Amyloidosis cutis dyschromia is a rare genetic skin condition that causes a mix of lighter and darker patches on the skin. The changes usually start in childhood and tend to be lifelong. People with amyloidosis cutis dyschromia typically feel well, and symptoms are mainly cosmetic rather than painful. Doctors describe this as a skin-limited condition, and it does not affect life expectancy. Treatment focuses on managing skin appearance with sun protection, gentle skincare, and sometimes dermatologic therapies.
Overview
Amyloidosis cutis dyschromiaSymptoms
Amyloidosis cutis dyschromia causes speckled, net-like patches of darker and lighter skin, usually on the arms, trunk, and neck. Features often begin in early childhood and are mostly painless, with mild itch or dryness in some.
Outlook and prognosis
Most people with amyloidosis cutis dyschromia have stable skin color changes that don’t affect overall health or lifespan. Spots may spread slowly, then level off; itching is uncommon but can occur. Regular dermatology check-ins help manage cosmetic concerns and monitor rare changes.
Causes and risk factors
Amyloidosis cutis dyschromia usually stems from inherited gene changes affecting skin proteins, sometimes appearing from childhood. Family history increases risk. Sun exposure and chronic friction may accentuate color changes, but lifestyle factors do not cause it.
Genetic influences
Genetics plays a central role in Amyloidosis cutis dyschromia, with most cases linked to inherited variants affecting skin cell turnover and protein handling. Some families show autosomal recessive patterns. Genetic testing isn’t always needed but can confirm the diagnosis and guide counseling.
Diagnosis
Doctors suspect amyloidosis cutis dyschromia from its patterned light-and-dark skin changes. Diagnosis is confirmed by skin biopsy showing amyloid; genetic tests may be considered in familial cases. Together, these steps form the genetic diagnosis of amyloidosis cutis dyschromia.
Treatment and drugs
Treatment for Amyloidosis cutis dyschromia focuses on easing skin discoloration and itch, and on slowing new spots. Dermatologists may use gentle light-based therapies, topical retinoids, or anti-itch creams. Regular sun protection and avoiding skin friction can help prevent flare‑ups.
Symptoms
Skin tone shifts can be the first thing people notice—patches of lighter and darker skin that don’t tan or fade the way nearby skin does. Early features of amyloidosis cutis dyschromia often begin in childhood, with color changes on the face, neck, trunk, and arms. The changes are often subtle at first, blending into daily life until they become more noticeable. Itch is usually mild, if present at all, and overall health is typically unaffected.
Light and dark patches scattered across the skin create a speckled, net-like look. These patches don’t tan or fade evenly compared with nearby skin. Many people notice them on both sun-exposed and covered areas.
The face, neck, trunk, and arms are most commonly affected. Palms and soles are usually spared.
The changes often start in early childhood. They may spread slowly for a time and then settle into a stable pattern. Most children feel well otherwise.
Itching is absent or mild for many people with amyloidosis cutis dyschromia. The skin is not painful, but the look of the spots can be bothersome.
How people usually first notice Amyloidosis cutis dyschromia?
People often first notice amyloidosis cutis dyschromia as a gradual patchwork of small, speckled light and dark spots on sun-exposed skin, especially the face, neck, and upper back. These first signs of amyloidosis cutis dyschromia usually appear in childhood or adolescence and tend not to itch or hurt, so families may bring them up during a routine check-up when the color contrast becomes more obvious. Doctors typically recognize the pattern on exam and confirm the diagnosis with a skin biopsy, which shows amyloid deposits in the upper layer of the skin.
Types of Amyloidosis cutis dyschromia
Amyloidosis cutis dyschromia is a rare skin-limited form of primary cutaneous amyloidosis. Broadly, symptoms are grouped into a few clinical variants that share the hallmark “salt-and-pepper” changes in skin color but differ in when they start, how widespread the patches become, and whether itching or texture changes show up. Not everyone will experience every type. Knowing the main variants of Amyloidosis cutis dyschromia can help people understand why the pattern on their skin looks a bit different from someone else’s.
Classic generalized
Diffuse speckled light-and-dark patches appear across the trunk and limbs, often beginning in childhood or adolescence. Skin usually feels smooth without raised bumps, and itching is mild or absent. The color contrast can be more visible on sun-exposed areas.
Segmental or localized
Mottled discoloration is limited to one region, such as a shoulder, lower back, or a single limb. Patches are smaller in area and may remain stable for years. People may notice edges that blend gradually into nearby normal skin.
Pruritic variant
The same salt-and-pepper discoloration appears, but itching is more frequent or bothersome. Scratching can make spots look slightly rough or more pronounced over time. Using gentle skin care and avoiding triggers can help reduce flare-ups.
Texture-predominant
Color change occurs with a faint, fine roughness when you run a finger across the area. The skin may feel slightly dry or sandpapery even when the color differences are subtle. Moisturizing can make the feel less noticeable.
Familial pattern
Similar discoloration shows up in multiple relatives across generations, suggesting an inherited form. Onset is usually earlier, and the spread can be wider than in sporadic cases. Discussing family history can clarify the types of Amyloidosis cutis dyschromia seen in your family.
What genetics can tell you about symptoms
Some people with amyloidosis cutis dyschromia have changes in genes that help skin cells handle wear-and-tear, leading to speckled light and dark patches and mild itch. Variants in keratin-handling or DNA-repair genes can make pigment uneven and trigger tiny amyloid deposits in the skin.
Causes and risk factors
Amyloidosis cutis dyschromia is most often linked to changes in the GPNMB gene that affect how skin cells handle waste.
These changes are usually inherited, but a new mutation can appear in a child without family history.
The buildup of abnormal skin protein helps explain early symptoms of Amyloidosis cutis dyschromia, like patchy light and dark areas.
Sun exposure and repeated friction can worsen the color changes, and the condition is reported more often in people from parts of Asia and the Middle East.
Some risks are modifiable (things you can change), others are non-modifiable (things you can’t).
Environmental and biological risk factors
Understanding what can raise the chance of amyloidosis cutis dyschromia helps you plan care and protect your skin over time. Doctors often group risks into internal (biological) and external (environmental). The points below reflect patterns seen in clinics and published case reports.
UV light can injure the upper skin layer and trigger protein changes that end up as amyloid. Color contrast may stand out more on frequently sun-exposed areas.
Ongoing minor rubbing or pressure creates micro-injury in the upper skin. This cell stress can release keratin fragments that seed amyloid.
Episodes of superficial inflammation and healing can leave behind stressed skin cells. That stress may increase keratin breakdown and amyloid formation in amyloidosis cutis dyschromia.
In this condition, amyloid in the skin forms from broken-down keratin released by damaged skin cells. Processes that increase cell wear and tear can raise the chance of deposits.
Genetic risk factors
Genetic changes play a central role in Amyloidosis cutis dyschromia. Some risk factors are inherited through our genes. In many families, early symptoms of Amyloidosis cutis dyschromia appear in childhood when both copies of a key skin gene are altered. Research points most strongly to variants in the GPNMB gene, though a small number of families have no identified change yet.
GPNMB gene variants: Loss-of-function changes in the GPNMB gene are the main known cause. They disrupt how skin cells manage pigment and clear cell debris, encouraging amyloid to form. This pattern often leads to childhood-onset mottled light and dark patches.
Autosomal recessive pattern: Amyloidosis cutis dyschromia usually occurs when a child inherits one nonworking copy of GPNMB from each parent. Carrier parents typically have normal skin. When both parents are carriers, each child has about a 1 in 4 (25%) chance to be affected.
Parental relatedness: Parents who are related by blood (consanguinity) are more likely to carry the same rare GPNMB change. This raises the chance a child will inherit two altered copies. Genetic counseling can help families understand this recurrence risk.
Family history: Having siblings or relatives with Amyloidosis cutis dyschromia suggests a shared inherited variant. In such families, future children may have a higher chance of being affected if both parents are carriers. Mapping who is affected across relatives helps identify who could benefit from testing.
Ancestry patterns: Amyloidosis cutis dyschromia has been reported more often in families from East and South Asia and the Middle East. This may reflect where cases have been recognized and where certain rare variants cluster. People of any background can be affected.
Variable expression: Even with the same GPNMB changes, skin findings can range from subtle to widespread. Age of onset and intensity can differ among relatives. People with the same risk factor can have very different experiences.
Other genes suspected: A minority of families meeting criteria for this condition have no detectable change in GPNMB on current tests. This points to additional genes involved in skin amyloid formation that remain to be discovered. Science continues to uncover how these elements interact.
Lifestyle risk factors
Amyloidosis cutis dyschromia is a genetic skin condition; lifestyle habits do not cause it, but they can influence symptom flares, pigment contrast, and skin comfort. Understanding how lifestyle affects Amyloidosis cutis dyschromia can help you reduce itching, prevent secondary darkening, and protect fragile skin. In this context, “lifestyle risk factors for Amyloidosis cutis dyschromia” refers to day‑to‑day choices that may worsen visibility or discomfort rather than create the condition.
Ultraviolet light can deepen hyperpigmented spots and make hypopigmented areas look more contrasting. Consistent photoprotection can limit new darkening and help stabilize overall skin tone.
Friction and scratching can inflame the skin and may exacerbate pigment changes in affected areas. Gentle fabrics and itch-control strategies reduce microtrauma that can lead to post‑inflammatory darkening.
Heat and heavy sweating can intensify itch, which can trigger more scratching and visible discoloration. Cooling measures and pacing activity help you exercise while minimizing flare‑ups.
Dryness increases itch and makes skin more prone to microtears that worsen dyschromia. Regular use of bland emollients supports the barrier and can reduce itch‑scratch cycles.
Risk prevention
Amyloidosis cutis dyschromia is usually inherited, so you can’t fully prevent the condition itself. Prevention is about lowering risk, not eliminating it completely. What helps most is protecting skin and avoiding triggers that can worsen the color changes or cause new spots to appear. Regular dermatology care can also catch problems early and guide safe treatments over time.
Daily broad‑spectrum sunscreen and shade can keep patches from darkening. UV‑safe clothing and hats reduce UV exposure that may trigger new color changes in amyloidosis cutis dyschromia. Reapply sunscreen during long outdoor time.
Use fragrance‑free cleansers and moisturizers to support the skin barrier. Harsh scrubs and acids can irritate skin and worsen mottled pigmentation in amyloidosis cutis dyschromia.
Treating itch with gentle moisturizers or doctor‑recommended creams reduces scratching. Less scratching lowers the chance of new or larger patches forming in amyloidosis cutis dyschromia.
Skip rough loofahs, tight seams, and repetitive rubbing on the same skin areas. Lowering friction helps prevent Koebner‑type reactions that can create new spots in amyloidosis cutis dyschromia.
Transmission
Amyloidosis cutis dyschromia is not an infection and does not spread between people. You cannot catch it through touch, coughing, sex, blood exposure, or shared towels.
Amyloidosis cutis dyschromia is usually inherited. It often happens when both parents carry a silent, non-working copy of a gene, and in that situation each pregnancy has about a 1 in 4 chance that a child will have the condition. Sometimes a new gene change appears for the first time in a child, so there may be no family history. A genetics professional can explain how Amyloidosis cutis dyschromia is inherited and the genetic transmission of Amyloidosis cutis dyschromia in your family.
When to test your genes
Consider genetic testing if you have lifelong, symmetric speckled skin color changes without itching, especially with a family history or if multiple relatives are affected. Testing can confirm the diagnosis, guide monitoring for rare systemic features, and avoid unnecessary biopsies. Talk with a dermatologist or geneticist to choose the right test.
Diagnosis
For many, the first step comes when everyday activities start feeling harder because of skin changes that draw questions or comments. Amyloidosis cutis dyschromia is usually recognized by its distinct, widespread mix of lighter and darker skin patches, then confirmed with simple skin tests. Many people feel relief just knowing what’s really going on. Doctors rely on the look and pattern first, then use a small skin sample and sometimes genetic tests to make a clear genetic diagnosis of Amyloidosis cutis dyschromia.
Doctors look for a fine, speckled mix of lighter and darker patches spread across much of the skin, often starting in childhood. Itching is usually mild or absent, and the face and trunk may show a net-like pattern. This overall look helps separate it from more common pigment conditions.
A dermatologist maps where the color changes are and checks texture and any tiny bumps. They also look for signs seen in other forms of primary cutaneous amyloidosis to see if features overlap. Findings on the palms, soles, nails, or mouth can help narrow the possibilities.
A handheld skin scope lets the clinician see the pigment network and dotted patterns more clearly. These close-up features can support the suspected diagnosis. It is painless and done at the bedside.
A small numbed sample confirms amyloid just under the surface layer of skin. The procedure takes minutes and usually leaves a tiny scar. Results guide next steps and help rule out look-alike disorders.
Stages of Amyloidosis cutis dyschromia
Amyloidosis cutis dyschromia does not have defined progression stages. It tends to cause a mottled mix of lighter and darker skin that often changes slowly over years, rather than moving through clear step-by-step phases. Early symptoms of amyloidosis cutis dyschromia may include faint, speckled color changes on the trunk, arms, or face that you or a family member gradually notice. Different tests may be suggested to help confirm the diagnosis—doctors usually examine the skin, review your history, and may take a small skin sample (biopsy) to look for amyloid and to rule out other causes of pigmentation change.
Outlook and prognosis
Looking ahead can feel daunting, but most people with Amyloidosis cutis dyschromia live full lives with careful skin care and routine monitoring. This condition mainly affects skin color—patches of lighter and darker areas—so the day-to-day impact is often cosmetic rather than dangerous. Many people ask, “What does this mean for my future?”, and the practical answer is that symptoms tend to be long lasting but usually don’t progress to organ disease when the diagnosis is truly limited to the skin.
Doctors call this the prognosis—a medical word for likely outcomes. Over time, most people with Amyloidosis cutis dyschromia notice that the pattern of discoloration stabilizes after a period of gradual spread in youth or early adulthood. Itching can come and go; early symptoms of Amyloidosis cutis dyschromia sometimes include mild itch or skin sensitivity that responds to moisturizers, sun protection, and gentle clothing choices. In medical terms, the long-term outlook is often shaped by both genetics and lifestyle.
Mortality from Amyloidosis cutis dyschromia itself is not expected; the condition is generally considered benign with respect to life span. That said, it is important to confirm that amyloid deposits are confined to the skin and to rule out any signs of internal involvement if new symptoms appear, such as unexplained weight loss, swelling, or nerve changes. Everyone’s journey looks a little different. Talk with your doctor about what your personal outlook might look like, including how to manage cosmetic concerns, monitor for changes, and consider genetic counseling if there’s a family history.
Long-term effects
Amyloidosis cutis dyschromia tends to be long-lasting, with skin color changes that usually begin in childhood and continue into adult life. Many notice the early symptoms of amyloidosis cutis dyschromia as speckled light-and-dark patches on the trunk and limbs that slowly widen over time. Long-term effects vary widely, and the condition is typically limited to the skin without affecting internal organs.
Patchy light-and-dark skin changes often appear in early childhood. They usually persist into adulthood.
Mottled areas of hyperpigmentation and hypopigmentation tend to remain over time. The overall pattern may slowly expand before stabilizing.
Features are confined to the skin in amyloidosis cutis dyschromia. It is not linked to systemic organ involvement or reduced life expectancy.
The spread is often gradual during childhood and adolescence. Many people then notice long periods of stability in adulthood.
How is it to live with Amyloidosis cutis dyschromia?
Living with Amyloidosis cutis dyschromia often means noticing patchy areas of lighter and darker skin that don’t hurt but can draw unwanted attention, questions, or stares. Daily life is usually physically unaffected, yet choosing clothing, makeup, or sun protection can become more intentional to minimize contrast and protect sensitive areas. Many find that clear information, support from dermatology and genetics teams, and honest conversations with friends, family, or coworkers ease social stress and build confidence. For loved ones, simple acts—using respectful language, avoiding assumptions, and asking how to be supportive—can make a real difference.
Treatment and drugs
Treatment for Amyloidosis cutis dyschromia focuses on easing itching and improving the look of the skin, since the color changes themselves are harmless but can be long‑lasting. Doctors sometimes recommend anti‑itch creams, gentle topical retinoids, or laser therapy to help blend color differences; results vary, and several sessions or months of use may be needed. Alongside medical treatment, lifestyle choices play a role, including daily sunscreen (SPF 30+), avoiding scratching, and using bland moisturizers to reduce irritation that can worsen discoloration. In some cases, dermatologists try procedures such as fractional laser or superficial chemical peels in carefully selected areas, weighing benefits against risks like temporary redness or post‑procedure darkening. Keep track of how you feel, and share this with your care team so they can adjust your plan and set realistic expectations about what improvement looks like over time.
Non-drug treatment
Living with patchy light-and-dark skin can affect clothing choices and confidence. For Amyloidosis cutis dyschromia, non-drug care focuses on soothing itch, protecting skin, and reducing the contrast of color changes. Non-drug treatments often lay the foundation for day-to-day control. Even if early symptoms of Amyloidosis cutis dyschromia are subtle, starting gentle routines early may help limit irritation.
Daily broad-spectrum sunscreen SPF 30+ and protective clothing help prevent tanning that makes color contrast more noticeable. Reapply every 2 hours outdoors and use hats and UPF-rated layers. Mineral formulas may suit sensitive skin.
Use fragrance-free moisturizers to support the skin barrier and ease itch. Lukewarm showers and mild cleansers help avoid dryness. Pat skin dry and moisturize within a few minutes.
Cool compresses or menthol or oatmeal lotions can calm itch without medicine. Limiting the scratch-itch cycle may reduce worsening of pigment changes. Keeping nails short lowers the risk of skin injury.
Skip rough scrubs, tight collars, and repetitive rubbing that can aggravate lesions. Choose soft, breathable fabrics and gentle laundry detergents. Switch to smooth washcloths or hands-only cleansing.
Your genes may have an impact on how drugs work for you
Some medicines for amyloidosis cutis dyschromia are processed differently depending on gene variants that affect drug‑metabolizing enzymes and transporters, which can change dose needs or side‑effect risk. Pharmacogenetic testing may help tailor therapy and monitoring for safer, steadier results.
Pharmacological treatments
Medicines for amyloidosis cutis dyschromia mainly aim to calm itch and reduce skin irritation, which can help protect the skin’s color pattern from further change. Uneven pigmentation can be slow to shift, so treatments focus on comfort and gradual improvement rather than quick lightening. Not everyone responds to the same medication in the same way. Starting care when early symptoms of amyloidosis cutis dyschromia—like new mottled patches plus itch—show up may help manage discomfort sooner.
This non-steroid cream can reduce inflammation and itch in amyloidosis cutis dyschromia. Some people see gradual softening of texture and less contrast over several months.
Works similarly to tacrolimus to calm immune-driven skin irritation. It may ease itching and help limit scratch-related darkening in amyloidosis cutis dyschromia.
This vitamin A–related medicine can slowly even texture and pigment in cutaneous amyloidosis. It needs regular blood tests and strict pregnancy precautions due to birth defect risk.
Speeds up skin cell turnover and may very gradually reduce mottling in amyloidosis cutis dyschromia. It can cause irritation and sun sensitivity, so gentle use and sunscreen help.
Genetic influences
Many families ask whether Amyloidosis cutis dyschromia is inherited. In most reported families, the condition follows an autosomal recessive pattern, meaning a child is affected when both parents pass on a silent gene change. A “carrier” means you hold the gene change but may not show symptoms. Variants in the GPNMB gene, which helps skin cells handle pigment and recycle proteins, are the most common genetic cause identified so far. If both parents are carriers, each pregnancy has a 1 in 4 (25%) chance of a child with Amyloidosis cutis dyschromia, a 1 in 2 (50%) chance of a carrier child, and a 1 in 4 (25%) chance of a child with no gene change. Severity and the pattern of skin color changes can differ from person to person, and genetic testing for Amyloidosis cutis dyschromia may confirm the cause and guide family planning.
Is Amyloidosis cutis dyschromia genetic?
Genetics plays a central role in Amyloidosis cutis dyschromia, with most cases linked to inherited variants affecting skin cell turnover and protein handling. Some families show autosomal recessive patterns. Genetic testing isn’t always needed but can confirm the diagnosis and guide counseling.
Pharmacogenetics—how genetics influence drug effects
Genetic changes can play a role in how Amyloidosis cutis dyschromia develops, and this can shape care, even if it doesn’t dictate a specific drug. In some families, inherited changes in a gene called GPNMB are linked to the condition; that finding helps confirm the diagnosis and consider counseling for relatives, but it doesn’t yet point to a targeted therapy. Most treatments still aim to ease pigment changes and itch—such as prescription creams, laser options, or, in selected cases, oral retinoids—and doctors adjust these based on skin response and side effects. Not every difference in response is genetic, but genetic makeup can influence how quickly the body processes oral retinoids and other medicines, so doses are started low and monitored with blood tests and check-ins. There are currently no validated drug–gene guides specific to this condition, and pharmacogenetic testing for Amyloidosis cutis dyschromia is not routinely used today. That said, knowing the genetic cause can be useful for planning care, avoiding unnecessary trials, and learning about clinical studies that may explore future targeted treatments.
Interactions with other conditions
Day to day, people with Amyloidosis cutis dyschromia often find that other skin issues—like eczema, very dry skin, or frequent rubbing—can make color changes and itch more noticeable. A condition may “exacerbate” (make worse) symptoms of another. When eczema flares, for example, scratching can increase bumps and uneven pigmentation, while treating the eczema well can calm the itch from Amyloidosis cutis dyschromia too.
Most importantly, this condition is usually limited to the skin and is not known to progress to internal organ (systemic) amyloidosis. It doesn’t typically change risks for heart, kidney, or nerve disease, but overlapping skin conditions can affect how treatments are chosen or how the skin looks over time. If you’re living with Amyloidosis cutis dyschromia alongside another diagnosis, ask your care team to coordinate a plan so therapies for one problem don’t aggravate the other, and so similar-looking conditions aren’t mistaken for it during flares.
How genes can cause diseases
Humans have more than 20,000 genes, each carrying out one or a few specific functions in the body. One gene instructs the body to digest lactose from milk, another tells the body how to build strong bones and another prevents the body's cells from beginning to multiply uncontrollably and developing into cancer. As all of these genes combined are the building instructions for our body, a defect in one of these genes can have severe health consequences.
Through decades of genetic research, we know the genetic code of any healthy/functional human gene. We have also identified that in certain positions on a gene, some individuals may have a different genetic letter from the one you have. We call these hotspots "Genetic Variations" or "Variants" in short. In many cases, studies have been able to show that having the genetic letter "G" in the position makes you healthy, but having the letter "A" in the same position disrupts the gene function and causes a disease. Genopedia allows you to view these variants in genes and summarizes all that we know from scientific research, which genetic letters (Genotype) have good or bad consequences on your health or on your traits.
History
Throughout history, people have described mottled or speckled skin that didn’t tan or darken like the surrounding areas, often starting in childhood and spreading slowly. Families sometimes remembered a grandparent with tiny gray-brown spots and lighter patches on the neck and arms, while others in the same family had only faint freckling. For many, this meant questions about appearance more than health problems, since the skin usually felt normal and didn’t itch.
First described in the medical literature as a patterned change in skin color with tiny deposits under the surface, amyloidosis cutis dyschromia was initially recognized in small case reports from parts of Asia. Early doctors focused on what they could see: widespread “salt-and-pepper” color changes on the trunk and limbs, usually without scarring. Over time, descriptions became more precise, noting that hair, nails, and general health were usually unaffected, and that symptoms tended to progress slowly before stabilizing.
From these first observations, clinicians began to notice family clusters. Inheritance patterns were noticed, suggesting a genetic contribution in at least some people. As more relatives were examined across generations, reports suggested both women and men could be affected, with onset often in school-age years. Skin samples under the microscope showed the same small, characteristic protein deposits in the upper layer of the skin, confirming a shared process even when the pattern of light and dark spots varied.
In recent decades, knowledge has built on a long tradition of observation. Advances in genetics helped link a subset of amyloidosis cutis dyschromia to changes in genes involved in maintaining skin cell balance and protein handling. This clarified why the condition sits within the broader group of cutaneous amyloidoses—conditions where certain proteins build up in the skin—but remains distinct because it mainly causes color changes rather than itching or thickened plaques.
Looking back helps explain why amyloidosis cutis dyschromia was once considered rare, now recognized as more widely distributed but still uncommon. Earlier reports came largely from specific regions and specialty clinics, so milder cases were likely missed. With improved dermatology training and access to noninvasive tools, clinicians now recognize the early symptoms of amyloidosis cutis dyschromia more readily and can distinguish it from other causes of skin color change, such as sun damage or post-inflammatory spots.
Despite evolving definitions, the core picture has stayed consistent: a lifelong, mostly cosmetic skin condition marked by mixed lighter and darker areas, small deposits seen on biopsy, and a tendency to run in some families. Today’s understanding blends careful historical descriptions with genetic insights, guiding more accurate diagnosis, counseling about inheritance when relevant, and supportive care focused on skin appearance and sun protection.