Phytophotodermatitis can be prevented by staying indoors after handling the above substances. However, the primary triggering mechanism is UV-A radiation (320–380 nm) which windows are not guaranteed to filter out.

Many different topical and oral medications can be used to treat the inflammatory reaction of phytophotodermatitis. A dermatologist may also prescribe a bleaching cream to help treat the hyperpigmentation and return the skin pigmentation back to normal. If they do not receive treatment, the affected sites may develop permanent hyperpigmentation or hypopigmentation.

Phytophotodermatitis, also known as "lime disease" (not to be confused with "Lyme disease"), "Berloque dermatitis", or "Margarita photodermatitis" is a chemical reaction which makes skin hypersensitive to ultraviolet light. It is frequently mistaken for hereditary conditions such as atopic dermatitis or chemical burns, but it is caused by contact with the photosensitizing compounds—such as furanocoumarins—found naturally in some plants and vegetables like parsnips, citrus fruits and more. Symptoms include burning, itching and large blisters that slowly accumulate over time. One of the earliest descriptions of this disease was made by Darrell Wilkinson, a British dermatologist in the 1950s.

In all cases of suspected NEH, a skin biopsy should be performed, because the clinical symptoms are non specific, but the histopathological findings on the biopsy are specific. The biopsy shows characteristic changes of the eccrine glands, the major sweat glands of the body.

In NEH, eccrine gland necrosis, and neutrophils surroundings the eccrine glands, are typical findings on biopsy. If the chemotherapy has recently been administered, chemotherapy induced neutropenia may be present, and, as a result, the neutrophils may be absent. But the other characteristic finding, i.e. eccrine gland necrosis, can still be seen. A vacuolar interface dermatitis also is visible in glands and ducts, along with necrosis of the lining cells.

In addition, in patients receiving chemotherapy, keratinocyte atypia can be seen.

A single case report suggested that oral dapsone may be useful for prevention. However, the efficacy of oral dapsone as prevention has not been demonstrated very clearly until now.

Riehl melanosis is a form of contact dermatitis, beginning with pruritus, erythema, and pigmentation that gradually spreads which, after reaching a certain extent, becomes stationary. The pathogenesis of Riehl melanosis is believed to be sun exposure following the use of some perfumes or creams (a photocontact dermatitis).

Excision biopsy is required to confirm the diagnosis of saree cancer. In many cases local excision with skin grafting is considered the appropriate treatment.

Different ways of wearing the petticoat may help saree-wearers to prevent saree cancer. Some such strategies are:

- Loosening the petticoat

- Changing the usual rope-like belt to broader ones that reduce pressure on the area

- Continuously changing the level at which the petticoat is tied

Scratch dermatitis (also known as "flagellate pigmentation from bleomycin") is a cutaneous condition characterized by linear hyperpigmented streaks are seen on the chest and back.

Erythema (from the Greek "erythros", meaning red) is redness of the skin or mucous membranes, caused by hyperemia (increased blood flow) in superficial capillaries. It occurs with any skin injury, infection, or inflammation. Examples of erythema not associated with pathology include nervous blushes.

There are a wide range of depigmenting treatments used for hyperpigmentation conditions, and responses to most are variable.

Most often treatment of hyperpigmentation caused by melanin overproduction (such as melasma, acne scarring, liver spots) includes the use of topical depigmenting agents, which vary in their efficacy and safety, as well as in prescription rules. Several are prescription only in the US, especially in high doses, such as hydroquinone, azelaic acid, and koijic acid. Some are available without prescription, such as niacinamide, or cysteamine hydrochloride. Hydroquinone was the most commonly prescribed hyperpigmentation treatment before the long-term safety concerns were raised, and the use of it became more regulated in several countries and discouraged in general by WHO. For the US only 2% is at present sold over-the-counter, and 4% needs prescription. In the EU hydroquinone was banned from cosmetic applications. Treatments that do not involve topical agents are also available, including fraction lasers and dermabrasion.

It can be caused by infection, massage, electrical treatment, acne medication, allergies, exercise, solar radiation (sunburn), cutaneous radiation syndrome, mercury toxicity, blister agents, niacin administration, or waxing and tweezing of the hairs—any of which can cause the capillaries to dilate, resulting in redness. Erythema is a common side effect of radiotherapy treatment due to patient exposure to ionizing radiation.

A study in Sweden showed that 21.5% of smokers and 3% of nonsmokers (genetic pigmentation or unknown cause) had lesions that could be classified as an oral melanin pigmentation. A gingival melanin index in 4 degrees was established. Already with a consumption of 1-3 cigarettes a day 9.3% of all 20.333 examined showed a smoker's melanosis. Pipe smokers had smoker's melanosis in 16.8%. One year after the start of cigarette smoking a clinically visible smoker's melanosis could be seen in 12.3% of women, and 17% among men.

In cigarette smokers who quit smoking, the number of individuals with smoker's melanosis becomes slowly less frequent after 2–3 months, but can still be seen in a few former smokers three years after smoking stop.

Although clinically visible genetic melanin pigmentations in the mouth are present in several ethnic groups all over the world, more mucosal areas will be melanin-pigmentet if tobacco products are used. Smoker's melanosis is found in India, Italy, Japan, Nigeria, Sweden, Turkey, USA, and several other countries.

Smoker's melanosis is expected to be found also in other tissue surfaces exposed to tobacco and tobacco smoke, for instance lips and in skin of the fingers holding the cigarette. Future studies will also show if the use of tobacco exaggerates the pigmentation of skin.

Lesions usually disappear between 3 months to 3 years for those who stop smoking. Smoker's melanosis is a benign, normal physiological reaction, and does not develop into cancer. If it does not disappear, however, a biopsy can verify the diagnosis. If Smoker's melanosis is destroyed by excessive smoking, as in the hard palate of reverse smokers, who smoke with the glowing part of the cigarette inside the mouth for different reasons, a pale depigmented surface is first seen, indicating the loss of the protecting melanin. Then a red inflammation sometimes occurs and cancer development may follow. In reverse smokers it is important to inspect regularly the areas with smoker's melanosis to detect any melanin destruction, in order to stop smoking in time and thus prevent a cancer to develop.

Even though the ideal method of diagnosis of melanoma should be complete excisional biopsy, the location of the melanoma may require alternatives. Dermatoscopy of acral pigmented lesions is very difficult but can be accomplished with diligent attention. Initial confirmation of the suspicion can be done with a small wedge biopsy or small punch biopsy. Thin deep wedge biopsies can heal very well on acral skin, and small punch biopsies can give enough clue to the malignant nature of the lesion. Once this confirmatory biopsy is done, a second complete excisional skin biopsy can be performed with a narrow surgical margin (1 mm). This second biopsy will determine the depth and invasiveness of the melanoma, and will help to define what the final treatment will be. If the melanoma involves the nail fold and the nail bed, complete excision of the nail unit might be required. Final treatment might require wider excision (margins of 0.5 cm or more), digital amputation, lymphangiogram with lymph node dissection, or chemotherapy.

Millipede burns are a cutaneous condition caused by some millipedes that secrete a toxic liquid that causes a brownish pigmentation or burn when it comes into contact with the skin. Some millipedes produce quinones in their defensive secretions, which have been reported to cause brown staining of the skin.

Shiitake mushroom dermatitis (also known as "flagellate mushroom dermatitis", "mushroom worker's disease", and "shiitake-induced toxicoderma") is an intensely pruritic dermatitis characterized by disseminated 1mm erythematous micropapules seen in a linear grouped arrangement secondary to Koebnerization due to patient scratching. It is caused by the ingestion of shiitake mushrooms and was first described in 1977 by Nakamura. Although it is rarely seen outside of China and Japan due to a lower incidence of shiitake consumption outside these regions, there is a well-established association between flagellate dermatitis and shiitake mushroom (Lentinula edodes) ingestion. Bleomycin ingestion may also cause similar findings. On physical exam, one key difference between the two is that post-inflammatory hyperpigmentation changes are usually seen with bleomycin-induced flagellate dermatitis and are not typically present with shiitake mushroom induced flagellate dermatitis. The median time of onset from ingestion of shiitake mushrooms is typically 24 hours, ranging from 12 hours to 5 days. Most patients completely recover by 3 weeks, with or without treatment. Although the pathogenesis of shiitake induced flagellate dermatitis is not clear, the theory most argued for is a toxic reaction to lentinan, a polysaccharide isolated from shiitake mushrooms. However, Type I and Type IV allergic hypersensitivities have also been supported by the 24-hour median time of onset, clearance in 3–21 days, severe pruritus, benefit of steroids and antihistamines, and lack of grouped outbreaks in people exposed to shared meals containing shiitake mushrooms. Most cases reported shortly after its discovery were due to consumption of raw shiitake mushrooms, but several cases have since been reported after consumption of fully cooked mushrooms.

There are 4 possible mechanisms to how this change may occur:

1. Accumulation of melanin, the skin pigment

2. Accumulation of drug or one of its products under any layer of the skin (usually the dermis or epidermis)

3. Accumulation of iron throughout the dermis from drug-induced post-inflammatory changes

4. The synthesis of special pigments, under direct influence of the drug

Poikiloderma vasculare atrophicans (PVA), sometimes referred to as parapsoriasis variegata or parapsoriasis lichenoides is a cutaneous condition (skin disease) characterized by hypo- or hyperpigmentation (diminished or heightened skin pigmentation, respectively), telangiectasia and skin . Other names for the condition include prereticulotic poikiloderma and atrophic parapsoriasis. The condition was first described by pioneer American pediatrician Abraham Jacobi in 1906. PVA causes areas of affected skin to appear speckled red and inflamed, yellowish and/or brown, gray or grayish-black, with scaling and a thinness that may be described as "cigarette paper". On the surface of the skin, these areas may range in size from small patches, to plaques (larger, raised areas), to neoplasms (spreading, tumor-like growths on the skin).

Mycosis fungoides, a type of skin lymphoma, may be a cause of PVA. The condition may also be caused by, associated with or accompany any of the following conditions or disorders: other skin lymphomas, dermatomyositis, lupus erythematosus, Rothmund-Thompson syndrome, Kindler syndrome, dyskeratosis congenita, and chronic radiodermatitis. Rare causes include arsenic ingestion, and the condition can also be idiopathic.

PVA may be considered a rare variant of cutaneous T-cell lymphoma, a non-Hodgkin's form of lymphoma affecting the skin. It may also be included among a number of similar conditions that are considered as precursors to mycosis fungoides. PVA is believed to be a syndrome closely associated with large-plaque parapsoriasis and its cohort retiform parapsoriasis; including PVA, all three conditions fit within an updated view of the once ambiguous classification scheme known as parapsoriasis.

PVA usually has an underlying cause, attributed to existing skin diseases and disorders associated with a cutaneous lymphoma or inflammation. Mycosis fungoides is the common lymphoma believed to cause PVA, although it may be considered a precursor when the lymphoma is (hidden) and undiagnosed. Large plaque parapsoriasis is another common causes of PVA. Less common causes include autoimmune-related connective tissue diseases such as lupus, dermatomyositis and scleroderma. Dermatoses and those that are genetically inspired, called genodermatoses, may also be an underlying cause of PVA. Among them, xeroderma pigmentosum and Rothmund-Thomson syndrome (poikiloderma congenita) are thought to be the most prominent. Ingestion of substances containing arsenic, such as arsphenamine, has also been suggested as a least common cause. PVA can also be idiopathic (of unknown cause), as seen in a small number of cases.

Chrysiasis (Gk, "chrysos" – 'gold', "osis" – 'condition of') is a dermatological condition induced by the parenteral administration of gold salts, usually for the treatment of rheumatoid arthritis. Such treatment has been superseded as the best practice for treating the disease because of "numerous side effects and monitoring requirements, their limited efficacy, and very slow onset of action".

Similar to silver, a gold preparation used parenterally for a long period may rarely produce a permanent skin pigmentation – especially if the skin is exposed to sunlight or artificial ultraviolet radiation.

The skin's pigmentation (in this condition) has been described as uniformly gray, grayish purple, slate gray, or grayish blue, and is usually limited to exposed portions of the body. It may involve the conjunctivae over the scleras but usually not the oral mucosa. Location of pigment predominantly in the upper dermis leads to the blue component of skin color through the scattering phenomenon. It is much less likely to be deposited in the nails and hair.

Chrysiasis was said to have been much more common when medicines containing traces of gold were used for treatment of tuberculosis (commonplace forms of treatment nearly fifty years ago). Treatments containing gold traces were also used to treat cases of rheumatoid arthritis – but because the dose used for tuberculosis was higher than for arthritis, it has not afflicted many subscribing to such treatments.

Gold can be identified in the skin chemically by light microscopy, electron microscopy, and spectroscopy.

There is no way to reverse or treat chrysiasis.

The diagnosis is clinical. Amalgam tattoo can be distinguished from other causes of localized oral pigmentation because it does not change significantly in size or color, although it may appear to slowly enlarge for several months after the initial implantation of the metal particles. Some amalgam tattoos appear radio-opaque on radiographs (i.e. they show up on x-rays), although in many cases amalgam tattoos have no radiographic features since the responsible particle(s) of amalgam are very small even though clinically the area of discolored mucosa is much larger.

If necessary, the diagnosis can be confirmed histologically by excisional biopsy, which excludes nevi and melanomas. If a biopsy is taken, the histopathologic appearance is:

- Pigmented fragments of metal within connective tissue

- Staining of reticulin fibers with silver salts

- A scattered arrangement of large, dark, solid fragments or a fine, black or dark brown granules

- Large particles may be surrounded by chronically inflamed fibrous tissue

- Smaller particles surrounded by more significant inflammation, which may be granulomatous or a mixture of lymphocytes and plasma cells

Histological signs of acral lentiginous melanoma include:

- atypical melanocytes

- dermal invasion

- desmoplasia

According to Scolyer "et al.", ALM "is usually characterized in its earliest recognisable form as single atypical melanocytes scattered along the junctional epidermal layer".

Drug-induced pigmentation of the skin may occur as a consequence of drug administration, and the mechanism may be postinflammatory hyperpigmentation in some cases, but frequently is related to actual deposition of the offending drug in the skin.The incidence of this change varies and depends on the type of medication involved. Some of the most common drugs involved are NSAIDs, Antimalarials, psychotropic drugs, Amiodarone, cytotoxic drugs, tetracyclines and heavy metals such as silver and gold (must be ingested not just worn).

Diagnosis is clinical, based on observation. Biopsy is rarely required.

Theoretically, routine use of a dental dam during dental procedures which involve amalgam should reduce the risk of amalgam tattoo.

The saree is common female attire in the Indian subcontinent. It is a piece of long (generally ) cloth which can be made of various materials: cotton, silk, nylon, chiffon or synthetic fabric. It is worn over an inner skirt (petticoat) which is tightened around the waist by a thick cotton cord. This is the traditional costume of most Indian women. The saree is attached to the waist throughout the day in the hot and humid climate. The waist is often soiled with dust and sweat and remains without proper cleaning. This causes changes in pigmentation and mild scaling over the waist. This, in turn, causes chronic irritation and gradually malignancy may develop in the skin at the waistline.