Subcutaneous fat necrosis of the newborn (SCFN or SFN) is a rare form of lobular panniculitis occurring in newborns that is usually self-remitting and non-recurring. Proposed causes include perinatal stress, local trauma, hypoxia and hypothermia, though the exact cause is unknown. It has been suggested that the brown fat seen in newborns is more sensitive to hypoxic injury than fat seen in adults, and that such hypoxia, usually in the context of a complicated birth, leads to the fat necrosis. Complications can include hypercalcemia, hyperlipidemia and thrombocytopenia, and can present months after the onset of SCFN symptoms.

Sclerema neonatorum is a rare and severe skin condition that is characterized by diffuse hardening of the subcutaneous tissue with minimal inflammation. It usually affects premature, ill newborns. Prognosis is poor.

Minimal inflammation helps distinguish sclerema neonaturum from subcutaneous fat necrosis of the newborn.

Neutrophilic lobular panniculitis is a cutaneous condition characterized by inflammation of the subcutaneous fat.

Localized lipodystrophy is a skin condition characterized by the loss subcutaneous fat localized to sites of insulin injection.

In sheep, intrauterine growth restriction can be caused by heat stress in early to mid pregnancy. The effect is attributed to reduced placental development causing reduced fetal growth. Hormonal effects appear implicated in the reduced placental development. Although early reduction of placental development is not accompanied by concurrent reduction of fetal growth; it tends to limit fetal growth later in gestation. Normally, ovine placental mass increases until about day 70 of gestation, but high demand on the placenta for fetal growth occurs later. (For example, research results suggest that a normal average singleton Suffolk x Targhee sheep fetus has a mass of about 0.15 kg at day 70, and growth rates of about 31 g/day at day 80, 129 g/day at day 120 and 199 g/day at day 140 of gestation, reaching a mass of about 6.21 kg at day 140, a few days before parturition.)

In adolescent ewes (i.e. ewe hoggets), overfeeding during pregnancy can also cause intrauterine growth restriction, by altering nutrient partitioning between dam and conceptus. Fetal growth restriction in adolescent ewes overnourished during early to mid pregnancy is not avoided by switching to lower nutrient intake after day 90 of gestation; whereas such switching at day 50 does result in greater placental growth and enhanced pregnancy outcome. Practical implications include the importance of estimating a threshold for "overnutrition" in management of pregnant ewe hoggets. In a study of Romney and Coopworth ewe hoggets bred to Perendale rams, feeding to approximate a conceptus-free live mass gain of 0.15 kg/day (i.e. in addition to conceptus mass), commencing 13 days after the midpoint of a synchronized breeding period, yielded no reduction in lamb birth mass, where compared with feeding treatments yielding conceptus-free live mass gains of about 0 and 0.075 kg/day.

In both of the above models of IUGR in sheep, the absolute magnitude of uterine blood flow is reduced. Evidence of substantial reduction of placental glucose transport capacity has been observed in pregnant ewes that had been heat-stressed during placental development.

Warfarin-induced skin necrosis (or, more generally, Anticoagulant-induced skin necrosis) is a condition in which skin and subcutaneous tissue necrosis (tissue death) occurs due to acquired protein C deficiency following treatment with anti-vitamin K anticoagulants (4-hydroxycoumarins, such as warfarin).

Warfarin necrosis is a rare but severe complication of treatment with warfarin or related anticoagulants. The typical patient appears to be an obese, middle aged woman (median age 54 years, male to female ratio 1:3). This drug eruption usually occurs between the third and tenth days of therapy with warfarin derivatives. The first symptoms are pain and redness in the affected area. As they progress, lesions develop a sharp border and become petechial, then hard and purpuric. They may then resolve or progress to form large, irregular, bloody bullae with eventual necrosis and slow-healing eschar formation. Favored sites are breasts, thighs, buttocks and penis, all areas with subcutaneous fat. In rare cases, the fascia and muscle are involved.

Development of the syndrome is associated with the use of large loading doses at the start of treatment.

Warfarin necrosis usually occurs three to five days after drug therapy is begun, and a high initial dose increases the risk of its development. Heparin-induced necrosis can develop both at sites of local injection and - when infused intravenously - in a widespread pattern.

In warfarin's initial stages of action, inhibition of protein C and Factor VII is stronger than inhibition of the other vitamin K-dependent coagulation factors II, IX and X. This results from the fact that these proteins have different half-lives: 1.5 to six hours for factor VII and eight hours for protein C, versus one day for factor IX, two days for factor X and two to five days for factor II. The larger the initial dose of vitamin K-antagonist, the more pronounced these differences are. This coagulation factor imbalance leads to paradoxical activation of coagulation, resulting in a hypercoagulable state and thrombosis. The blood clots interrupt the blood supply to the skin, causing necrosis. Protein C is an innate anticoagulant, and as warfarin further decreases protein C levels, it can lead to massive thrombosis with necrosis and gangrene of limbs.

Notably, the prothrombin time (or international normalized ratio, INR) used to test the effect of warfarin is highly dependent on factor VII, which explains why patients can have a therapeutic INR (indicating good anticoagulant effect) but still be in a hypercoagulable state.

In one third of cases, warfarin necrosis occurs in patients with an underlying, innate and previously unknown deficiency of protein C. The condition is related to purpura fulminans, a complication in infants with sepsis (blood stream infection) which also involves skin necrosis. These infants often have protein C deficiency as well. There have also been cases in patients with other deficiency, including protein S deficiency, activated protein C resistance (Factor V Leiden) and antithrombin III deficiency.

Although the above theory is the most commonly accepted theory, others believe that it is a hypersensitivity reaction or a direct toxic effect.

Fat necrosis is a form of necrosis characterized by the action upon fat by digestive enzymes.

In fat necrosis the enzyme lipase releases fatty acids from triglycerides. The fatty acids then complex with calcium to form soaps. These soaps appear as white chalky deposits.

It is usually associated with trauma of the pancreas or acute pancreatitis.

It can also occur in the breast, the salivary glands and neonates after a traumatic delivery.

Alpha-1 antitrypsin deficiency panniculitis is a panniculitis associated with a deficiency of the α-antitrypsin enzyme.

Angiolipoleiomyoma is an acquired, solitary, asymptomatic acral nodule, characterized histologically by well-circumscribed subcutaneous tumors composed of smooth muscle cells, blood vessels, connective tissue, and fat.

Lipodermatosclerosis is a form of panniculitis associated with chronic venous insufficiency that presents with brown indurations on the front of the shins. It may be associated with pain and other signs of chronic venous insufficiency. The exact cause is unknown.

Other forms include:

- Subcutaneous fat necrosis of the newborn, a form of panniculitis occurring in newborns that is usually self-resolving, that may be a result of hypoxic injury to relatively high levels of brown fat.

- Sclerema neonatorum, affecting premature births.

- Weber–Christian disease, a symmetrical form of the disease of unknown origin occurring in middle-aged women.

- Lupus erythematosus panniculitis, panniculitis associated with lupus erythematosus.

- Forms associated with use of high doses of systemic corticosteroids during rapid corticosteroid withdrawal, and from the injection of silicone or mineral oils.

Angiomatosis is a non-neoplastic condition characterised by nests of proliferating capillaries arranged in a lobular pattern, displacing adjacent muscle and fat. It consists of many angiomas.

These tend to be cavernous hemangiomas, which are sharply defined, sponge-like tumors composed of large, dilated, cavernous vascular spaces.

Prognosis depends on the size and location of the tumour, untreated angiomatosis may lead to blindness and/ or permanent brain damage. Death may occur, with complications in the kidney or brain.

The exact cause of lipodermatosclerosis is unknown. Venous disease, such as venous incompetence, venous hypertension, and body mass ("obesity") may be relevant to the underlying pathogenesis.

Increased blood pressure in the veins (venous hypertension) can cause diffusion of substances, including fibrin, out of capillaries. Fibrotic tissue may predispose the tissue to ulceration. Recurrent ulceration and fat necrosis is associated with lipodermatosclerosis. In advanced lipodermatosclerosis the proximal leg swells from chronic venous obstruction and the lower leg shrinks from chronic ulceration and fat necrosis resulting in the inverted coke bottle appearance of the lower leg.

Lipodermatosclerosis is most commonly diagnosed in middle-aged women.

The origin of lipodermatosclerosis is probably multifactorial, involving tissue hypoxia, leakage of proteins into the interstitium, and leukocyte activation. Studies of patients with lipodermatosclerosis have demonstrated significantly decreased concentrations of cutaneous oxygen associated with decreased capillary density. Capillaries are virtually absent in areas of fibrotic scars, leading to a condition known as atrophie blanche or livedoid vasculopathy.

Prolonged hyperbilirubinemia (severe jaundice) can result in chronic bilirubin encephalopathy (kernicterus). Quick and accurate treatment of neonatal jaundice helps to reduce the risk of neonates developing kernicterus.

Infants with kernicterus may have a fever or seizures. High pitched crying is an effect of kernicterus. Scientists used a computer to record and measure cranial nerves 8, 9 and 12 in 50 infants who were divided into two groups equally depending upon bilirubin concentrations. Of the 50 infants, 43 had tracings of high pitched crying.

Exchange transfusions performed to lower high bilirubin levels are an aggressive treatment.

Involutional lipoatrophy is a cutaneous condition, and is an idiopathic lipoatrophy characterized clinically by non-inflammatory focal loss of fat.

Idiopathic localized involutional lipoatrophy (ILIL) is a rare and nosologically imprecise condition characterized by a focal loss of subcutaneous tissue on one or several sites, occurring without any significant triggering factor or auto-immune background, and regressing spontaneously within a few months.

IUGR affects 3-10% of pregnancies. 20% of stillborn infants have IUGR. Perinatal mortality rates are 4-8 times higher for infants with IUGR, and morbidity is present in 50% of surviving infants.

According to the theory of thrifty phenotype, intrauterine growth restriction triggers epigenetic responses in the fetus that are otherwise activated in times of chronic food shortage. If the offspring actually develops in an environment rich in food it may be more prone to metabolic disorders, such as obesity and type II diabetes.

Lipoatrophy is the term describing the localized loss of fat tissue. This may occur as a result of subcutaneous injections of insulin in the treatment of diabetes, from the use of Human Growth Hormone or from subcutaneous injections of Copaxone used for the treatment of multiple sclerosis. In the latter case, an injection may produce a small dent at the injection site. Lipoatrophy occurs in HIV-associated lipodystrophy, one cause of which is an adverse drug reaction that is associated with some antiretroviral drugs.

A more general term for an abnormal or degenerative condition of the entire body's adipose tissue is "lipodystrophy".

AGL with autoimmune origin is responsible for about 25% of all AGL reports. Those with autoimmune origin stems from other autoimmune diseases, most commonly with juvenile dermatomyositis and autoimmune hepatitis, but also occurs with rheumatoid arthritis, systemic lupus erythematous, and Sjogren syndrome.

About 25% of previously reported AGL is associated with panniculitis. Panniculitis is an inflammatory nodules of the subcutaneous fat, and in this type of AGL, adipose destruction originates locally at the infection or inflammation site and develops into generalized lipodystrophy.

Lipodermatosclerosis (also known as "chronic panniculitis with lipomembranous changes", "hypodermitis sclerodermiformis", "sclerosing panniculitis", and "stasis panniculitis") is a skin and connective tissue disease. It is a form of lower extremity panniculitis, an inflammation of the layer of fat under the epidermis.

Centrifugal abdominal lipodystrophy (also known as "Centrifugal lipodystrophy," "Lipodystrophia centrifugalis abdominalis infantalis") is a skin condition characterized by areas of subcutaneous fat loss that slowly enlarge.

On the other hand, there is evidence that HIV-1 infection on its own contributes to the development of the lipodystrophic phenotype by interfering with some key genes of adipocyte differentiation and mitochondrial function on patients which have not received antiretroviral treatment.

Lipohypertrophy is a medical term that refers to a lump under the skin caused by accumulation of extra fat at the site of many subcutaneous injections of insulin. It may be unsightly, mildly painful, and may change the timing or completeness of insulin action. It is a common, minor, chronic complication of diabetes mellitus.

Typical injection site hypertrophy is several inches or cm across, smoothly rounded, and somewhat firmer than ordinary subcutaneous fat. There may be some scar tissue as well, but the major component is adipose tissue, as insulin exerts a hypertrophic effect on adipose cells. To avoid lipohypertrophy, persons with diabetes mellitus who inject insulin daily for an extended period of time are advised to "rotate" their injections among several areas (usually upper, outer arms, outer thighs, abdomen below and around the umbilicus, and the upper parts of the buttocks). Rotation charts are often provided as part of diabetes education to help prevent lipohypertrophy.

Lipohypertrophy usually will gradually disappear over months if injections in the area are avoided.

It is a common misconception that the lump is largely scar tissue, as injection site hypertrophy is much rarer and milder with injections of other hormones and medications which lack the specific ability of insulin to stimulate adipose hypertrophy.

In a sense, the "opposite" of injection site lipohypertrophy is injection site lipoatrophy, in which the subcutaneous fat around an injected area "melts away" over a few weeks or months, leaving unsightly, well-demarcated depressions in the skin. The mechanism of this local lipoatrophy is not understood and may involve autoimmunity or local inflammation.

Lipoatrophia annularis (also known as "Ferreira–Marques lipoatrophia") is a skin condition affecting primarily women, characterized by the loss of subcutaneous fat in the upper extremity.

It is a form of lipodystrophy.