Swyer–James syndrome (SJS, also called Swyer–James–Macleod's syndrome) is a rare lung disorder found by English chest physician William Mathiseon Macleod, and (simultaneously) by physician Paul Robert Swyer and radiologist George James in the 1950s in Canada.

Swyer–James syndrome is a manifestation of postinfectious obliterative bronchiolitis. In SJS, the involved lung or portion of the lung does not grow normally and is slightly smaller than the opposite lung. The characteristic radiographic appearance is that of pulmonary hyperlucency, caused by overdistention of the alveoli in conjunction with diminished arterial flow. and has been linked to adenovirus type 21.

In appearance Swyer–James normally leaves shadowing in a CT scan in the upper lobar regions of one or (rarely) both lungs. Patients with the illness operate in much the same way as patients with mild bronchiectasis. As a result, the illness can go undiagnosed for some time. With current pharmaceutical developments, the prognosis is good for sufferers of the illness to lead normal and healthy lives.

Schwartz–Jampel syndrome (SJS) is a rare genetic disease caused by a mutation in the HSPG2 gene, which makes the protein perlecan, and causing osteochondrodysplasia associated with myotonia.

Most people with Schwartz–Jampel syndrome have a nearly normal life expectancy.

Relationships between the disease and perlecan deficiency have been studied.

SJS usually begins with fever, sore throat, and fatigue, which is commonly misdiagnosed and therefore treated with antibiotics. SJS and TEN are often heralded by fever, sore throat, cough, and burning eyes for 1 to 3 days. Patients with SJS and TEN frequently experience burning pain of their skin at the start of disease. Ulcers and other lesions begin to appear in the mucous membranes, almost always in the mouth and lips, but also in the genital and anal regions. Those in the mouth are usually extremely painful and reduce the patient's ability to eat or drink. Conjunctivitis of the eyes occurs in about 30% of children who develop SJS. A rash of round lesions about an inch across arises on the face, trunk, arms and legs, and soles of the feet, but usually not the scalp.

Stevens–Johnson syndrome (SJS) is a milder form of toxic epidermal necrolysis (TEN). These conditions were first recognised in 1922. A classification first published in 1993, that has been adopted as a consensus definition, identifies Stevens–Johnson syndrome, toxic epidermal necrolysis, and SJS/TEN overlap. All three are part of a spectrum of severe cutaneous reactions (SCAR) which affect skin and mucous membranes. The distinction between SJS, SJS/TEN overlap, and TEN is based on the type of lesions and the amount of the body surface area with blisters and erosions. It is agreed that the most reliable method to classify EM, SJS, and TEN is based on lesion morphology and extent of epidermal detachment. Blisters and erosions cover between 3% and 10% of the body in SJS, 11–30% in SJS/TEN overlap, and over 30% in TEN. The skin pattern most commonly associated with SJS is widespread, often joined or touching (confluent), papuric spots (macules) or flat small blisters or large blisters which may also join together. These occur primarily on the torso.

SJS, TEN, and SJS/TEN overlap can be mistaken for erythema multiforme. Erythema multiforme, which is also within the SCAR spectrum, differs in clinical pattern and etiology. Although both SJS and TEN can also be caused by infections, they are most often adverse effects of medications.

Nearly all people with TEN have oral, eye and genital involvement as well. Painful crusts and erosions may develop on any mucosal surface. The mouth becomes blistered and eroded, making eating difficult and sometimes necessitating feeding through a nasogastric tube through the nose or a gastric tube directly into the stomach. The eyes can become swollen, crusted, and ulcerated, leading to potential blindness. The most common problem with the eyes is severe conjunctivitis.

Initial skin findings include red-purple, dusky, flat spots known as macules that start on the trunk and spread out from there. These skin lesions then transform into large blisters. The affected skin can then become necrotic or sag from the body and peel off in great swaths.

The hallmark symptom of SS is a generalized dryness, typically including dry mouth and keratoconjunctivitis sicca (dry eyes), part of what are known as sicca ("dryness") symptoms. Sicca syndrome also incorporates vaginal dryness and chronic bronchitis. SS may cause skin, nose, and vaginal dryness, and may affect other organs of the body, including the muscles (myositis), kidneys, blood vessels, lungs, liver, biliary system, pancreas, peripheral nervous system (distal axonal neuropathy or small fiber peripheral neuropathy) and brain. Some people have gastrointestinal or esophageal diseases such as GERD, achlorhydria or gastroparesis. Chronic pain with accompanying fatigue and brain fog may also occur.

Skin dryness in some people with SS may be the result of lymphocytic infiltration into skin glands. The symptoms may develop insidiously, with the diagnosis often not considered for several years, because the complaints of sicca may be otherwise attributed to medications, a dry environment, aging, or may be regarded as not of severity warranting the level of investigation necessary to establish the presence of the specific underlying autoimmune disorder.

SS can damage vital organs of the body with symptoms that may plateau or worsen, or go into remission as with other autoimmune diseases. Some people may experience only the mild symptoms of dry eyes and mouth, while others have symptoms of severe disease. Many patients can treat problems symptomatically. Others are forced to cope with blurred vision, constant eye discomfort, recurrent mouth infections, swollen parotid glands, dysphonia (vocal disorders including hoarseness), and difficulty in swallowing and eating. Debilitating fatigue and joint pain can seriously impair quality of life. Some patients can develop renal (kidney) involvement (autoimmune tubulointerstitial nephritis) leading to proteinuria (excess protein in urine), urinary concentrating defect, and distal renal tubular acidosis.

Sjögren syndrome (SjS, SS) is a long-term autoimmune disease in which the moisture-producing glands of the body are affected. This results primarily in the development of a dry mouth and dry eyes. Other symptoms can include dry skin, a chronic cough, vaginal dryness, numbness in the arms and legs, feeling tired, muscle and joint pains, and thyroid problems. Those affected are at an increased risk (5%) of lymphoma.

While the exact cause is unclear, it is believed to involve a combination of genetics and an environmental trigger such as exposure to a virus or bacteria. It can occur independently of other health problems (primary Sjögren syndrome) or as a result of another connective tissue disorder (secondary Sjögren syndrome). The inflammation that results progressively damages the glands. Diagnosis is by biopsy of moisture-producing glands and blood tests looking for specific antibodies. On biopsy there are typically lymphocytes within the glands.

Treatment is directed at the person's symptoms. For dry eyes artificial tears, medications to reduce inflammation, punctal plugs, or surgery to shut the tear ducts, may be tried. For a dry mouth, chewing gum (preferably sugar free), sipping water, or a saliva substitute may be used. In those with joint or muscle pain, ibuprofen may be used. Medications that can cause dryness, such as antihistamines, may also be stopped.

The disease was described in 1933 by Henrik Sjögren, after whom it is named; however, a number of earlier descriptions of people with the symptoms exist. Between 0.2% and 1.2% of the population are affected, with half having the primary form and half the secondary form. Females are affected about ten times as often as males and it commonly begins in middle age; however, anyone can be affected. Among those without other autoimmune disorders, life expectancy is unchanged.

AGEP is an acute febrile drug eruption characterized by numerous small, primarily non-follicular, sterile pustules, arising within large areas of red swollen skin.

The eruption follows a self-limiting course and will end before a week provided the causative agent (e.g. medication) is discarded. It is accompanied by fever, a high number of neutrophils and eosinophils in the blood, liver inflammation, and sometimes by facial swelling. The mortality rate is about 5% and the differential diagnosis includes Stevens–Johnson syndrome (SJS). Contrary to SJS, in AGEP, mucosa are not affected, which means that there are no blisters in the mouth or vagina.

The treatment is (1) stop the offending drug (antibiotics), (2) symptomatic (fever), and (3) for complications (hepatitis).

The most common type of eruption is a morbilliform (resembling measles) or erythematous rash (approximately 90% of cases). Less commonly, the appearance may also be urticarial, papulosquamous, pustular, purpuric, bullous (with blisters) or lichenoid. Angioedema can also be drug-induced (most notably, by angiotensin converting enzyme inhibitors).

The condition varies from a mild, self-limited rash (E. multiforme minor) to a severe, life-threatening form known as erythema multiformer major (or erythema multiforme majus) that also involves mucous membranes.

Consensus classification:

- Erythema multiforme minor—typical targets or raised, edematous papules distributed

- Erythema multiforme major—typical targets or raised, edematous papules distributed acrally with involvement of one or more mucous membranes; epidermal detachment involves less than 10% of total body surface area (TBSiA)

- SJS/TEN—widespread blisters predominant on the trunk and face, presenting with erythematous or pruritic macules and one or more mucous membrane erosions; epidermal detachment is less than 10% TBSA for Stevens-Johnson syndrome and 30% or more for toxic epidermal necrolysis.

The mild form usually presents with mildly itchy (but itching can be very severe), pink-red blotches, symmetrically arranged and starting on the extremities. It often takes on the classical "target lesion" appearance, with a pink-red ring around a pale center. Resolution within 7–10 days is the norm.

Individuals with persistent (chronic) erythema multiforme will often have a lesion form at an injury site, e.g. a minor scratch or abrasion, within a week. Irritation or even pressure from clothing will cause the erythema sore to continue to expand along its margins for weeks or months, long after the original sore at the center heals.

The underlying mechanism can be immunological (such as in drug allergies) or non-immunological (for example, in photodermatitis or as a side effect of anticoagulants). A fixed drug eruption is the term for a drug eruption that occurs in the same skin area every time the person is exposed to the drug. Eruptions can occur frequently with a certain drug (for example, with phenytoin), or be very rare (for example, Sweet's syndrome following the administration of colony-stimulating factors).

Erythema multiforme (EM) is a skin condition of unknown cause; it is a type of erythema possibly mediated by deposition of immune complexes (mostly IgM-bound complexes) in the superficial microvasculature of the skin and oral mucous membrane that usually follows an infection or drug exposure. It is an uncommon disorder, with peak incidence in the second and third decades of life. The disorder has various forms or presentations, which its name reflects ("multiforme", "", from "" + ""). Target lesions are a typical manifestation. Two types, one mild to moderate and one severe, are recognized (erythema multiforme minor and erythema multiforme major).

Erythema multiforme major (also known as "erythema multiforme majus") is a form of rash with skin loss or epidermal detachment.

The term "erythema multiforme majus" is sometimes used to imply a bullous (blistering) presentation.

According to some sources, there are two conditions included on a spectrum of this same disease process:

- Stevens–Johnson syndrome (SJS)

- Toxic epidermal necrolysis (TEN) which described by Alan Lyell and previously called Lyell syndrome[5].

In this view, EM major, SJS and TEN are considered a single condition, distinguished by degree of epidermal detachment.

However, a consensus classification separates erythema multiforme minor, erythema multiforme major, and SJS/TEN as three separate entities.