Angiolymphoid hyperplasia with eosinophilia (also known as: "Epithelioid hemangioma," "Histiocytoid hemangioma," "Inflammatory angiomatous nodule," "Intravenous atypical vascular proliferation," "Papular angioplasia," "Inflammatory arteriovenous hemangioma," and "Pseudopyogenic granuloma") usually presents with pink to red-brown, dome-shaped, dermal papules or nodules of the head or neck, especially about the ears and on the scalp.

It, or a similar lesion, has been suggested as a feature of IgG4-related skin disease, which is the name used for skin manifestations of IgG4-related disease.

Lymphoid hyperplasia is the rapid growth proliferation of normal cells that resemble lymph tissue.

Jessner lymphocytic infiltrate of the skin is a cutaneous condition characterized by a persistent papular and plaque-like skin eruption which can occur on the neck, face and back and may re-occur. This is an uncommon skin disease and is a benign collection of lymph cells. Its cause is not known and can be hereditary. It is named for Max Jessner. It is thought to be equivalent to lupus erythematosus tumidus.

It can occur as the result of ACE inhibitors and a number of medications used to treat multiple sclerosis including glatiramer acetate.

Intravascular papillary endothelial hyperplasia (also known as "Masson's hemangio-endotheliome vegetant intravasculaire," "Masson's lesion," "Masson's pseudoangiosarcoma," "Masson's tumor," and "Papillary endothelial hyperplasia") is a rare, benign tumor. It may mimic an angiosarcoma, with lesions that are red or purplish 5-mm to 5-cm papules and deep nodules on the head, neck, or upper extremities.

Follicular hyperplasia (or "reactive follicular hyperplasia" or "lymphoid nodular hyperplasia") is a type of lymphoid hyperplasia. It is caused by a stimulation of the B cell compartment. It is caused by an abnormal proliferation of secondary follicles and occurs principally in the cortex without broaching the lymph node capsule. The follicles are cytologically polymorphous, are often polarized, and vary in size and shape. Follicular hyperplasia is distinguished from follicular lymphoma in its polyclonality and lack of bcl-2 protein expression, whereas follicular lymphoma is monoclonal, and does express bcl-2).

Cutaneous lymphoid hyperplasia refers to a groups of benign cutaneous disorders characterized by collections of lymphocytes, macrophages, and dendritic cells in the skin. Conditions included in this groups are:

- Cutaneous lymphoid hyperplasia with nodular pattern, a condition of the skin characterized by a solitary or localized cluster of asymptomatic erythematous to violaceous papules or nodules

- Cutaneous lymphoid hyperplasia with bandlike and perivascular patterns, a condition of the skin characterized by skin lesions that clinically resemble mycosis fungoides

Atypical hyperplasia is a benign (noncancerous) cellular hyperplasia in which cells show some atypia. In this condition, cells look abnormal under a microscope and are increased in number.

Atypical hyperplasia is a high-risk premalignant lesion of the breast. It is believed that atypical ductal hyperplasia (ADH) is a direct precursor for low-grade mammary ductal carcinoma, whereas atypical lobular hyperplasia (ALH) serves as a risk indicator.

Papuloerythroderma of Ofuji is a rare disorder most commonly found in Japan, characterized by pruritic papules that spare the skinfolds, producing bands of uninvolved cutis, creating the so-called deck-chair sign. Frequently there is associated blood eosinophilia. Skin biopsies reveal a dense lymphohistiocytic infiltrate, eosinophils in the papillary dermis, and increased Langerhans cells (S-100 positive). Systemic steroids are the treatment of choice and may result in long-term remissions.

It was characterized in 1984.

Use of PUVA in treatment has been described.

Some specific reactive lymphadenopathies with a predominantly follicular pattern:

- Rheumatoid arthritis

- Sjogren syndrome

- IgG4-related disease (IgG4-related lymphadenopathy)

- Kimura disease

- Toxoplasmosis

- Syphilis

- Castleman disease

- HIV-associated lymphadenopathy

- Progressive transformation of germinal centers (PTGC)

The treatment of hyperplasia would consist upon "which"; in the case of benign prostate hyperplasia the combination of alpha-1-receptor blockers and 5-alpha-reductase inhibitors are effective.

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.

If the causative factor persists, tissue will become more fibrous over time.

Sebaceous hyperplasia is a disorder of the sebaceous glands in which they become enlarged, producing flesh-colored or yellowish, shiny, often umbilicated bumps on the face. Newly formed nodules often swell with sweating (which is pathognomonic for the condition), but this diminishes over time.

Sebaceous glands are glands located within the skin and are responsible for secreting an oily substance named sebum. They are commonly associated with hair follicles but they can be found in hairless regions of the skin as well. Their secretion lubricates the skin, protecting it from drying out or becoming irritated.

Sebaceous hyperplasia generally affects newborns as well as middle-aged to elderly adults. The symptoms of this condition are 1–5 mm papules on the skin, mainly on the forehead, nose and cheeks, and seborrheic facial skin. The papules may be cauliflower-shaped. In infants, acne is sometimes associated with sebaceous hyperplasia.

Treatment is by surgical excision (complete removal) of the fibrous tissue overgrowth and addressing the causative factor to prevent recurrence of the lesion. Other sources suggest that surgical excision may not be required in all cases. Common techniques for removal of the excess tissue include traditional removal with a surgical scalpel, electrical scalpel, or laser excision with a laser scalpel, e.g. a carbon dioxide laser, , Neodymium-YAG laser, or diode laser. The poorly fitting denture can be adapted to fit better (a "reline") or a new denture constructed. Alternatively, the section of flange that is sharp/over-extended can be smoothed and reduced with a drill.

It is one common source of appendicitis, as it may cause an obstruction of the appendiceal lumen, resulting in the subsequent filling of the appendix with mucus, causing it to distend and internal pressure to increase.

The European Medicines Agency (EMA) estimated the prevalence of HES at the time of granting orphan drug designation for HES in 2004 at 1.5 in 100,000 people, corresponding to a current prevalence of about 8,000 in the EU, 5,000 in the U.S., and 2,000 in Japan.

Patients who lack chronic heart failure and those who respond well to Prednisone or a similar drug have a good prognosis. However, the mortality rate rises in patients with anaemia, chromosomal abnormalities or a very high white blood cell count.

Multifocal micronodular pneumocyte hyperplasia (MMPH) is a subtype of pneumocytic hyperplasia (hyperplasia of pneumocytes lining pulmonary alveoli).

Several synonymous terms have been done for this entity: adenomatoid proliferation of alveolar epithelium, papillary alveolar hamartoma, multifocal alveolar hyperplasia, multinodular pneumocyte hyperplasia.

These multifocal lesions are observed in tuberous sclerosis, and can be associated with lymphangioleiomyomatosis and perivascular epithelioid cell tumour (PEComa or clear cell "sugar tumor")).

It can be diagnosed through lung biopsy using thoracoscopy.

This type of gingival enlargement is sometimes termed "drug induced gingival enlargement" or "drug influenced gingival enlargement", abbreviated to "DIGO". Gingival enlargement may also be associated with the administration of three different classes of drugs, all producing a similar response: Gingival overgrowth is a common side effect of phenytoin, termed "Phenytoin-induced gingival overgrowth" (PIGO).

- anticonvulsants (such as phenytoin, phenobarbital, lamotrigine, vigabatrin, ethosuximide, topiramate and primidone NOT common for valproate)

- calcium channel blockers (antihypertensives such as nifedipine, amlodipine, and verapamil). The dihydropyridine derivative isradipidine can replace nifedipine and does not induce gingival overgrowth.

- cyclosporine, an immunosuppresant.

Of all cases of DIGO, about 50% are attributed to phenytoin, 30% to cyclosporins and the remaining 10-20% to calcium channel blockers.

Drug-induced enlargement has been associated with a patient's genetic predisposition, and its association with inflammation is debated. Some investigators assert that underlying inflammation is necessary for the development of drug-induced enlargement, while others purport that the existing enlargement induced by the drug effect compounds plaque retention, thus furthering the tissue response. Careful attention to oral hygiene may reduce the severity of gingival hyperplasia. In most cases, discontinuing the culprit drug resolves the hyperplasia.

Treatment primarily consists of reducing eosinophil levels and preventing further damage to organs. Corticosteroids, such as Prednisone, are good for reducing eosinophil levels and antineoplastics are useful for slowing eosinophil production. Surgical therapy is rarely utilised, however splenectomy can reduce the pain due to spleen enlargement. If damage to the heart (in particular the valves), then prosthetic valves can replace the current organic ones. Follow-up care is vital for the survival of the patient, as such the patient should be checked for any signs of deterioration regularly. After promising results in drug trials (95% efficiency in reducing blood eosinophil count to acceptable levels) it is hoped that in the future hypereosinophilic syndrome, and diseases related to eosinophils such as asthma and eosinophilic granulomatosis with polyangiitis, may be treated with the monoclonal antibody Mepolizumab currently being developed to treat the disease. If this becomes successful, it may be possible for corticosteroids to be eradicated and thus reduce the amount of side effects encountered.

Nodular regenerative hyperplasia is a form of liver hyperplasia associated with portal hypertension.

Nodular regenerative hyperplasia (NRH) is a rare liver condition characterized by a widespread benign transformation of the hepatic parenchyma into small regenerative nodules. NRH may lead to the development of non-cirrhotic portal hypertension. There are no published systematic population studies on NRH and our current knowledge is limited to case reports and case series. NRH may develop "via" autoimmune, hematological, infectious, neoplastic, or drug-related causes. It is associated with rheumatoid arthritis, Felty syndrome, myeloproliferative disorders, liver, kidney and bone marrow transplantation, cytotoxic drugs like azathioprine, mercaptopurine, thioguanine, antiretroviral drugs for HIV like didanosine and vitamin A. The disease is usually asymptomatic, slowly or non-progressive unless complications of portal hypertension develop. Accurate diagnosis is made by histopathology, which demonstrates diffuse micronodular transformation without fibrous septa. Lack of perinuclear collagen tissue distinguishes NRH from typical regenerative nodules in the cirrhotic liver. While the initial treatment is to address the underlying disease, ultimately the therapy is directed to the management of portal hypertension. The prognosis of NRH depends on both the severity of the underlying illness and the prevention of secondary complications of portal hypertension. In this review we detail the epidemiology, pathogenesis, diagnosis, management, and prognosis of NRH.

It can be a complication of azathioprine therapy.

Gingival enlargement, (also termed gingival overgrowth, hypertrophic gingivitis, gingival hyperplasia, or gingival hypertrophy, and sometimes abbreviated to GO), is an increase in the size of the gingiva (gums). It is a common feature of gingival disease. Gingival enlargement can be caused by a number of factors, including inflammatory conditions and the side effects of certain medications. The treatment is based on the cause. A closely related term is epulis, denoting a localized tumor (i.e. lump) on the gingiva.

Thymus hyperplasia (or thymic hyperplasia) refers to an enlargement ("hyperplasia") of the thymus.

It is not always a disease state. The size of the thymus usually peaks during adolescence, and atrophies in the following decades. Before the immune function of the thymus was well understood, the enlargement was sometimes seen as a cause for alarm, and justification for surgical reduction. This approach is much less common today.

It can be associated with myasthenia gravis.

MRI can be used to distinguish it from thymoma.

Pneumocytic hyperplasia is an hyperplasia of pneumocytes lining pulmonary alveoli.

Salivary gland hyperplasia is hyperplasia of the terminal duct of salivary glands.

There are two types:

- Acinar adenomatoid hyperplasia

- Ductal adenomatoid hyperplasia