Papular mucinosis affects adults of both sexes equally and appears between ages 30 and 80. Recently, it has been reported in patients infected with the HIV/AIDS virus.

Verrucous lupus erythematosus (also known as "Hypertrophic lupus erythematosus") presents with non-pruritic papulonodular lesions on the arms and hands, resembling keratoacanthoma or hypertropic lichen planus.

Lupus can develop in any age but most commonly in ages 15 to 44 with varying results. Typically, the manifestation of the disease tends to be more acute in those affected who are of younger age. Women are more likely to get it than men. Patients with juvenile onset Lupus in particular, are vulnerable to mucocutaneous manifestations of the disease (alopecia, skin rash, and ulceration of the mucus membranes) more so than any other age group. However, patients with late onset Lupus have a much higher mortality rate. Nearly 50% of those with late onset Lupus die of their affliction. Women who are of childbearing age are also particularly at risk.

Papular mucinosis (also known as "Scleromyxedema," "Generalized lichen myxedematosus," and "Sclerodermoid lichen myxedematosus") is a rare skin disease. Localized and disseminated cases are called papular mucinosis or lichen myxedematosus while generalized, confluent papular forms with sclerosis are called scleromyxedema. Frequently, all three forms are regarded as papular mucinosis. However, some authors restrict it to only mild cases. Another form, acral persistent papular mucinosis is regarded as a separate entity.

As PNP is ultimately caused by the presence of a tumor, it is not contagious. There is no known way to predict who will become afflicted with it. Patients with cancer are therefore a group at risk. Although PNP has been known to affect all age groups, it is more likely to afflict middle-aged to older patients.

The cause of prurigo nodularis is unknown, although other conditions may induce PN. PN has been linked to Becker's nevus, linear IgA disease, an autoimmune condition, liver disease and T cells. Systemic pruritus has been linked to cholestasis, thyroid disease, polycythaemia rubra vera, uraemia, Hodgkins disease, HIV and other immunodeficiency diseases. Internal malignancies, liver failure, renal failure, and psychiatric illnesses have been considered to induce PN, although more recent research has refuted a psychiatric cause for PN. Patients report an ongoing battle to distinguish themselves from those with psychiatric disorders such as delusions of parasitosis and other psychiatric conditions.

Pemphigus ( or ) is a rare group of blistering autoimmune diseases that affect the skin and mucous membranes. The name is derived from the Greek root "pemphix" meaning "pustule".

In pemphigus, autoantibodies form against desmoglein. Desmoglein forms the "glue" that attaches adjacent epidermal cells via attachment points called desmosomes. When autoantibodies attack desmogleins, the cells become separated from each other and the epidermis becomes "unglued", a phenomenon called acantholysis. This causes blisters that slough off and turn into sores. In some cases, these blisters can cover a significant area of the skin.

Originally, the cause of this disease was unknown, and "pemphigus" was used to refer to any blistering disease of the skin and mucosa. In 1964, researchers found that the blood of patients with pemphigus contained antibodies to the layers of skin that separate to form the blisters. In 1971, an article investigating the autoimmune nature of this disease was published.

Pemphigus foliaceus has been recognized in pet dogs, cats, and horses and is the most common autoimmune skin disease diagnosed in veterinary medicine. Pemphigus foliaceus in animals produces clusters of small vesicles that quickly evolve into pustules. Pustules may rupture, forming erosions or become crusted. Left untreated, pemphigus foliaceus in animals is life-threatening, leading to not only loss of condition but also secondary infection.

Pemphigus vulgaris is a very rare disorder described in pet dogs and cats. Paraneoplastic pemphigus has been identified in pet dogs.

Substantial data have been found to indicate that certain ethnic populations could be more at risk for Lupus Erythematosus, and have a better or worse prognosis. Asian, African, and Native Americans are more likely to get Lupus than Caucasians. Caucasians seem to generally have a more mild manifestation of the disease. Their survival rates after five years were typically around 94%-96%, while patients of African, and some Asian ethnicities had survival rates closer to 79%-92%. The only documented ethnicity that had a higher survival rate than Caucasians were Koreans, who had survival rates nearer to 98%. Among Caucasians, the most common causes of death were complications involving the cardiovascular system, the respiratory system and problems with malignancies. Atherosclerotic cardiovascular disease is more prevalent in African American Lupus patients compared to Caucasians with Lupus.

Prurigo nodularis (PN), also known as nodular prurigo, is a skin disease characterised by pruritic (itchy) nodules which usually appear on the arms or legs. Patients often present with multiple excoriated lesions caused by scratching. PN is also known as Hyde prurigo nodularis, "Picker's nodules", atypical nodular form of neurodermatitis circumscripta, lichen corneus obtusus.

Lichen simplex chronicus is a distinct clinical entity.

In 2016, interferon gamma/CXCL10 axis was hypothesized to be a target for treatments that reverse inflammation. Apremilast is undergoing investigation as a potential treatment .

Nodular lichen myxedematosus is a cutaneous condition characterized by multiple nodules on the limbs and trunk, with a mild or absent papular component.

The cause of lichen planus is unknown, but it is not contagious and does not involve any known pathogen. It is thought to be a T cell mediated autoimmune reaction (where the body's immune system targets its own tissues). This autoimmune process triggers apoptosis of the epithelial cells. Several cytokines are involved in lichen planus, including tumor necrosis factor alpha, interferon gamma, interleukin-1 alpha, interleukin 6, and interleukin 8. This autoimmune, T cell mediated, process is thought to be in response to some antigenic change in the oral mucosa, but a specific antigen has not been identified.

Where a causal or triggering agent is identified, this is termed a lichenoid reaction rather than lichen planus. These may include:

- Drug reactions, with the most common inducers including gold salts, beta blockers, traditional antimalarials (e.g. quinine), thiazide diuretics, furosemide, spironolactone, metformin and penicillamine.

- Reactions to amalgam (metal alloys) fillings (or when they are removed/replaced),

- Graft-versus-host disease lesions, which chronic lichenoid lesions seen on the palms, soles, face and upper trunk after several months.

- Hepatitis, specifically hepatitis B and hepatitis C infection, and primary biliary cirrhosis.

It has been suggested that lichen planus may respond to stress, where lesions may present during times of stress. Lichen planus can be part of Grinspan's syndrome.

It has also been suggested that mercury exposure may contribute to lichen planus.

Lichen sclerosus may have a genetic component. Higher rates of lichen sclerosus have been reported among twins and among family members.

If the lesions are mild, the patient will be subject to a good deal of pain. If the lesions are severe, the overall quality of life is devastating. The impaired skin barrier function commonly leads to localized infection, which sepsis and death may follow. The pain from the oral and pharyngeal ulcers interfere with eating, which can compromise nutritional health.

The general prognosis for PNP is poor. It is more hopeful if the tumor is benign, but in the case of malignant tumors, the mortality rate is roughly 90%. The two most commonly associated types of tumors are non-Hodgkin lymphoma and chronic lymphocytic lymphoma; nearly all of these patients die within two years of diagnosis. This is attributed to the effects of the tumor combined with the negative side effects of the medication administered to treat PNP.

Roughly 1/3 of the deaths from PNP stem from pulmonary insufficiency which is brought about by the action of PNP on the respiratory mucosa. It manifests as dyspnea and progresses to bronchiolitis obliterans (non-reversible obstructive lung disease) via an unknown mechanism.

Atypical lichen myxedematosus (also known as "Intermediate lichen myxedematosus") is a skin condition caused by fibroblasts producing abnormally large amounts of mucopolysaccharides.

Autoimmunity is a process in which the body fails to recognize itself and therefore attacks its own cells and tissue. Specific antibodies have been found in LS. Furthermore, there seems to be a higher prevalence of other autoimmune diseases such as diabetes mellitus type 1, vitiligo and thyroid disease.

Discrete papular lichen myxedematosus is a skin condition caused by fibroblasts producing abnormally large amounts of mucopolysaccharides characterized by the occurrence of waxy, flesh-colored papules.

Lichen myxedematosus is a group of cutaneous disorders considered mucinoses. Conditions included in this group are:

Urticaria is a vascular reaction of the skin characterized by the appearance of wheals, which are firm, elevated swelling of the skin. Angioedema, which can occur alone or with

urticaria, is characterized by a well-defined, edematous swelling that involves subcutaneous tissues, abdominal organs, or upper airway.

- Acquired C1 esterase inhibitor deficiency

- Acute urticaria

- Adrenergic urticaria

- Anaphylaxis

- Aquagenic urticaria

- Cholinergic urticaria

- Chronic urticaria (ordinary urticaria)

- Cold urticaria

- Dermatographism (dermographism)

- Episodic angioedema with eosinophilia (Gleich's syndrome)

- Exercise urticaria (exercise-induced urticaria)

- Galvanic urticaria

- Heat urticaria

- Hereditary angioedema (Quincke's edema)

- Localized heat contact urticaria

- Mast cell-independent urticaria

- Physical urticaria

- Primary cold contact urticaria

- Pressure urticaria (delayed pressure urticaria)

- Reflex cold urticaria

- Schnitzler syndrome

- Secondary cold contact urticaria

- Solar urticaria

- Systemic capillary leak syndrome

- Urticarial allergic eruption

- Urticaria-like follicular mucinosis

- Vibratory angioedema

The classification of exfoliative dermatitis into Wilson-Brocq (chronic relapsing), Hebra or pityriasis rubra (progressive), and Savill (self-limited) types may have had historical value, but it currently lacks pathophysiologic or clinical utility.

Generally, lichen nitidus is asymptomatic and self-limited; therefore, no treatment is required. However, if persistent pruritus is present, or the appearance “...interferes with daily activities or outlook...” topical glucocorticoids may be tried. If the disease process is symptomatic, generalized and extensive, oral glucocorticoids may be indicated. Other reported treatments include PUVA, UVA/UVB phototherapy, astemizole, acitretin, and etretinate.

When appears with sun/humidity; air conditioning (cool dry air) reduces swelling and discomfort.

Primary cutaneous amyloidosis is a form of amyloidosis associated with oncostatin M receptor. This type of amyloidosis has been divided into the following types:

- Macular amyloidosis is a cutaneous condition characterized by itchy, brown, rippled macules usually located on the interscapular region of the back. Combined cases of lichen and macular amyloidosis are termed biphasic amyloidosis, and provide support to the theory that these two variants of amyloidosis exist on the same disease spectrum.

- Lichen amyloidosis is a cutaneous condition characterized by the appearance of occasionally itchy lichenoid papules, typically appearing bilaterally on the shins.

- Nodular amyloidosis is a rare cutaneous condition characterized by nodules that involve the acral areas.

Localized lichen myxedematosus is a group of skin condition caused by fibroblasts producing abnormally large amounts of mucopolysaccharides, a disease for which there is no treatment.

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