Depigmentation is the lightening of the skin, or loss of pigment. Depigmentation of the skin can be caused by a number of local and systemic conditions. The pigment loss can be partial (injury to the skin) or complete (caused by vitiligo). It can be temporary (from tinea versicolor) or permanent (from albinism).

Most commonly, depigmentation of the skin is linked to people born with vitiligo, which produces differing areas of light and dark skin. These individuals, if they so decided to use a lightning process to even out their skin tone, could apply a topical cream containing the organic compound monobenzone to lessen the remaining pigment. The brand drug incorporating 20% monobenzone is Benoquin, made by ICN.

Increasingly, people who are not afflicted with the vitiligo experiment with lower concentrations of monobenzone creams in the hope of lightning their skin tone evenly. An alternate method of lightning is to use the chemical mequinol over an extended period of time. Both monobenzone and mequinol produce dramatic skin whitening, but react very differently. Mequinol leaves the skin looking extremely pale. However, tanning is still possible. It is important to notice that the skin will not go back to its original color after the none treatment of mequinol. Mequinol should not be used by people that are allergic to any ingredient in mequinol, if you are pregnant, if you have eczema, irritated or inflamed skin, an increased number of white blood cells or if you are sensitive to sunlight or must be outside for prolonged periods of time. Mequinol is used in Europe in concentrations ranging from 2-20% and is approved in many countries for the treatment of solar lentigines. Monobenzone applied topically completely removes pigment in the long term and vigorous sun-safety must to be adhered to for life to avoid severe sun burn and melanomas. People using monobenzone without previously having vitiligo do so because standard products containing hydroquinone or other lightning agents are not effective for their skin and due to price and active ingredient strength. However, monobenzone is not recommended for skin conditions other than vitiligo.

For stubborn pigmented lesions the Q-switched ruby laser, cryotherapy or TCA peels can be used to ensure the skin remains pigment-free.

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.

In cases of extensive vitiligo the option to de-pigment the unaffected skin with topical drugs like monobenzone, mequinol, or hydroquinone may be considered to render the skin an even colour. The removal of all the skin pigment with monobenzone is permanent and vigorous. Sun-safety must be adhered to for life to avoid severe sunburn and melanomas. Depigmentation takes about a year to complete.

Liver spots (also known as age spot, solar lentigo, "lentigo senilis", "old age spot", "senile freckle") are es on the skin associated with aging and exposure to ultraviolet radiation from the sun. They range in color from light brown to red or black and are located in areas most often exposed to the sun, particularly the hands, face, shoulders, arms and forehead, and the scalp if bald.

The spots derive their name from the fact that they were once incorrectly believed to be caused by liver problems, but they are physiologically unrelated to the liver, save for a similar color. From the age of 40 onward the skin is less able to regenerate from sun exposure, and liver spots are very common in this age group, particularly in those who spend time in the sun.

In the overwhelming majority of cases, liver spots pose no threat and require no treatment, though they occasionally have been known to obscure the detection of skin cancer. However, despite being a benign condition, liver spots are sometimes considered unsightly and some people choose to have them removed. This can be done by electrosurgery, laser treatment, cryotherapy, or the use of depigmentation agents, such as hydroquinone, tretinoin, topical cysteamine, azelaic acid or alpha hydroxy acids.

Differently from the melanotic nevi and the verrucous nevi on the skin, age spots change with time in color and in shape. Misrepair-accumulation aging theory proposes a hypothesis on the development of age spots. Firstly, the development of a flat spot is a result of accumulation of aged basal cells. When the skin is aged, some aged cells that contain lipofuscin bodies cannot be removed. An aged cell will affect the functionality of the local tissue and promote the aging of its neighbor cells. By a feedback loop, more and more neighbor cells become aged and lipofuscin-containing. They aggregate and form a spot with an irregular shape. Secondly, protruding of a flat spot is a result of the death of aged cells in the spot and release of lipofuscin bodies. Isolation of the un-digestible lipofuscin bodies in a fibrotic capsule is essential for maintaining the structural integrity of the tissue. Successive encapsulation of dead cells and lipofuscin bodies results in the growth of a spot in three dimensions. The dense lipofuscin bodies in the capsule make a protruding spot soft and dark in color.

Halo nevi are estimated to be present in approximately 1% of the general population, and are found to be more prevalent in people with vitiligo, malignant melanoma, or Turner syndrome. All races and sexes are equally susceptible to this disease, although a familial tendency has been reported. The average age of onset is in a person's teenage years.

As halo nevi are only of cosmetic significance, no treatment is required, and patients will be asymptomatic. Although halo nevi are harmless, it is important to monitor the lesion on regular basis. Watch out for any changes in appearance of existing or new halo nevi. If there is any change in appearance or is associated with pain, itch, and infection, a doctor should be consulted immediately to exclude the possibility of melanoma.

A lentigo () (plural lentigines, ) is a small pigmented spot on the skin with a clearly defined edge, surrounded by normal-appearing skin. It is a harmless (benign) hyperplasia of melanocytes which is linear in its spread. This means the hyperplasia of melanocytes is restricted to the cell layer directly above the basement membrane of the epidermis where melanocytes normally reside. This is in contrast to the "nests" of multi-layer melanocytes found in moles (melanocytic nevi). Because of this characteristic feature, the adjective "lentiginous" is used to describe other skin lesions that similarly proliferate linearly within the basal cell layer.

Lentigines are distinguished from freckles (ephelis) based on the proliferation of melanocytes. Freckles have a relatively normal number of melanocytes but an increased "amount" of melanin. A lentigo has an increased "number" of melanocytes. Freckles will increase in number and darkness with sunlight exposure, whereas lentigines will stay stable in their color regardless of sunlight exposure.

Lentigines by themselves are benign, however one might desire the removal or treatment of some of them for cosmetic purposes. In this case they can be removed surgically, or lightened with the use of topical depigmentation agents. Some common depigmentation agents such as azelaic acid and kojic acid seem to be inefficient in this case, however other agents might work well (4% hydroquinone, 5% topical cysteamine, 10% topical ascorbic acid).

Conditions characterized by lentigines include:

- Lentigo simplex

- Solar lentigo (Liver spots)

- PUVA lentigines

- Ink spot lentigo

- LEOPARD syndrome

- Mucosal lentigines

- Multiple lentigines syndrome

- Moynahan syndrome

- Generalized lentiginosis

- Centrofacial lentiginosis

- Carney complex

- Inherited patterned lentiginosis in black persons

- Partial unilateral lentiginosis

- Peutz-Jeghers syndrome

- Lentigo maligna

- Lentigo maligna melanoma

- Acral lentiginous melanoma

Radiation burns are caused by exposure to high levels of radiation. Levels high enough to cause burn are generally lethal if received as a whole-body dose, whereas they may be treatable if received as a shallow or local dose.

Fluoroscopy may cause burns if performed repeatedly or for too long.

Similarly, Computed Tomography and traditional Projectional Radiography have the potential to cause radiation burns if the exposure factors and exposure time are not appropriately controlled by the operator.

A study of radiation induced skin injuries has been performed by the Food and Drug Administration (FDA) based on results from 1994, followed by an advisory to minimize further fluoroscopy-induced injuries. The problem of radiation injuries due to fluoroscopy has been further investigated in review articles in 2000, 2001, 2009 and 2010.

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

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).

Lymphoma is the most common type of blood-related cancer in horses and while it can affect horses of all ages, it typically occurs in horses aged 4–11 years.

Tumors related to squamous-cell carcinoma (SCC) can appear anywhere on the body, but they are most often located in non-pigmented skin near mucocutaneous junctions (where skin meets mucous membranes) such as on the eyelids, around the nostrils, lips, vulva, prepuce, penis or anus. The tumors are raised, fleshy, often ulcerated or infected and may have an irregular surface. Rarely, primary SCC develops in the esophagus, stomach (non-glandular portion), nasal passages and sinuses, the hard palate, gums, guttural pouches and lung. The eyelid is the most common site, accounting for 40-50% of cases, followed by male (25-10% of cases) and female (10% of cases) genitalia. Horses with lightly pigmented skin, such as those with a gray hair coat or white faces, are especially prone to developing SCC, and some breeds, such as Clydesdales, may have a genetic predisposition. Exposure of light-colored skin to UV light has often been cited as a predisposing factor, but lesions can occur in dark skin and in areas that are not usually exposed to sunlight, such as around the anus. Buildup of smegma ("the bean" in horseman's terms) on the penis is also linked to SCC and is thought to be a carcinogen through penile irritation. Pony geldings and work horses are more prone to developing SCC on the penis, due to less frequent penile washing when compared to stallions. Equine papillomavirus-2 has also been found within penile SCCs, but has not been determined to cause SCC.

Genital HPV infections have an estimated prevalence in the US of 10–20% and clinical manifestations in 1% of the sexually active adult population. US incidence of HPV infection has increased between 1975 and 2006. About 80% of those infected are between the ages of 17–33. Although treatments can remove the warts, they do not remove the HPV, so warts can recur after treatment (about 50–73% of the time). Warts can also spontaneously regress (with or without treatment).

Traditional theories postulated that the virus remained in the body for a lifetime. However, studies using sensitive DNA techniques have shown that through immunological response the virus can either be cleared or suppressed to levels below what polymerase chain reaction (PCR) tests can measure. One study testing genital skin for subclinical HPV using PCR found a prevalence of 10%.

Gardasil (sold by Merck & Co.) is a vaccine that protects against human papillomavirus types 6, 11, 16 and 18. Types 6 and 11 cause genital warts, while 16 and 18 cause cervical cancer. The vaccine is preventive, not therapeutic, and must be given before exposure to the virus type to be effective, ideally before the beginning of sexual activity. The vaccine is approved by the US Food and Drug Administration for use in both males and females as early as 9 years of age.

In the UK, Gardasil replaced Cervarix in September 2012 for reasons unrelated to safety. Cervarix had been used routinely in young females from its introduction in 2008, but was only effective against the high-risk HPV types 16 and 18, neither of which typically causes warts.

During pregnancy and breastfeeding, women must ingest enough nutrients for themselves and their child, so they need significantly more protein and calories during these periods, as well as more vitamins and minerals (especially iron, iodine, calcium, folic acid, and vitamins A, C, and K). In 2001 the FAO of the UN reported that iron deficiency afflicted 43 percent of women in developing countries and increased the risk of death during childbirth. A 2008 review of interventions estimated that universal supplementation with calcium, iron, and folic acid during pregnancy could prevent 105,000 maternal deaths (23.6 percent of all maternal deaths).

Frequent pregnancies with short intervals between them and long periods of breastfeeding add an additional nutritional burden.

Malnutrition and being underweight are more common in the elderly than in adults of other ages. If elderly people are healthy and active, the aging process alone does not usually cause malnutrition. However, changes in body composition, organ functions, adequate energy intake and ability to eat or access food are associated with aging, and may contribute to malnutrition. Sadness or depression can play a role, causing changes in appetite, digestion, energy level, weight, and well-being. A study on the relationship between malnutrition and other conditions in the elderly found that malnutrition in the elderly can result from gastrointestinal and endocrine system disorders, loss of taste and smell, decreased appetite and inadequate dietary intake. Poor dental health, ill-fitting dentures, or chewing and swallowing problems can make eating difficult. As a result of these factors, malnutrition is seen to develop more easily in the elderly.

Rates of malnutrition tend to increase with age with less than 10 percent of the "young" elderly (up to age 75) malnourished, while 30 to 65 percent of the elderly in home care, long-term care facilities, or acute hospitals are malnourished. Many elderly people require assistance in eating, which may contribute to malnutrition. Because of this, one of the main requirements of elderly care is to provide an adequate diet and all essential nutrients.

In Australia malnutrition or risk of malnutrition occurs in 80 percent of elderly people presented to hospitals for admission. Malnutrition and weight loss can contribute to sarcopenia with loss of lean body mass and muscle function. Abdominal obesity or weight loss coupled with sarcopenia lead to immobility, skeletal disorders, insulin resistance, hypertension, atherosclerosis, and metabolic disorders. A paper from the "Journal of the American Dietetic Association" noted that routine nutrition screenings represent one way to detect and therefore decrease the prevalence of malnutrition in the elderly.

Pinta (also known as Azul, Carate, Empeines, Lota, Mal del Pinto and Tina) is a human skin disease endemic to Mexico, Central America, and South America caused by infection with a spirochete, "Treponema pallidum carateum", which is morphologically and serologically indistinguishable from the bacterium that causes syphilis.

Pinta, the least severe of treponemal infections being limited to the skin, is thought to be transmitted by skin-to-skin contact (similar to bejel and yaws), and after an incubation period of two to three weeks, produces a raised papule, which enlarges and becomes hyperkeratotic (scaly/flaky). Lesions are usually present in the exposed surface of arms and legs. Local lymph nodes might be enlarged. Three to 9 months later, further thickened and flat lesions (pintids) appear all over the body. These generally resolve, but a proportion of people with pinta will go on to develop late-stage disease, characterised by widespread pigmentary change with a mixture of hyperpigmentation and depigmentation which can be disfiguring.

Chloroquine retinopathy, also known as Bull's eye maculopathy, is a retinopathy (damage of the retina) caused by the drugs chloroquine or hydroxychloroquine, which are sometimes used in the treatment of autoimmune disorders such as rheumatoid arthritis and systemic lupus erythematosus. This eye toxicity limits long-term use of the drugs.

Both agents bind to melanin pigment in the RPE, and this may serve to concentrate the drugs or to prolong their adverse effects.

If the Hirschsprung's disease is treated in time, ABCD sufferers live otherwise healthy lives. If it is not found soon enough, death often occurs in infancy. For those suffering hearing loss, it is generally regressive and the damage to hearing increases over time. Digestive problems from the colostomy and reattachment may exist, but most cases can be treated with laxatives. The only other debilitating symptom is hearing loss, which is usually degenerative and can only be treated with surgery or hearing aids.

Kwashiorkor is a form of severe protein–energy malnutrition characterized by edema, irritability, ulcerating dermatoses, and an enlarged liver with fatty infiltrates. Sufficient calorie intake, but with insufficient protein consumption, distinguishes it from marasmus. Kwashiorkor cases occur in areas of famine or poor food supply. Cases in the developed world are rare.

Jamaican pediatrician Cicely Williams introduced the name into the medical community in a 1935 "Lancet" article, two years after she published the disease's first formal description in the Western medical literature. The name is derived from the Ga language of coastal Ghana, translated as "the sickness the baby gets when the new baby comes" or "the disease of the deposed child", and reflecting the development of the condition in an older child who has been weaned from the breast when a younger sibling comes. Breast milk contains proteins and amino acids vital to a child's growth. In at-risk populations, kwashiorkor may develop after a mother weans her child from breast milk, replacing it with a diet high in carbohydrates, especially sugar.

Affected individuals are typically 20 to 50 years old. The female to male ratio is 2:1. By definition, there is no history of either surgical or accidental ocular trauma. VKH is more common in Asians, Latinos, Middle Easterners, American Indians, and Mexican Mestizos; it is much less common in Caucasians and in blacks from sub-Saharan Africa.

VKH is associated with a variety of genetic polymorphisms that relate to immune function. For example, VKH has been associated with human leukocyte antigens (HLA) HLA-DR4 and DRB1/DQA1, copy-number variations (CNV) of complement component 4, a variant IL-23R locus and with various other non-HLA genes. HLA-DRB1*0405 in particular appears to play an important susceptibility role.