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.

Nevus anemicus is a congenital disorder characterized by macules of varying size and shape that are paler than the surrounding skin and cannot be made red by trauma, cold, or heat. The paler area is due to the blood vessels within the area which are more sensitive to the body’s normal vasoconstricting chemicals.

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.

This benign patch appears on the skin at birth or in early childhood. In most people these are under 10cm in size. If there is doubt about the diagnosis, rubbing the area causes the skin around the lesion to become red while the lesion itself does not change in color. Often the patches are difficult to see against the background color of the patient’s skin, but if sunburn develops, then the white area stands out prominently. The involved area is lighter than the normal skin, not because of a loss of pigment occurs, but because blood vessels are constricted, producing a permanent blanching of the area. This blanching is a functional rather than a structural abnormality, presumed to be caused by local increased sensitivity to catecholamines. Although the cutaneous vasculature appears normal histologically, the blood vessels within the nevus do not respond to injection of vasodilators. It has been postulated that the persistent pallor may represent a sustained localized adrenergic vasoconstriction. Results of a skin biopsy would be interpreted as normal and only physiological testing can reveal the nevus in contrast to normal skin. Stroking the patch elicits no red flare. Only the normal skin would react with a characteristic erythematous response. Examination under a Wood lamp can also reveal the nevus anemicus patch will not emphasize as a patch of vitiligo would.

Hyperpigmentation can be caused by sun damage, inflammation, or other skin injuries, including those related to acne vulgaris. People with darker skin tones are more prone to hyperpigmentation, especially with excess sun exposure.

Many forms of hyperpigmentation are caused by an excess production of melanin. Hyperpigmentation can be diffuse or focal, affecting such areas as the face and the back of the hands. Melanin is produced by melanocytes at the lower layer of the epidermis. Melanin is a class of pigment responsible for producing colour in the body in places such as the eyes, skin, and hair. As the body ages, melanocyte distribution becomes less diffuse and its regulation less controlled by the body. UV light stimulates melanocyte activity, and where concentration of the cells is greater, hyperpigmentation occurs. Another form of hyperpigmentation is post inflammatory hyperpigmentation. These are dark and discoloured spots that appear on the skin following acne that has healed.

Hyperpigmentation is associated with a number of diseases or conditions, including the following:

- Addison's disease and other sources of adrenal insufficiency, in which hormones that stimulate melanin synthesis, such as melanocyte-stimulating hormone (MSH), are frequently elevated.

- Cushing's disease or other excessive adrenocorticotropic hormone (ACTH) production, because MSH production is a byproduct of ACTH synthesis from proopiomelanocortin (POMC).

- Acanthosis nigricans—hyperpigmentation of intertriginous areas associated with insulin resistance.

- Melasma, also known as "chloasma"—patchy hyperpigmentation

- Acne scarring from post-inflammatary hyperpigmentation

- Linea nigra—a hyperpigmented line found on the abdomen during pregnancy.

- Peutz-Jeghers syndrome—an autosomal dominant disorder characterized by hyperpigmented macules on the lips and oral mucosa and gastrointestinal polyps.

- Exposure to certain chemicals such as salicylic acid, bleomycin, and cisplatin.

- Smoker's melanosis

- Coeliac disease

- Cronkite-Canada syndrome

- Porphyria

- Tinea fungal infections such as ringworm

- Haemochromatosis—a common but debilitating genetic disorder characterized by the chronic accumulation of iron in the body.

- Mercury poisoning—particularly cases of cutaneous exposure resulting from the topical application of mercurial ointments or skin-whitening creams.

- Aromatase deficiency

- Nelson's syndrome

- Grave's disease

- As a result of tinea cruris.

Hyperpigmentation can sometimes be induced by dermatological laser procedures.

There are various causes of madarosis.

- Ophthalmological conditions: blepharitis is an infection of the eyelid. Anterior blepharitis is either "staphylococcal blepharitis,"or "seborrhoeic blepharitis" and posterior blepharitis is due to the meibomian gland.

- Dermatologic conditions: there are multiple types of dermatological conditions that can result in madarosis. These include Atopic dermatitis, Seborrhoeic dermatitis atopic dermatitis, and Psoriasis on the eyelids can result in madarosis. Others include: frontal fibrosing alopecia, ulerythema ophryogenes, acne rosacea, telogen effluvium, follicular mucinosis, and cutaneous sarcoidosis.

- Nutritional defects: Severe malnutrition can cause chronic hair loss. Hypoproteinemia causes hair loss by early onset of telogen. Zinc deficiencies like acrodermatitis enteropathica, can lead to the loss of eyebrow/eyelash hair. Other deficiencies like biotin and iron make it possible for loss of hair as well.

- Infections: There are many bodily infections that can cause the loss of eyelashes/eyebrows. The most common infection may be leprosy, such as lepromatous leprosy. Syphilis or other viral infections like herpes or HIV can cause the loss of eye hair as well. Fungal infections, like paracoccidioidomycosis, trichophyton, or microsporum, are also possible infection causes.

- Trauma: Most trauma injuries cause madarosis from the psychological standpoint, known as trichotillomania

- Drugs/Medications: Crack cocaine or chemotherapy drugs. Other drugs include:propranolol, valproic acid, barbiturates, MMR vaccine, botulinum toxin, epinephrine, antithyroid drugs, anticoagulants, and lipid-lowering drugs

- Genetics

- Autoimmune disorders: alopecia areata, discoid lupus erythematosus, chronic cutaneous lupus erythmatosus, Graham-Little syndrome, and Parry Romberg syndrome

- Other diseases: hypothyroidism, hyperthyroidism, hypoparathyroidism, hypopituitarism, and amyloidosis

There only prevention method is determining the underlying condition before treatment options are too late.

Sarcoidosis involves the skin in about 25% of patients. The most common lesions are erythema nodosum, plaques, maculopapular eruptions, subcutaneous nodules, and lupus pernio. Treatment is not required, since the lesions usually resolve spontaneously in two to four weeks. Although it may be disfiguring, cutaneous sarcoidosis rarely causes major problems.

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.

The most common method of treatment includes radiotherapy and/or surgical excision .

Morpheaform sarcoidosis is a very rare cutaneous condition characterized by specific cutaneous skin lesions of sarcoidosis accompanied by substantial fibrosis, simulating morphea.

Erythrodermic sarcoidosis is a cutaneous condition and very rare form of sarcoidosis.

Hypopigmented sarcoidosis is a cutaneous condition characterized by areas of hypopigmented skin. It is usually diagnosed in darkly pigmented races and may be the earliest sign of sarcoidosis.

Papular sarcoid is a cutaneous condition characterized by papules, which are the most common morphology of cutaneous sarcoidosis.

Ichthyosiform sarcoidosis is a cutaneous condition resembling ichthyosis vulgaris or acquired ichthyosis, with fine scaling usually on the distal extremities, by caused by sarcoidosis.

There are two major pathways. In the non-scarring pathway, the hair follicles remain intact which could potentially be reversed with the proper diagnosis and treatments. In the Scaring pathway, the follicles are permanently lost due to tissue damage, autrophy, or inflammation.

The severity of the pre-existing condition determines which type of madarosis occurs.

- Ophthalmologic conditions: there are multiple types of infections and are common. The gray line of the eye is a line that divides the eyelid into parts: anterior part is skin and muscle while posterior is tarsus and conjunctiva. The blepharitis is classified based on the type of eyelid involvement. Anterior blepharitis is either "staphylococcal blepharitis,"or "seborrhoeic blepharitis" which have symptoms of the presence of scales that are along the hair shaft. Posterior blepharitis is usually due to meibomian gland dysfunction.

- Dermatologic conditions: there are multiple types of dermatological conditions that can result in madarosis dependent on the location. Atopic dermatitis is associated with allergic disorders and affects the lower eyelid. Seborrhoeic dermatitis can be seen as the scaling of the eyebrows. Loss of eyebrows is commonly seen from both atopic and seborrhoeic dermatitis due to continuous scratching/touching. Psoriasis on the eyelids can result in madarosis. Others include: frontal fibrosing alopecia, ulerythema ophryogenes, acne rosacea, telogen effluvium, follicular mucinosis, and cutaneous sarcoidosis.

- Nutritional Defects: Zinc is important in hair growth and the lack of zinc can cause hair loss, specifically madarosis.The main proteins in hair are biotin and iron so deficiencies would result in a loss of hair.

- Infections: Unilateral madarosis (only one eye) may occur in tuberculoid leprosy from granulomatous infiltration of hair follicles ultimately destroying them. Infections like syphilis by causing a moth-eaten appearance of the eyebrow hair loss. Viral infections like herpes or HIV can cause scarring of the eyelid, causing loss of hair. Various fungal infections like paracoccidioidomycosis can cause lesions and changes in the hair locations of the eyelid.

- Trauma: Trichotillomania is a psychological disorder where the hair is pulled out or breakage occurs when anxious. Both trichoteiromania (hair loss from constant rubbing) and trichotemnomania (hair loss from constant shaving of the hair) can result in hair loss.

- Drugs/Medications: The heart medication amiodarone has been reported to commonly cause loss of eyelashes and eyebrows. Cocaine abuse has shown hair loss due to the hot vapors traveling up causing burning of the hair of the eyebrows or eyelashes. Radiotherapy and chemotherapy can cause hair loss due to the eradication of the hair cells, especially when used to treat ocular tumors.

- Genetics: Some of the diseases listed in the causes can be inherited.

Chronic exposure to ultraviolet light can result in skin thickening as well as elastic destruction of the skin. At least in one instance, the occupational exposure to the UVA light of the sun (UVB is blocked by many car windows) resulted in skin destruction on one side of the face.

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.

Pagetoid reticulosis (also known as "acral mycoses fungoides", "localized epidermotropic reticulosis", "mycosis fungoides palmaris et plantaris", "unilesional mycosis fungoides", and "Woringer–Kolopp disease") is a cutaneous condition, an uncommon lymphoproliferative disorder, sometimes considered a form of mycosis fungoides.

Tumid lupus erythematosus (also known as "lupus erythematosus tumidus") is a rare, but distinctive entity in which patients present with edematous erythematous plaques, usually on the trunk.

Lupus erythematosus tumidus (LET) was reported by Henri Gougerot and Burnier R. in 1930. It is a photosensitive skin disorder, a different subtype of cutaneous lupus erythematosus (CLE) from discoid lupus erythematosus (DLE) or subacute CLE (SCLE). LET is usually found on sun-exposed areas of the body. Skin lesions are edematous, urticarialike annular papules and plaques. Topical corticosteroids are not effective as treatment for LET, but many will respond to chloroquine. LET resolves with normal skin, no residual scarring, no hyperpigmentation or hypopigmentation. Cigarette smokers who have LET may not respond very well to chloroquine.

It has been suggested that it is equivalent to Jessner lymphocytic infiltrate of the skin.

The challenge has always been how to deliver the siRNA using a topical method or retroviral vectors and ex vivo gene transfer. In 2011/12 a team at Northwestern University claim to have solved the topical delivery of siRNA dilemma. Personalized siRNA can be delivered in a commercial moisturizer or phosphate-buffered saline, and do not require barrier disruption or transfection agents, such as liposomes, peptides, or viruses. "Topical application of nucleic acids offers many potential therapeutic advantages for suppressing genes in the skin, and potentially for systemic gene delivery. However, the epidermal barrier typically precludes entry of gene-suppressing therapy unless the barrier is disrupted. We now show that spherical nucleic acid nanoparticle conjugates (SNA-NCs), gold cores surrounded by a dense shell of highly oriented, covalently immobilized siRNA, freely penetrate almost 100% of keratinocytes in vitro, mouse skin, and human epidermis within hours after application."

This new discovery may soon offer hope to all suffering from mono-genetic diseases such as EHK. This may lead to promising personalized, topically delivered gene therapy of cutaneous tumors, skin inflammation, and dominant negative genetic skin disorders.

UPDATE: OCTOBER 2014

As of late, Paller reports "we are using a new nanotechnology-based technique called 'spherical nucleic acids' (SNAs) to suppress the production of the abnormal keratin 10 gene that is the most common change leading to epidermolytic ichthyosis. We continue to screen candidate SNAs to find a few that clearly suppress the abnormal keratin 10 gene much more than the normal keratin 10 gene. In the meantime, we have developed several tools towards this effort, which can also be used by other researchers. Most recently we've developed a special 'lentivirus reporter construct' in which we can see through changes in fluorescence whether or not our SNA works."

Dr. Paller and her team recently received more good news with regard to progressing their research. "We just received a grant from the National Institutes of Health (NIH) to continue this effort based on our preliminary data collected with FIRST's funding support. FIRST has been instrumental in furthering our research efforts related to ichthyosis," she said.

Overheating: The scaling of the skin prevents normal sweating so hot weather and/or vigorous exercise can cause problems.

Eye problems: The eyelids can be pulled down by the tightness of the skin and this can make eyelids (but usually just the lower one) very red and they are prone to drying and irritation.

Constriction bands: Very rarely children with this condition can have tight bands of skin around their fingers or toes (usually at the tips) that can prevent proper blood circulation to the area.

Hair loss: Severe scaling of the skin on the scalp can lead to patchy loss of hair, but this is rarely permanent.

Usually observed at birth or shortly thereafter in 94% of patients, in other reports, patients did not develop skin lesions until 3 months or even 2 years after birth. Females are typically affected more often than males (64%).

Epidermolytic ichthyosis (EI), (also known as "epidermolytic hyperkeratosis (EHK)", "bullous congenital ichthyosiform erythroderma (BCIE), bullous ichthyosiform erythroderma, or bullous congenital ichthyosiform erythroderma Brocq) is a rare and severe form of ichthyosis this skin disease affects around 1 in 300,000 people.

It involves the clumping of keratin filaments.

Other than identifying and treating any underlying conditions in secondary livedo, idiopathic livedo reticularis may improve with warming the area.

The appearance is often described as a shiny film looking like a layer of vaseline. The eyelids and mouth may have the appearance of being forced open due to the tightness of the skin. There can be associated eversion of the eyelids (ectropion).

Collodion baby can have severe medical consequences, mainly because the baby can lose heat and fluid through the abnormal skin. This can lead to hypothermia and dehydration. Strategies to prevent these problems are the use of emollients or nursing the baby in a humidified . There is also an increased risk of skin infection and mechanical compression, leading to problems like limb ischemia. There is also a risk of intoxication by cutaneous absorption of topical products, for example salicylate intoxication (similar to aspirin overdose) due to keratolytics.

The condition is not thought to be painful or in itself distressing to the child. Nursing usually takes place in a neonatal intensive care unit, and good intensive care seems to have improved the prognosis markedly. The collodion membrane should peel off or "shed" 2 to 4 weeks after birth, revealing the underlying skin disorder.

The condition can resemble but is different from harlequin type ichthyosis.

Favre–Racouchot syndrome (also known as "Favre–Racouchot disease", and "nodular cutaneous elastosis with cysts and comedones") is a disorder consisting of multiple open comedones that occurs in skin damaged by sunlight, especially under and lateral of the eyes. The comedones are widened openings for hair follicles and sebaceous glands filled with material.

The prognosis is favorable in most patients with an isolated cutaneous abnormality. In the majority of cases, both the vivid red marking and the difference in circumference of the extremities regress spontaneously during the first year of life. It is theorized that this may be due to the normal maturation process, with thickening of the epidermis and dermis. Improvements for some patients can continue for up to 10 years, while in other cases, the marbled skin may persist for the patient's lifetime.

One study reported an improvement in lesions in 46% of patients within 3 years. If CMTC persists into adulthood, it can result in complaints due to paresthesia, increased sensitivity to cold and pain, and the formation of ulcers.

Few reports included long-term follow up of CMTC into adolescence and adulthood. While about 50% of patients seem to show definite improvement in the reticular vascular pattern, the exact incidence and cause of persistent cases are unknown.

Blue nevus (also known as "blue neuronevus", "dermal melanocytoma", and "nevus bleu") is a type of melanocytic nevus. The blue colour is caused by the pigment being deeper in the skin than in ordinary nevi. In principle they are harmless but they can sometimes be mimicked by malignant lesions, i.e. some melanomas can look like a blue nevus.

Ionizing radiation-induced cutaneous conditions result from exposure to ionizing radiation.

- Acute radiodermatitis

- Chronic radiation keratosis

- Chronic radiodermatitis

- Eosinophilic, polymorphic, and pruritic eruption associated with radiotherapy

- Fluoroscopy burn

- Radiation acne

- Radiation cancer

- Radiation dermatitis (radiodermatitis)

- Radiation recall reaction

- Radiation-induced erythema multiforme

- Radiation-induced hypertrophic scar

- Radiation-induced keloid

- Radiation-induced morphea