White patches are the visible part. What decides your treatment is invisible: whether the disease is still spreading, how long each patch has been there, and where on the body it sits. This section covers all of it.
Vitiligo is an autoimmune condition. The melanocytes — the cells that make pigment — are destroyed or switched off in patches, and the skin left behind has no colour. It is not an infection, it is not caused by anything you ate, and it cannot be passed to anyone else by touch.
It affects roughly one person in a hundred worldwide, and India carries one of the highest burdens of any country. Around a fifth of patients have a close relative with it, so a family history is common without being deterministic — most children of a parent with vitiligo never develop it.
The clinically important distinction is not how big the patches are. It is whether the disease is active — still producing new patches or expanding old ones — or stable. Almost every treatment decision on this page follows from that one answer.
Active disease has to be stopped before anything can be rebuilt. New patches in the last six months, patches with blurred edges, or depigmentation appearing where the skin was scratched or injured all point to activity.
Face and neck respond best; hands, feet and lips respond least, because they have the fewest pigment reservoirs to repopulate from. Patches present for many years respond more slowly.
Pigment cells survive in hair follicles even when they are gone from the surrounding skin, and repigmentation usually starts as small dark dots around each hair. If the hairs inside a patch have turned white too, that reservoir is depleted — which is why those patches respond poorly to creams and light, and why surgery exists.
There is no single vitiligo treatment. There is a sequence, and where you enter it depends on activity, site and duration.
| Treatment | What it does | Best suited to |
|---|---|---|
| Topical steroids | Suppresses the immune attack; halts spread | Recent, active, limited patches |
| Calcineurin inhibitors | Immune-modulating without steroid thinning | Face, eyelids, folds — thin skin |
| Topical JAK inhibitors | Blocks the specific immune signal in vitiligo | Facial and limited non-segmental disease |
| NB-UVB phototherapy | Stimulates surviving melanocytes to repopulate | Widespread disease; the workhorse treatment |
| Excimer laser | Targeted high-dose light on individual patches | Few, small, localised patches |
| Oral mini-pulse steroids | Arrests rapidly progressing disease | Actively spreading vitiligo |
| Melanocyte transplant | Moves your own pigment cells into the patch | Stable disease only, 12 months quiet |
| Punch / blister grafting | Transplants pigmented skin fragments | Small stable patches, lips, extremities |
Nothing on this list cures vitiligo. Each is a way of stopping the disease, restoring colour, or both — and most patients need more than one.
Active disease is quietened first — usually topicals, sometimes a short oral course. Repigmenting skin while new patches appear is running up a down escalator.
Phototherapy, targeted light and topicals, given long enough to judge. Six to eight weeks is a check, not a verdict; three to six months is a verdict.
Some patches recolour fully, some partially, some not at all. What remains after a proper medical trial is what surgery is for.
Grafting into active disease fails and can trigger new patches at the donor site. Twelve quiet months is the threshold.
Melanocyte transplant and punch grafting move your own pigment cells into skin that has none left. For stable patches on hands, lips and other stubborn sites, it is often the only thing that will work.
It requires an operating list, the skill to harvest and place cells, and the judgement to refuse patients whose disease is not stable. This practice has done it for decades — and it began life as a vitiligo hospital, which is why.
How graft surgery worksNo new patches, no expansion, no koebnerisation for twelve months. Being told to wait is a common answer.
Send photographs before booking travel. A video consultation can settle whether the trip is worth making.
No. No treatment available anywhere cures vitiligo, and any clinic promising a cure is making a claim it cannot support.
What treatment does reliably achieve is stopping the spread, and repigmenting a significant proportion of affected skin in many patients — particularly on the face and trunk, and particularly when treated early.
No. It is an autoimmune condition, not an infection. It cannot spread by touch, by sharing food, by using the same towel, or by any other contact.
Usually not. Most vitiligo remains limited, and the pattern in the first year or two is broadly predictive. A minority does progress widely, which is precisely why active disease is treated promptly rather than watched.
Facial patches often show the first specks of colour within two to three months of consistent phototherapy. Hands and feet may take much longer or not respond at all. Six to eight weeks is the first review, not the deadline.
No food causes vitiligo, and no diet has been shown to reverse it. The advice about avoiding citrus, milk and sour foods together is folklore with no evidence behind it. Eating well matters; a restrictive diet does not.
It can be. Thyroid disease is the most common association, which is why thyroid function is usually checked at the first visit. Diabetes and pernicious anaemia are less frequent associations.
Yes, it can. Repigmented skin can lose colour again, particularly if treatment stops abruptly or the disease reactivates, which is why maintenance and review continue after the visible result.
Not a treatment plan sold on the spot. Message the clinic and bring your history.