The exact cause of poikiloderma is unknown; however, extended sun exposure, namely the ultraviolet light emitted by the sun, is the primary factor.

Albeit difficult, treatment of poikiloderma involves the delivery of multiple wavelengths of intense pulsed light (IPL) to the affected area.

Types include:

- Poikiloderma vasculare atrophicans

- Poikiloderma of Civatte

- Hereditary sclerosing poikiloderma

Actinic keratosis is very common, with an estimated 14% of dermatology visits related to AKs. It is seen more often in fair-skinned individuals, and rates vary with geographical location and age. Other factors such as exposure to ultraviolet (UV) radiation, certain phenotypic features, and immunosuppression can also contribute to the development of AKs.

Men are more likely to develop AK than women, and the risk of developing AK lesions increases with age. These findings have been observed in multiple studies, with numbers from one study suggesting that approximately 5% of women ages 20–29 develop AK compared to 68% of women ages 60–69, and 10% of men ages 20–29 develop AK compared to 79% of men ages 60–69.

Geography seems to play a role in the sense that individuals living in locations where they are exposed to more UV radiation throughout their lifetime have a significantly higher risk of developing AK. Much of the literature on AK comes from Australia, where prevalence of AK is estimated at 40–50% in adults over 40, as compared to the United States and Europe, where prevalence is estimated at under 11–38% in adults. One study found that those who immigrated to Australia after age 20 had fewer AKs than native Australians in all age groups.

Often, hypopigmentation can be brought on by laser treatments; however, the hypopigmentation can be treated with other lasers or light sources.

It is seen in:

- Albinism

- Idiopathic guttate hypomelanosis

- Leprosy

- Lleucism

- Phenylketonuria

- Pityriasis alba

- Vitiligo

- Angelman syndrome

- Tinea versicolor

- An uncommon adverse effect of imatinib therapy

The patches of pityriasis alba may last from 1 month to about one year, but commonly on the face last a year. However it is possible that the white patches may last for more than 1 year on the face.

Any dermatitis may heal leaving pale skin, as may excessive use of corticosteroid creams used to treat episodes of eczema. The hypopigmentation is due to both reduced activity of melanocytes with fewer and smaller melanosomes.

The condition is most often seen in children between the ages of 3 and 16 years and is more common in males than females. However adults can also suffer from this disease.

It may occur more frequently in lighter-skinned patients, but is more apparent in those with darker complexions.

Up to a third of US school children may at some stage have this condition. Single-point prevalence studies from India have shown variable rates from 8.4%,

to 31%.

Other studies have shown prevalence rates in Brazil of 9.9%,

Egypt 13.49%,

Romania 5.1%,

Turkey 12% where higher rates were seen in those with poor socioeconomic conditions,

and just 1% in school children in Hong Kong.

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.

It is thought that UV radiation induces mutations in the keratinocytes of the epidermis, promoting the survival proliferation of these atypical cells. Eventually, this leads to the formation of AKs. In particular, mutations in the p53 tumor suppressor gene have been found in 30–50% of AK lesion skin samples.

- Extent of sun exposure: Cumulative sun exposure leads to an increased risk for development of AKs. In one U.S. study, AKs were found in 55% of fair-skinned men with high cumulative sun exposure, and in only 19% of fair-skinned men with low cumulative sun exposure in an age-matched cohort (the percents for women in this same study were 37% and 12% respectively). Furthermore, the use of sunscreen (SPF 17 or higher) has been found to significantly reduce the development of AK lesions, and also promotes the regression of existing lesions.

- History of sunburn: Studies show that even a single episode of painful sunburn as a child can increase an individual's risk of developing AK as an adult. Six or more painful sunburns over the course of a lifetime was found to be significantly associated with the likelihood of developing AK.

This skin disease commonly affects adolescents and young adults, especially in warm and humid climates. The yeast is thought to feed on skin oils (lipids), as well as dead skin cells. Infections are more common in people who have seborrheic dermatitis, dandruff, and hyperhidrosis.

Vitamins are one of many of the nutritional factors that change the outward appearance of a dog. The fat soluble vitamins A and E play a critical role in maintaining skin health. Vitamin A, which can also be supplemented as beta-carotene, prevents the deterioration of epithelial tissues associated with chronic skin diseases and aging. A deficiency in vitamin A can lead to scaly of skin and other dermatisis related issues like alopecia Vitamin E is an antioxidant. Vitamin E neutralizes free radicals that accumulate in highly proliferative cells like skin and prevent the deterioration of fibrous tissue caused by these ionized molecules. There are also a couple of water-soluble vitamins that contribute to skin health. Riboflavin (B2) is a cofactor to the metabolism of carbohydrates and when deficient in the diet leads to cracked, brittle skin. Biotin (B7) is another B vitamin that, when deficient, leads to alopecia.

Dyschromia refers to an alteration of the color of the skin or nails.

"Hyperchromia" can refer to hyperpigmentation, and "hypochromia" can refer to hypopigmentation.

"Dyschromatoses" involve both hyperpigmented and hypopigmented macules.

Variations in genes that are part of the immune system or part of melanocytes have both been associated with vitiligo. It is also thought to be caused by the immune system attacking and destroying the melanocytes of the skin. A genomewide association study found approximately 36 independent susceptibility loci for generalized vitiligo.

Although multiple hypotheses have been suggested as potential triggers that cause vitiligo, studies strongly imply that changes in the immune system are responsible for the condition. Vitiligo has been proposed to be a multifactorial disease with genetic susceptibility and environmental factors both thought to play a role.

The TYR gene encodes the protein tyrosinase, which is not a component of the immune system, but is an enzyme of the melanocyte that catalyzes melanin biosynthesis, and a major autoantigen in generalized vitiligo. The NIH states that sunburns can cause the disease but there is not good evidence to support this.

Preliminary evidence suggests a possible association with eating gluten.

In cases of tinea versicolor caused by the fungus "Malassezia furfur", lightening of the skin occurs due to the fungus's production of azelaic acid, which has a slight bleaching effect.

Minerals have many roles in the body, which include acting as beneficial antioxidants. Selenium is an essential nutrient, that should be present in trace amounts in the diet. Like other antioxidants, selenium acts as a cofactor to neutralize free radicals. Other minerals act as essential cofactors to biological processes relating to skin health. Zinc plays a crucial role in protein synthesis, which aids in maintaining elasticity of skin. By including zinc in the diet it will not only aid in the development of collagen and wound healing, but it will also prevent the skin from becoming dry and flaky. Copper is involved in multiple enzymatic pathways. In dogs, a deficiency in copper results in incomplete keratinization leading to dry skin and hypopigmentation. The complicated combination of trace minerals in the diet are a key component of skin health and a part of a complete and balanced diet.

Males and Females get Mongolian spots equally. A hospital-based, cross-sectional, prospective study was conducted in the Department of Dermatology, Venereology and Leprosy, BLDE University, Shri B. M. Patil Medical College Hospital and Research Center, Bijapur. One thousand neonates delivered in the Department of Obstetrics and Gynecology of the same institution was surveyed for the presence of skin lesions. The study was conducted in the period of November 2007 to May 2009. The study showed that 467 males were born with Mongolian spots and 380 females were born with Mongolian spots. The results showed there was no statistical significance in males and females born with Mongolian spots. Within the same study, different racial groups were recorded and documented. The study showed that among the Australian neonate, 25.5% were born with Mongolian spots. In the Iranian neonate, 71-81% were reported, in the Japanese neonate 81.5%, in the Turkish neonate 13.2%, in the caucasian neonate 62.8%, in the African American neonate 86.6%, and in the Indian neonate 72-89% were reported in having Mongolian spots. The populations with the most incidences of Mongolian spots were Iranian, Japanese, African American, and Indian.

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.

Mongolian spots, or Dermal melanocytosis, result from failure of complete melanocyte migration into the epidermis before birth with ensuing dermal nesting and melanin production. If there are many spots, or a spot covers a large area, it may be a sign of an underlying disorder, such as a metabolism problem called GM1 gangliosidosis Type 1. Recent data suggest that Mongolian spots may be associated with inborn errors of metabolism. Inborn errors of metabolism arise from single gene defect, most often involving an enzyme function, which leads to disruption of a specific metabolic pathway giving rise to abnormalities in the synthesis or catabolism or proteins, fats or carbohydrates. The most common condition associated with Mongolian spots is Hurler's disease followed by GM1 gangliosidosis Type 1. The clinical manifestations in Mongolian spots in inborn errors of metabolism are spots deeper in color and have a generalized distribution involving dorsal and ventral trunk in addition to sacral region and extremities. They are persistent and in some cases an indistinct feathery border has been described. Another possible cause is through genetic inheritance. Mongolian spots have been diagnosed on several occasions through family history, Mongolian spots were linked with an autosomal dominant inheritance. The majority of the neonatal cutaneous lesions are physiological and transient requiring no therapy. It is necessary to differentiate between benign and clinically significant skin lesions in newborn. Therefore, it is important to be aware of the innocent transient skin lesions in newborn and differentiate these from other serious conditions, which will help avoid unnecessary therapy to the neonates. Parents can be assured of good prognosis of these skin manifestations.

Many conditions affect the human integumentary system—the organ system covering the entire surface of the body and composed of skin, hair, nails, and related muscle and glands. The major function of this system is as a barrier against the external environment. The skin weighs an average of four kilograms, covers an area of two square meters, and is made of three distinct layers: the epidermis, dermis, and subcutaneous tissue. The two main types of human skin are: glabrous skin, the hairless skin on the palms and soles (also referred to as the "palmoplantar" surfaces), and hair-bearing skin. Within the latter type, the hairs occur in structures called pilosebaceous units, each with hair follicle, sebaceous gland, and associated arrector pili muscle. In the embryo, the epidermis, hair, and glands form from the ectoderm, which is chemically influenced by the underlying mesoderm that forms the dermis and subcutaneous tissues.

The epidermis is the most superficial layer of skin, a squamous epithelium with several strata: the stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale. Nourishment is provided to these layers by diffusion from the dermis, since the epidermis is without direct blood supply. The epidermis contains four cell types: keratinocytes, melanocytes, Langerhans cells, and Merkel cells. Of these, keratinocytes are the major component, constituting roughly 95 percent of the epidermis. This stratified squamous epithelium is maintained by cell division within the stratum basale, in which differentiating cells slowly displace outwards through the stratum spinosum to the stratum corneum, where cells are continually shed from the surface. In normal skin, the rate of production equals the rate of loss; about two weeks are needed for a cell to migrate from the basal cell layer to the top of the granular cell layer, and an additional two weeks to cross the stratum corneum.

The dermis is the layer of skin between the epidermis and subcutaneous tissue, and comprises two sections, the papillary dermis and the reticular dermis. The superficial papillary dermis with the overlying rete ridges of the epidermis, between which the two layers interact through the basement membrane zone. Structural components of the dermis are collagen, elastic fibers, and ground substance. Within these components are the pilosebaceous units, arrector pili muscles, and the eccrine and apocrine glands. The dermis contains two vascular networks that run parallel to the skin surface—one superficial and one deep plexus—which are connected by vertical communicating vessels. The function of blood vessels within the dermis is fourfold: to supply nutrition, to regulate temperature, to modulate inflammation, and to participate in wound healing.

The subcutaneous tissue is a layer of fat between the dermis and underlying fascia. This tissue may be further divided into two components, the actual fatty layer, or panniculus adiposus, and a deeper vestigial layer of muscle, the panniculus carnosus. The main cellular component of this tissue is the adipocyte, or fat cell. The structure of this tissue is composed of septal (i.e. linear strands) and lobular compartments, which differ in microscopic appearance. Functionally, the subcutaneous fat insulates the body, absorbs trauma, and serves as a reserve energy source.

Conditions of the human integumentary system constitute a broad spectrum of diseases, also known as dermatoses, as well as many nonpathologic states (like, in certain circumstances, melanonychia and racquet nails). While only a small number of skin diseases account for most visits to the physician, thousands of skin conditions have been described. Classification of these conditions often presents many nosological challenges, since underlying etiologies and pathogenetics are often not known. Therefore, most current textbooks present a classification based on location (for example, conditions of the mucous membrane), morphology (chronic blistering conditions), etiology (skin conditions resulting from physical factors), and so on. Clinically, the diagnosis of any particular skin condition is made by gathering pertinent information regarding the presenting skin lesion(s), including the location (such as arms, head, legs), symptoms (pruritus, pain), duration (acute or chronic), arrangement (solitary, generalized, annular, linear), morphology (macules, papules, vesicles), and color (red, blue, brown, black, white, yellow). Diagnosis of many conditions often also requires a skin biopsy which yields histologic information that can be correlated with the clinical presentation and any laboratory data.

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.

Pallor is a pale color of the skin that can be caused by illness, emotional shock or stress, stimulant use, or anemia, and is the result of a reduced amount of oxyhaemoglobin and is visible in skin conjuctivae or mucous membrane.

Pallor is more evident on the face and palms. It can develop suddenly or gradually, depending on the cause. It is not usually clinically significant unless it is accompanied by a general pallor (pale lips, tongue, palms, mouth and other regions with mucous membranes). It is distinguished from similar presentations such as hypopigmentation (lack or loss of skin pigment) or simply a fair complexion.

There does not yet exist a specific treatment for IP. Treatment can only address the individual symptoms.

The symptoms are equivalent to photodermatitis, but vary in severity.

The skin condition is a cutaneous phototoxic inflammatory eruption resulting from contact with light-sensitizing botanical substances—particularly from the plant families Umbelliferae, Rutaceae, Moraceae, and Leguminosae—and ultraviolet light, typically from sun exposure. Phytophotodermatitis usually results in hyperpigmentation of the skin that often appears like a bruise. This may be accompanied by blisters or burning. The reaction typically begins within 24 hours of exposure and peaks at 48–72 hours after the exposure.

Phytophotodermatitis can affect people of any age. Because of the bruise-like appearance that is usually in the shape of handprints or fingerprints, it can be mistaken in children for child abuse.

IP is inherited in an X-linked dominant manner. IP is lethal in most, but not all, males. A female with IP may have inherited the IKBKG mutation from either parent or have a new gene mutation. Parents may either be clinically affected or have germline mosaicism. Affected women have a 50% risk of transmitting the mutant IKBKG allele at conception; however, most affected male conceptuses miscarry. Thus, the effective ratio for liveborn children from a mother carrying the mutation is 33% unaffected females, 33% affected females, and 33% unaffected males. Genetic counseling, prenatal testing, and preimplantation genetic diagnosis is available.

In females, the cells expressing the mutated IKBKG gene due to lyonization selectively die around the time of birth so the X-inactivation is extremely skewed.

IP is caused by mutations in a gene called NEMO (NF-κB essential modulator).