12-phase flow (12)

1. 1FRAME
   Frame as a CHRONIC, often progressive/relapsing T-cell-mediated AUTOIMMUNE melanocyte-loss disease (depigmentation, not hypopigmentation) managed on an extent/activity/site-stratified ladder with autoimmune-comorbidity screening + psychological support as first-class outcomes — NOT a benign cosmetic finding. EVERY patient is screened for the autoimmune cluster (thyroid #1, T1DM, alopecia areata, pernicious anaemia, Addison) and for depression/anxiety/stigma (amplified in skin of colour). The treatable/serious not-to-miss is pityriasis versicolor, leprosy, and hypopigmented mycosis fungoides/CTCL masquerading as vitiligo.
   advance: chronic autoimmune-depigmentation framing set; comorbidity + psychosocial + versicolor/leprosy/CTCL escape routes noted
2. 2ENTRY
   Recognise acquired well-demarcated DEPIGMENTED macules with Wood-lamp bright accentuation vs the segmental/blaschkoid entry vs the active-disease (confetti/trichrome/Koebner) entry vs the autoimmune-comorbidity/severe-distress entry; capture extent (% BSA, facial vs non-facial) up front as the primary therapy-gating axis.
   inputs: depigmentation_extent_and_bsa
   actions: workup.chronic_pruritus
   advance: entry trigger present; extent (% BSA, facial vs non-facial) recorded
3. 3CONTEXT
   Build the diagnosis + treatment context: confirm true depigmentation (Wood-lamp bright chalk/blue-white accentuation, sharp margins), assign subtype (non-segmental vs segmental vs mixed), grade ACTIVITY (confetti macules, trichrome, Koebner, leukotrichia, rapid spread), map site distribution (face/neck best repigmentation; acral/leukotrichic poor), Fitzpatrick phototype + contrast, the autoimmune-comorbidity screen (thyroid #1, T1DM, AA, pernicious anaemia, Addison), and a structured psychosocial + depression/anxiety assessment (a core, not optional, axis).
   inputs: subtype_nonsegmental_vs_segmental_vs_mixed, disease_activity_signs, lesion_site_distribution, autoimmune_comorbidity_screen, psychosocial_burden_and_mood_screen, fitzpatrick_skin_phototype
   actions: workup.chronic_pruritus
   advance: true depigmentation confirmed; subtype + activity + site + comorbidity + psychosocial context established
4. 4RED_FLAGS
   Pityriasis (tinea) versicolor (fine branny scale, KOH spaghetti-and-meatballs, dull-yellow Wood-lamp — hypopigment not depigment) → route the dermatophyte engine, antifungal not immunosuppression. Leprosy (anaesthetic hypopigmented patch, nerve thickening, endemic exposure) → urgent leprosy work-up. Hypopigmented mycosis fungoides / CTCL (persistent atypical/poikilodermatous patches, often skin of colour, treatment-resistant) → SKIN BIOPSY before chronic immunomodulation. Rapidly progressive ACTIVE vitiligo (confetti + Koebner + trichrome) → expedite arrest-progression therapy.
   inputs: koh_scaly_or_anaesthetic_or_atypical_features
   actions: panel.cbc
   advance: versicolor / leprosy / CTCL / rapidly-active disease screened and routed/escalated if present
5. 5INITIAL_WORKUP
   Vitiligo is a clinical + Wood-lamp diagnosis — no test confirms it. Targeted workup is (a) the autoimmune-comorbidity screen (TSH/thyroid function ± anti-TPO; consider T1DM glucose/HbA1c, B12 for pernicious anaemia per symptoms) and (b) baseline labs before an oral mini-pulse corticosteroid where indicated (CBC, LFT, glucose). Skin biopsy ONLY for diagnostic uncertainty or to exclude hypopigmented mycosis fungoides/CTCL; KOH if versicolor plausible.
   inputs: tsh_thyroid_function, cbc_with_differential, lft, glucose_hba1c_for_t1dm_screen
   actions: panel.cbc, panel.thyroid, panel.lft, panel.renal
   advance: autoimmune comorbidity screen done; pre-mini-pulse safety labs drawn if systemic step likely; biopsy/KOH only if indicated
6. 6BRANCHING_WORKUP
   Leukoderma decision tree: Wood-lamp bright accentuation + symmetric acral/periorificial + sharp margins → vitiligo; fine scale + KOH-positive + dull-yellow fluorescence → pityriasis versicolor (route derm.tinea-dermatophytosis.core.v1); ill-defined hypopigmentation with fine scale on cheeks of an atopic child → pityriasis alba (route/associate derm.atopic-dermatitis.core.v1); follows preceding inflammation/injury, not bright on Wood-lamp → post-inflammatory hypopigmentation; congenital stable off-white patch with hyperpigmented island (no progression) → nevus depigmentosus / piebaldism; pale patch that disappears on diascopy → nevus anaemicus; depigmented rim around a mole → halo nevus; genital atrophic white plaques → lichen sclerosus; anaesthetic patch + nerve thickening + endemic → leprosy; occupational phenol/catechol exposure → chemical leukoderma; persistent atypical/poikilodermatous patches → BIOPSY for hypopigmented mycosis fungoides/CTCL.
   inputs: koh_scaly_or_anaesthetic_or_atypical_features
   actions: workup.chronic_pruritus
   advance: vitiligo confirmed clinically/Wood-lamp OR an alternative leukoderma assigned + routed; versicolor/leprosy/CTCL actively excluded
7. 7DIFFERENTIAL
   Terminal leukoderma differential with named pivots: vitiligo (acquired progressive symmetric DEPIGMENTATION + Wood-lamp bright accentuation + acral/periorificial + Koebner/confetti pivot) vs pityriasis versicolor (fine scale + KOH spaghetti-and-meatballs + dull-yellow fluorescence pivot — route derm.tinea-dermatophytosis.core.v1) vs pityriasis alba (atopic child + fine-scale facial HYPOpigmentation pivot — derm.atopic-dermatitis.core.v1) vs post-inflammatory hypopigmentation (antecedent dermatosis/injury + not bright on Wood-lamp pivot) vs idiopathic guttate hypomelanosis (small stable porcelain macules on sun-exposed limbs pivot) vs nevus depigmentosus / piebaldism (congenital, stable, non-progressive ± hyperpigmented islands pivot) vs nevus anaemicus (vasoconstrictive — disappears on diascopy pivot) vs halo nevus (depigmented rim around melanocytic naevus pivot) vs lichen sclerosus (atrophic genital white plaques + sclerosis pivot) vs leprosy (anaesthetic patch + nerve thickening + endemic pivot) vs chemical/occupational leukoderma (phenol/catechol exposure pivot) vs hypopigmented mycosis fungoides/CTCL (persistent atypical/poikilodermatous + BIOPSY pivot — NOT vitiligo).
   advance: single best diagnosis selected; versicolor/leprosy/CTCL actively excluded; subtype (non-segmental vs segmental vs mixed) + activity assigned
8. 8RISK_STRATIFICATION
   Severity = extent (% BSA, facial vs non-facial) × subtype × ACTIVITY × site repigmentation-potential × psychosocial impact (VASI/F-VASI/T-VASI + VES/Vitiligo Noticeability Scale scored clinically — schema-blocked as registry calculators, captured narratively; INFO/VGICG success = 80–100% target-lesion repigmentation, PMID 30030843). Limited stable non-segmental (≤10% BSA, no activity) → topical first-line. Active or extensive (confetti/Koebner/trichrome, >facial, rapidly progressive) → arrest-progression + phototherapy ± systemic. Stable segmental / refractory localised → surgical candidacy. Severe psychosocial distress upgrades urgency independent of extent.
   inputs: depigmentation_extent_and_bsa, disease_activity_signs, psychosocial_burden_and_mood_screen
   advance: extent × subtype × activity × site tier + escalation decision + psychosocial-urgency modifier assigned
9. 9TREATMENT
   Photoprotection + camouflage + psychological support always + the extent/activity/site-stratified ladder. Limited non-segmental (≤10% BSA): topical ruxolitinib 1.5% cream (FDA-approved repigmentation ≥12 y, ≤10% BSA — TRuE-V), topical corticosteroid (non-facial), topical calcineurin inhibitor (face/folds/children, steroid-sparing). Active/progressive or extensive: narrowband-UVB phototherapy (mainstay for widespread) ± topical; targeted 308-nm excimer for localised; oral mini-pulse corticosteroid to ARREST rapidly progressive disease. Stable segmental / refractory localised: surgical melanocyte–keratinocyte transplant (non-pharm; documented stable ≥6–12 mo only). Adjuncts/non-pharm: photoprotection, cosmetic camouflage + psychological support (core QoL), depigmentation with monobenzone for extensive recalcitrant universal disease (IRREVERSIBLE — counsel), maintenance topical after repigmentation to prevent relapse. Comorbidity gating: pregnancy/lactation → defer JAK/systemic/phototherapy, cautious minimal topical CNI/steroid; AVOID chronic systemic corticosteroids (mini-pulse only); phototherapy skin-cancer/photosensitiser caution; counsel slow response (≥3–6 mo, facial best, acral/leukotrichia poor).
   inputs: pregnancy_lactation, age, disease_stability_duration_for_surgery, creatinine
   advance: photoprotection/camouflage/psychological support offered; extent/activity-appropriate ladder step started; agent gated on age/pregnancy/stability; ≥3–6-mo response + relapse counselled
10. 10DISPOSITION
    Entirely outpatient/derm-clinic — vitiligo is not an admission disease. Phototherapy + topical-JAK + surgical transplant via dermatology; route pityriasis versicolor OUT to derm.tinea-dermatophytosis.core.v1, leprosy to the appropriate infectious-disease pathway, hypopigmented MF/CTCL to biopsy + cutaneous-lymphoma care; refer mental-health for significant depression/anxiety/stigma; pediatric extensive disease → pediatric-dermatology + phototherapy/topical-ruxolitinib-eligibility pathway.
    inputs: psychosocial_burden_and_mood_screen
    advance: disposition documented; outpatient derm follow-up + mental-health/peds referrals as indicated; mimics routed OUT
11. 11MONITORING
    Disease: repigmentation response by VASI/F-VASI/T-VASI + Vitiligo Noticeability Scale at 3 / 6 / 9–12 mo (slow — counsel ≥3–6 mo before judging; facial responds best, acral/leukotrichic poorly; INFO/VGICG success = 80–100% target-lesion repigmentation, PMID 30030843; TRuE-V F-VASI75 50.3% @52 wk continuous, PMID 40156697). Activity re-assessment (new confetti/Koebner/trichrome → re-escalate to arrest). Drug safety: topical ruxolitinib application-site acne/pruritus + JAK class label + BSA/duration limit; oral mini-pulse — short-course glycaemic/BP/mood vigilance, NOT chronic; phototherapy cumulative-dose + photodamage/skin-cancer surveillance; topical-steroid atrophy at long-term/facial sites. Autoimmune-comorbidity surveillance (re-screen thyroid). Relapse after stopping — maintenance counselled.
    inputs: cbc_with_differential, glucose_hba1c_for_t1dm_screen
    actions: panel.cbc, panel.thyroid
    advance: repigmentation + activity re-assessed at 3/6/9–12 mo; drug-class safety on schedule; comorbidity re-screened
12. 12FOLLOWUP
    Chronic-disease maintenance: counsel the often progressive/relapsing course + realistic site-dependent repigmentation expectations (face/neck best; acral, bony-prominence, and leukotrichic lesions poor; segmental more stable but less topical-responsive), maintenance topical 1–2×/wk after repigmentation to prevent relapse, lifelong autoimmune (thyroid #1, T1DM, AA, pernicious anaemia, Addison) + mental-health surveillance, photoprotection (depigmented skin burns, no melanin photoprotection) + camouflage + peer-support signposting, irreversibility counselling before any monobenzone depigmentation, and step-up/step-down + surgical-candidacy (stable ≥6–12 mo) criteria. Dermatology continuity; re-evaluate diagnosis (biopsy) if the course is atypical or treatment-resistant (hypopigmented MF/CTCL).
    inputs: autoimmune_comorbidity_screen, psychosocial_burden_and_mood_screen
    actions: workup.chronic_pruritus
    advance: course/relapse + site-dependent repigmentation-expectation counselling + maintenance + comorbidity + mental-health surveillance + photoprotection/camouflage documented