may be unilateral or bilateral), and may affect larger areas delineated by Blaschko's lines (invisible lines representing the developmental growth pattern of the skin). It may also involve the melanocytes of hair follicles, leading to depigmentation of affected hairs. 
  • The most commonly involved dermatome is that of the trigeminal nerve.
• Mixed vitiligo — segmental and non-segmental forms exist concurrently. 

[Gawkrodger, 2008; Ezzedine, 2012; Taieb, 2013; de Menezes, 2016; Ezzedine, 2016; Bergqvist, 2020; Bergqvist, 2021; Eleftheriadou, 2022; van Geel, 2023]

How common is it?

• Vitiligo is the most common depigmenting skin disorder, affecting 0.5–2% of the population worldwide. However, the reported prevalence of vitiligo in the literature varies according to the study population and geographical location of the studies [Bergqvist, 2020; Eleftheriadou, 2022].
  • Variations in reported prevalence rates may be due to higher reporting where social and cultural stigma are common, or where lesions are more evident in darker-skinned people [Bergqvist, 2020].
• Childhood onset is common (affecting around 30% of people with vitiligo), although it is uncommon in children aged under 2 years, with the majority of cases (89%) occurring after the age of 4 years [Ezzedine, 2016; Eleftheriadou, 2022].
  • Onset increases through the first two decades of life, with almost 50% of people presenting before the age of 20 years, and nearly 70–80% before the age of 30 years.
• Segmental vitiligo accounts for 5–16% of overall vitiligo cases. It occurs at a younger age, before 10 years in 41% of cases and before the age of 30 years in 87% of cases [Bergqvist, 2021].
• Prevalence is evenly distributed between the two sexes (although women and girls often seek consultation more frequently), and different ethnic groups and skin types are equally affected [Bergqvist, 2021].

What causes it?

• Vitiligo is a multifactorial disorder caused by the selective loss of functioning melanocytes (pigment cells) in the skin due to destruction of, or damage to, these cells, resulting in patches of decreased pigment or depigmented skin, hair, or mucous membranes. The exact pathogenetic mechanism is unknown, but a number of mechanisms have been proposed, including genetic autoimmune responses; oxidative stress; generation of inflammatory mediators; and melanocyte detachment mechanisms. Multiple mechanisms may work jointly to contribute to the destruction of melanocytes.  
  • In non-segmental vitiligo, the cause of melanocyte loss is thought to be autoimmune destruction of melanocytes by lymphocytes — there are associations with other autoimmune diseases, and melanocyte-specific lymphocytes have been found both in the blood and at the margins of active vitiligo lesions.
  • In segmental vitiligo, the cause was thought to be neuronal (given the unilateral distribution pattern). However, there is not enough evidence to support this theory, and more recent evidence suggests there may be an overlapping inflammatory or autoimmune pathogenesis for both segmental and non-segmental vitiligo, as melanocyte-specific lymphocytes identical to non-segmental vitiligo have been found in people with segmental vitiligo [Bergqvist, 2020].
• Proposed triggers for vitiligo disease onset and relapse include [Boissy, 2004; Taieb, 2013; Ezzedine, 2016]:
  • Sustained stress or anxiety.
  • Skin trauma, including the Koebner phenomenon (where depigmentation develops at sites of trauma, such as cuts, abrasions, or sunburn).
  • Environmental exposure to chemicals (such as phenolic/catecholic derivatives that may be present in oils, disinfectants, hair dyes, or deodorants). 

[Taieb, 2013; Ezzedine, 2016; Bergqvist, 2020; Bergqvist, 2021; Eleftheriadou, 2022; van Geel, 2023]

What are the risk factors?

Possible risk factors for vitiligo include:

• A family history of vitiligo.
  • About 20% of people with vitiligo have at least one first-degree relative with vitiligo, and the relative risk of vitiligo for first-degree relatives is increased by 7- to 10-fold [Bergqvist, 2020].
• A personal or family history of other autoimmune diseases, including [Gawkrodger, 2008; Ezzedine, 2016; Bergqvist, 2020]:
  • Thyroid disease (most common, particularly Hashimoto's thyroiditis). See the CKS topic on Hypothyroidism for more information. 
  • Addison's disease, pernicious anaemia, systemic lupus erythematosus, diabetes mellitus, alopecia areata, rheumatoid arthritis, psoriasis, and inflammatory bowel disease. See the CKS topics on Addison's disease, Anaemia - B12 and folate deficiency, Diabetes - type 1, Alopecia areata, Rheumatoid arthritis, Psoriasis, Crohn's disease, and Ulcerative colitis for more information. 

What are the complications?

• Possible complications of vitiligo include psychosocial issues, including poor body image, low self-esteem, embarrassment, difficulty in social and sexual relationships, social isolation, stigmatization, anxiety, and depression [Gawkrodger, 2008; Taieb, 2013; Ezzedine, 2016; Bergqvist, 2020]. See the CKS topics on Generalized anxiety disorder and Depression for more information.
• • The prevalence of psychosocial impact varies with the person's site and extent of disease, skin type, ethnicity, and cultural background. It may particularly affect people with darker skin pigmentation, as skin changes may be more noticeable. Effects may be exacerbated by the chronic, unpredictable nature of the disease [Taieb, 2013].
    • A meta-analysis of 21 studies (n = 3259) in 11 countries that compared people with vitiligo with a healthy control group, found that people with vitiligo often had concomitant anxiety (OR = 6:14 [95% CI: 3.35–11.24]). The pooled prevalence of anxiety in female patients was significantly higher than that in males (OR = 2:24 [95% CI: 1.31–3.84]). Subgroup analysis showed that the pooled prevalence of clinical anxiety disorder and anxiety symptoms was 12% (95% CI: 7%–16%, I2 = 76:3%) and 34% (95% CI: 21%–46%), respectively [Liu, 2021].

What is the prognosis?

• The prognosis of vitiligo depends on the person's age, disease subtype, distribution, activity, and extent [Ezzedine, 2016; Bergqvist, 2020]. 
• Vitiligo is a chronic and persistent disorder characterized by periods of disease activity and inactivity. Spontaneous repigmentation is uncommon, but may occur without any therapeutic intervention, or after sun exposure [Gawkrodger, 2008; Ezzedine, 2016]. 
  • Non-segmental vitiligo is characterized by unpredictable periods of disease activity, when there may be rapid progression over weeks to months, and long periods of relative inactivity and stability. Hair depigmentation may appear later in the course of the disease [Ezzedine, 2016; Bergqvist, 2020]. 
    • The face, neck, trunk, and mid-extremities respond best to therapy, while the lips and distal extremities are more resistant to treatment [Bergqvist, 2020].
    • After successful repigmentation, the rate of relapse in vitiligo lesions is about 44% in the first year after discontinuation of the treatment [van Geel, 2023].
  • Segmental vitiligo typical of childhood tends to stabilize rapidly and is usually less progressive than non-segmental disease [de Menezes, 2016; Plensdorf, 2017]. It usually spreads rapidly within the involved segment over a 3–24 month period [Ezzedine, 2016].
    • Once repigmentation has occurred, relapse is rare. However, disease recurrence can occur after years of lesion stability [Ezzedine, 2016; Bergqvist, 2020].

When should I suspect vitiligo?

• Suspect a diagnosis of vitiligo if there are areas of skin (or hair) depigmentation — lesions are usually asymptomatic, but itch may occur before lesions appear.
• Lesions are characterised by: 
  • Colour
    • Skin macules and patches may initially appear pale and hypopigmented before eventually becoming chalky white and depigmented. Occasionally, they have a white centre with an intermediate, pale area around (so-called 'trichrome' vitiligo).
  • Margins
    • Lesions are typically well-demarcated. 
    • Occasionally, inflammation is seen at the advancing edge of a lesion.
  • On palpation
    • Lesions are flat and non-scaly.
  • Extent and distribution
    • Lesions may be localized or generalized.
    • Lesions are often bilateral and symmetrical. They may be unilateral in early non-segmental vitiligo, or in segmental vitiligo when confined to part or all of one or more dermatomes or areas delineated by Blaschko's lines.
    • Lesions can appear anywhere, but the sites most commonly affected are the fingers and wrists, axillae, groin, and genitalia, and the skin around the eyes and mouth. Mucosal areas (including the mouth) can be prominent in people with darker skin pigmentation. The fingers, hands, and face are often affected first. 
    • Vitiligo may exhibit the Koebner phenomenon, with depigmentation developing at sites of mechanical trauma (such as abrasions or burns) or friction (such as waistbands).
    • Hair roots can be affected, resulting in white eyelashes and white hair (which may be patchy). 
  • Progression
    • Without treatment, individual lesions usually enlarge over time. 
    • Rarely, vitiligo can spread to cover almost all of the skin.
• The website DermNet (www.dermnetnz.org) has some useful images of different presentations of vitiligo.
• Suspect an alternative diagnosis if there are other clinical features such as scaling, inflammation, induration, skin swelling, or scarring.

How should I assess a person with suspected vitiligo?

• If a person has a suspected diagnosis of vitiligo, determine whether it is non-segmental or segmental following clinical examination.
• Take a medical history and ask about:
  • The person's age. 
  • The speed of onset, extent and duration of lesions, lesion activity and spread, and rate of progression or regression of lesions.
  • The impact on the person's quality of life, psychosocial impact, or other complications. See the CKS topics on Generalized anxiety disorder and Depression for more information.
  • The person's skin type (skin colour and ability to tan), which may affect treatment options. See the section on Skin type classification for more information.
  • Any known triggers, including occupational history/exposure to chemicals.
  • Any known risk factors, such as family history of vitiligo, or personal or family history of thyroid dysfunction or other autoimmune disease.
  • Any previous episodes of spontaneous repigmentation, previous treatments and their effectiveness.
  • Current medication.
• Examine the person for:
  • The type of vitiligo (segmental, or non-segmental). 
  • The location (including mucosal or genital involvement) and the extent of lesions.
  • The presence of Koebner's phenomenon, confetti-like depigmentation, inflamed borders trichome vitiligo, or depigmented hairs, which may suggest more active disease.
  • The presence of halo nevi. 
  • Skin type (skin colour and ability to tan). 
• Estimate the affected body surface area using the Vitiligo Extent Score (VES) — an online calculator is available at www.vitiligo-calculator.com. 
  • Consider taking digital photographs as a benchmark to aid monitoring of disease and treatment effectiveness.  
• Screen for antithyroid antibodies and thyroid function in people with vitiligo (including children) to identify those at high risk of developing autoimmune thyroid disease. 
  • See the CKS topic on Hypothyroidism for more information.
• Consider arranging blood tests for other comorbid autoimmune diseases if the person's history, family history, and/or other test results are suggestive. 

What else might it be?

A broad range of conditions present with areas of depigmentation that may mimic vitiligo.

• Congenital
  • Albinism — a generalized depigmentation that includes the eyes and is evident from birth, with ocular abnormalities such as strabismus and nystagmus.  
  • Naevus anaemicus — a congenital disorder causing hypopigmented patches due to localized vasoconstriction.
  • Naevus depigmentosus — segmental hypopigmentation that is usually present at birth or in the first year of life, lesions may increase in size in proportion to the growth of the child. 
  • Piebaldism — an autosomal dominant condition in which there is an absence of melanocytes in affected areas of the skin. It usually presents at birth with a white forelock of hair, anterior body midline depigmentation, and bilateral shin depigmentation. The patches remain unchanged throughout life.
  • Tuberous sclerosis — an inherited disease, characterized by ash-leaf shaped, depigmented macules. Other features include angiofibromas, seizures and developmental delay.
• Post-inflammatory
  • Chemical/occupational depigmentation — for example, caused by phenolic/catecholic derivatives that are cytotoxic to melanocytes. Sources include adhesives, de-emulsifiers used in oil fields, deodorants, disinfectants, duplicating paper, formaldehyde resins, germicidal detergents, hair dyes, insecticides, latex gloves, motor oil additives, paints, photographic chemicals, plasticizers, printing ink, rubber antioxidants, soap antioxidants, synthetic oils, varnish, and lacquer resins.
  • Lichen sclerosus — characterized by itchy, white atrophic plaques most commonly affecting the genital and perianal areas.
  • Morphoea — a localized thickening of the dermis due to excess collagen.
  • Pityriasis alba — most commonly seen in children, patches are hypopigmented and dry, and the borders are diffuse and ill-defined. Scaling, however, may be very subtle. Typically, the lesions are seen on sun-exposed areas like the face and upper limbs, and are often precipitated after a period of tanning. 
  • Hypopigmentation following any inflammatory skin condition —  including eczema, psoriasis, lichen planus, scleroderma or systemic sclerosis, lupus erythematosus, and syphilis. 
  • Trauma-induced leukoderma.
• Infective
  • Pityriasis versicolor (or tinea versicolor) — a superficial yeast infection that can cause loss of pigment, particularly in young adults with darker skin. It presents as small (less than 1 cm in diameter), round, pale hypopigmented or pink macules, which have a fine, dry surface scale. They are usually found on the neck, upper trunk and chest, abdomen, and proximal extremities. See the CKS topic on Pityriasis versicolor for more information.
  • Progressive macular hypomelanosis — a common disorder which presents with circular patches of skin hypopigmentation. It is more common in people of darker skin colour. It mainly affects the trunk, and rarely extends to the arms, legs, or neck. 
  • Tuberculoid leprosy — a few sharply defined red patches with raised borders, or a single larger hypopigmented patch less than 10 cm in diameter. There is loss of sensation in lesions, and affected nerves are thickened and tender on palpation. 
• Neoplastic
  • Cutaneous T-cell lymphoma (mycosis fungoides) — hypopigmented patches are associated with a typically 'wrinkled' appearance and dryness, with scaling which may be subtle. Patches vary in size and shape and may have a pinkish hue. The most commonly affected site is the buttocks. 
  • Melanoma-associated depigmentation — this can present as white areas of regression within the primary melanoma, or white patches can appear distant from the melanoma. 
• Other
  • Drug-induced depigmentation — for example, due to corticosteroids, chloroquine, fluphenazine, physostigmine, and imiquimod.
  • Halo naevus — a benign mole surrounded by a halo of depigmentation. It is caused by an immunological reaction against melanocytes and eventually the mole is destroyed. They are more common in summer when tanning of the surrounding skin makes the halo more prominent. 
  • Idiopathic guttate hypomelanosis — a benign, acquired condition commonly seen on the limbs of middle-aged to elderly individuals. Lesions appear as hypopigmented to depigmented discrete macules, usually 1–3 mm in size (rarely 10 mm or more).
  • Sarcoidosis — hypopigmented macules may occur over granulomas in the dermis or subcutaneous tissue. For more information, see the CKS topic on Sarcoidosis. 

Scenario: Management of vitiligo

From birth onwards.

Search strategy

Scope of search

A literature search was conducted for guidelines and systematic reviews on primary care management of vitiligo.

Search dates

March 2020 - April 2025

Key search terms

The terms listed below are the core search terms that were used for EBSCOhost MEDLINE (searched 29th March 2020). These were combined with filters to identify guidelines, systematic reviews and primary care relevant literature in EBSCOhost MEDLINE. The strategy was adapted for The Cochrane Library databases.

S3    S1 OR S2 
S2    AB vitiligo OR TI vitiligo 
S1    (MH "Vitiligo") 

Sources of guidelines

• National Institute for Health and Care Excellence (NICE)
• Scottish Intercollegiate Guidelines Network (SIGN)
• Royal College of Physicians
• Royal College of General Practitioners
• Royal College of Nursing
• NICE Evidence
• World Health Organization
• Guidelines International Network
• TRIP database
• Agency for Healthcare Research and Quality
• National Health and Medical Research Council (Australia)
• Royal Australian College of General Practitioners
• British Columbia Medical Association
• Canadian Medical Association
• Alberta Medical Association
• Michigan Quality Improvement Consortium
• Singapore Ministry of Health
• National Resource for Infection Control
• RefHELP NHS Lothian Referral Guidelines
• Medline (with guideline filter)
• Driver and Vehicle Licensing Agency
• NHS Health at Work (occupational health practice)

Sources of systematic reviews and meta-analyses

• The Cochrane Library:
  • Systematic reviews
  • Protocols
  • Database of Abstracts of Reviews of Effects
• Medline (with systematic review filter)
• EMBASE (with systematic review filter)

Sources of health technology assessments and economic appraisals

• NIHR Health Technology Assessment programme
• The Cochrane Library:
  • NHS Economic Evaluations
  • Health Technology Assessments
• Canadian Agency for Drugs and Technologies in Health
• International Network of Agencies for Health Technology Assessment

Sources of randomized controlled trials

• The Cochrane Library:
  • Central Register of Controlled Trials
• Medline (with randomized controlled trial filter)
• EMBASE (with randomized controlled trial filter)

Sources of evidence based reviews and evidence summaries

• Drug and Therapeutics Bulletin
• TRIP database
• Central Services Agency COMPASS Therapeutic Notes

Sources of national policy

• Department of Health
• Health Management Information Consortium (HMIC)

Patient experiences

• Healthtalk
• BMJ - Patient Journeys

Sources of medicines information

The following sources are used by CKS pharmacists and are not necessarily searched by CKS information specialists for all topics. Some of these resources are not freely available and require subscriptions to access content.

• British National Formulary (BNF)
• electronic Medicines Compendium (eMC)
• European Medicines Agency (EMEA)
• Medicines and Healthcare products Regulatory Agency (MHRA)
• REPROTOX
• Scottish Medicines Consortium
• Stockley's Drug Interactions
• TERIS
• TOXBASE
• Micromedex
• UK Medicines Information

Stakeholder engagement

Our policy

The external review process is an essential part of CKS topic development. Consultation with a wide range of stakeholders provides quality assurance of the topic in terms of:

• Clinical accuracy.
• Consistency with other providers of clinical knowledge for primary care.
• Accuracy of implementation of national guidance (in particular NICE guidelines).
• Usability.

Principles of the consultation process

• The process is inclusive and any individual may participate.
• To participate, an individual must declare whether they have any competing interests or not. If they do not declare whether or not they have competing interests, their comments will not be considered.
• Comments received after the deadline will be considered, but they may not be acted upon before the clinical topic is issued onto the website.
• Comments are accepted in any format that is convenient to the reviewer, although an electronic format is encouraged.
• External reviewers are not paid for commenting on the draft topics.
• Discussion with an individual or an organization about the CKS response to their comments is only undertaken in exceptional circumstances (at the discretion of the Clinical Editor or Editorial Steering Group).
• All reviewers are thanked and offered a letter acknowledging their contribution for the purposes of appraisal/revalidation.
• All reviewers are invited to be acknowledged on the website. All reviewers are given the opportunity to feedback about the external review process, enabling improvements to be made where appropriate.

Stakeholders

• Key stakeholders identified by the CKS team are invited to comment on draft CKS topics. Individuals and organizations can also register an interest to feedback on a specific topic, or topics in a particular clinical area, through the Getting involved section of the Clarity Informatics website.
• Stakeholders identified from the following groups are invited to review draft topics:
  • Experts in the topic area.
  • Professional organizations and societies (for example, Royal Colleges).
  • Patient organizations, Clarity has established close links with groups such as Age UK and the Alzheimer’s Society specifically for their input into new topic development, review of current topic content and advice on relevant areas of expert knowledge.
  • Guideline development groups where the topic is an implementation of a guideline.
  • The British National Formulary team.
  • The editorial team that develop MeReC Publications.
• Reviewers are provided with clear instructions about what to review, what comments are particularly helpful, how to submit comments, and declaring interests.

Patient engagement

Clarity Informatics has enlisted the support and involvement of patients and lay persons at all stages in the process of creating the content which include:

• Topic selection
• Scoping of topic
• Selection of clinical scenarios
• First draft internal review
• Second draft internal review
• External review
• Final draft and pre-publication

Our lay and patient involvement includes membership on the editorial steering group, contacting expert patient groups, organizations and individuals.

Evidence exclusion criteria

Our policy

Scoping a literature search, and reviewing the evidence for CKS is a methodical and systematic process that is carried out by the lead clinical author for each topic. Relevant evidence is gathered in order that the clinical author can make fully informed decisions and recommendations. It is important to note that some evidence may be excluded for a variety of reasons. These reasons may be applied across all CKS topics or may be specific to a given topic.

Studies identified during literature searches are reviewed to identify the most appropriate information to author a CKS topic, ensuring any recommendations are based on the best evidence. We use the principles of the GRADE and PICOT approaches to assess the quality of published research. We use the principles of AGREE II to assess the quality of published guidelines.

Standard exclusions for scoping literature:

• Animal studies
• Original research is not written in English

Possible exclusions for reviewed literature:

• Sample size too small or study underpowered
• Bias evident or promotional literature
• Population not relevant
• Intervention/treatment not relevant
• Outcomes not relevant
• Outcomes have no clear evidence of clinical effectiveness
• Setting not relevant
• Not relevant to UK
• Incorrect study type
• Review article
• Duplicate reference

Organizational, behavioural and financial barriers

Our policy

The CKS literature searches take into consideration the following concepts, which are discussed at the initial scoping of the topic.

• Feasibility
  • Studies are selected depending on whether the intervention under investigation is available in the NHS and can be practically and safely undertaken in primary care.
• Organizational and Financial Impact Analysis
• Studies are selected and evaluated on whether the intervention under investigations may have an impact on local clinical service provision or national impact on cost for the NHS. The principles of clinical budget impact analysis are adhered to, evaluated and recorded by the author. The following factors are considered when making this assessment and analysis.
  • Eligible population
  • Current interventions
  • Likely uptake of new intervention or recommendation
  • Cost of the current or new intervention mix
  • Impact on other costs
  • Condition-related costs
  • In-direct costs and service impacts
  • Time dependencies
• Cost-effectiveness or cost-benefit analysis studies are identified where available. 

We also evaluate and include evidence from NICE accredited sources which provide economic evaluations of recommendations, such as NICE guidelines. When a recommended action may not be possible because of resource constraints, this is explicitly indicated to healthcare professionals by the wording of the CKS recommendation.

Declarations of interest

Our policy

Clarity Informatics requests that all those involved in the writing and reviewing of topics, and those involved in the external review process to declare any competing interests. Signed copies are securely held by Clarity Informatics and are available on request with the permission of the individual. A copy of the declaration of interest form which participants are asked to complete annually is also available on request. A brief outline of the declarations of interest policy is described here and full details of the policy is available on the Clarity Informatics website. Declarations of interests of the authors are not routinely published, however competing interests of all those involved in the topic update or development are listed below. Competing interests include:

• Personal financial interests
• Personal family interest
• Personal non-financial interest
• Non-personal financial gain or benefit

Although particular attention is given to interests that could result in financial gains or losses for the individual, competing interests may also arise from academic competition or for political, personal, religious, and reputational reasons. An individual is not obliged to seek out knowledge of work done for, or on behalf of, the healthcare industry within the departments for which they are responsible if they would not normally expect to be informed.

Who should declare competing interests?

Any individual (or organization) involved in developing, reviewing, or commenting on clinical content, particularly the recommendations should declare competing interests. This includes the authoring team members, expert advisers, external reviewers of draft topics, individuals providing feedback on published topics, and Editorial Steering Group members. Declarations of interest are completed annually for authoring team and editorial steering group members, and are completed at the start of the topic update and development process for external stakeholders.

Competing interests declared for this topic:

None.