Inadequate nutrition or the consumption of tainted food are suspected. Both IgG and IgM autoantibodies to platelet and to glycoprotein IIb/IIIa is found in majority of patients.

PCH is a rare autoimmune haemolytic anaemia that can occur following an infection, when a microorganism triggers the formation of antibodies that cross-react with the P antigen on the red blood cell membrane (see article on the P antigen system). Viral infections that can cause PCH include measles, mumps, influenza, adenovirus, chickenpox, cytomegalovirus, and Epstein-Barr virus. Bacterial infections that can cause PCH include syphilis, "Haemophilus influenzae" and "Mycoplasma pneumoniae". PCH can also be a side effect of some vaccinations. Chronic idiopathic (of unknown cause) PCH also occurs, but it is rare.

Idiopathic pneumonia syndrome is a set of pneumonia-like symptoms (such as fever, chills, coughing, and breathing problems) that occur with no sign of infection in the lung. Idiopathic pneumonia syndrome is a serious condition that can occur after a stem cell transplant.

Acute PCH tends to be transient and self-limited, particularly in children. Chronic PCH associated with syphilis resolves after the syphilis is treated with appropriate antibiotics. Chronic idiopathic PCH is usually mild.

It has been suggested that idiopathic nonspecific interstitial pneumonia has an autoimmune mechanism, and is a possible complication of undifferentiated connective tissue disease.

Onyalai is limited to black populations in central southern Africa. The affected age range is from less than a year to 70 years and seems not to be gender-specific in the same manner as ITP. Cases generally peak between 11 and 20 years old.

Analysis of patient admissions in Namibia between 1981 and 1988 showed an incidence rate of onyalai to be 1.19% with the annual incidence varying between 0.96% and 1.66% of all admissions. The female to male ratio was 3:2. The mean age at presentation was 24.8 years (range 6 months to 80 years) and the mean hospital stay (and duration of clinical bleeding) was 7.68 days (ranging between 1–38 days). The treatment policy of commencing intravenous fluid on admission and a blood transfusion whenever the haemoglobin dropped below 10 g/dl in patients with active bleeding was associated with a mortality rate of 2.78% compared to 9.8% in cases recorded up to 1981.

ILD may be classified according to the cause. One method of classification is as follows:

1. Inhaled substances

- Inorganic

- Silicosis

- Asbestosis

- Berylliosis

- printing workers (eg. carbon bblack, ink mist)

- Organic

- Hypersensitivity pneumonitis

2. Drug-induced

- Antibiotics

- Chemotherapeutic drugs

- Antiarrhythmic agents

3. Connective tissue and Autoimmune diseases

- Rheumatoid arthritis

- Systemic lupus erythematosus

- Systemic sclerosis

- Polymyositis

- Dermatomyositis

4. Infection

- Atypical pneumonia

- Pneumocystis pneumonia (PCP)

- Tuberculosis

- "Chlamydia" trachomatis

- Respiratory Syncytial Virus

5. Idiopathic

- Sarcoidosis

- Idiopathic pulmonary fibrosis

- Hamman-Rich syndrome

- Antisynthetase syndrome

6. Malignancy

- Lymphangitic carcinomatosis

7. Predominantly in children

- Diffuse developmental disorders

- Growth abnormalities deficient alveolarisation

- Infant conditions of undefined cause

- ILD related to alveolar surfactant region

Non-specific interstitial pneumonia (NSIP) is a form of idiopathic interstitial pneumonia.

Idiopathic interstitial pneumonia (IIP), or noninfectious pneumonia are a class of diffuse lung diseases. These diseases typically affect the pulmonary interstitium, although some also have a component affecting the airways (for instance, Cryptogenic organizing pneumonitis). There are seven recognized distinct subtypes of IIP.

Macrophage-activation syndrome (MAS) is a severe, potentially life-threatening, complication of several chronic rheumatic diseases of childhood. It occurs most commonly with systemic-onset juvenile idiopathic arthritis (SoJIA). In addition, MAS has been described in association with systemic lupus erythematosus (SLE), Kawasaki disease, and adult-onset Still's disease. It is thought to be closely related and pathophysiologically very similar to reactive (secondary) hemophagocytic lymphohistiocytosis (HLH). The incidence of MAS is unknown as there is a wide spectrum of clinical manifestations, and episodes may remain unrecognized.

IPF has been recognized in several breeds of both dogs and cats, and has been best characterized in West Highland White Terriers. Veterinary patients with the condition share many of the same clinical signs as their human counterparts, including progressive exercise intolerance, increased respiratory rate, and eventual respiratory distress.

Prognosis is generally poor.

The cause of IPF is unknown but certain environmental factors and exposures have been shown to increase the risk of getting IPF. Cigarette smoking is the best recognized and most accepted risk factor for IPF, and increases the risk of IPF by about twofold. Other environmental and occupation exposures such as exposure to metal dust, wood dust, coal dust, silica, stone dust, biologic dusts coming from hay dust or mold spores or other agricultural products, and occupations related to farming/livestock have also been shown to increase the risk for IPF. There is some evidence that viral infections may be associated with idiopathic pulmonary fibrosis and other fibrotic lung diseases.

In many cases a trigger is identified, often a viral infection, or a medication. There is uncontrolled activation and proliferation of macrophages, and T lymphocytes, with a marked increase in circulating cytokines, such as IFN-gamma, and GM-CSF. The underlying causative event is unclear, and is the subject of ongoing research. In many cases of MAS, a decreased natural killer cell (NK-cell) function is found.

Interstitial lung disease (ILD), or diffuse parenchymal lung disease (DPLD), is a group of lung diseases affecting the interstitium (the tissue and space around the air sacs of the lungs). It concerns alveolar epithelium, pulmonary capillary endothelium, basement membrane, perivascular and perilymphatic tissues. It may occur when an injury to the lungs triggers an abnormal healing response. Ordinarily, the body generates just the right amount of tissue to repair damage. But in interstitial lung disease, the repair process goes awry and the tissue around the air sacs (alveoli) becomes scarred and thickened. This makes it more difficult for oxygen to pass into the bloodstream. The term ILD is used to distinguish these diseases from obstructive airways diseases.

In children, several unique forms of ILD exist which are specific for the young age groups. The acronym chILD is used for this group of diseases and is derived from the English name, Children’s Interstitial Lung Diseases – chILD.

Prolonged ILD may result in pulmonary fibrosis, but this is not always the case. Idiopathic pulmonary fibrosis is interstitial lung disease for which no obvious cause can be identified (idiopathic), and is associated with typical findings both radiographic (basal and pleural based fibrosis with honeycombing) and pathologic (temporally and spatially heterogeneous fibrosis, histopathologic honeycombing and fibroblastic foci).

In 2013 interstitial lung disease affected 595,000 people globally. This resulted in 471,000 deaths.

Classification can be complex, and the combined efforts of clinicians, radiologists, and pathologists can help in the generation of a more specific diagnosis.

Idiopathic interstitial pneumonia can be subclassified based on histologic appearance into the following patterns:

Usual interstitial pneumonia is the most common type.

In the absence of severe urinary tract obstruction (which generally requires surgery with omental wrapping), treatment is generally with glucocorticoids initially, followed by DMARDs either as steroid-sparing agents or if refractory on steroids. The SERM tamoxifen has shown to improve the condition in various small trials, although the exact mechanism of its action remains unclear.

Associations include:

- Riedel's thyroiditis

- previous radiotherapy

- sarcoidosis

- inflammatory abdominal aortic aneurysm

- drugs

Eosinophilia can be idiopathic (primary) or, more commonly, secondary to another disease. In the Western World, allergic or atopic diseases are the most common causes, especially those of the respiratory or integumentary systems. In the developing world, parasites are the most common cause. A parasitic infection of nearly any bodily tissue can cause eosinophilia.

Diseases that feature eosinophilia as a sign include:

- Allergic disorders

- Asthma

- Hay fever

- Drug allergies

- Allergic skin diseases

- Pemphigus

- Dermatitis herpetiformis

- IgG4-related disease

- Parasitic infections

- Addison's disease and stress-induced suppression of adrenal gland function

- Some forms of malignancy

- Acute lymphoblastic leukemia

- Chronic myelogenous leukemia

- Eosinophilic leukemia

- Clonal eosinophilia

- Hodgkin lymphoma

- Some forms of non-Hodgkin lymphoma

- Lymphocyte-variant hypereosinophilia

- Systemic mastocytosis

- Systemic autoimmune diseases

- Systemic lupus erythematosus

- Kimura disease

- Eosinophilic granulomatosis with polyangiitis

- Eosinophilic fasciitis

- Eosinophilic myositis

- Eosinophilic esophagitis

- Eosinophilic gastroenteritis

- Cholesterol embolism (transiently)

- Coccidioidomycosis (Valley fever), a fungal disease prominent in the US Southwest.

- Human immunodeficiency virus infection

- Interstitial nephropathy

- Hyperimmunoglobulin E syndrome, an immune disorder characterized by high levels of serum IgE

- Idiopathic hypereosinophilic syndrome.

- Congenital disorders

- Hyperimmunoglobulin E syndrome

- Omenn syndrome

- Familial eosinophilia

A number of conditions may cause the appearance of livedo reticularis:

- Cutis marmorata telangiectatica congenita, a rare congenital condition

- Sneddon syndrome – association of livedoid vasculitis and systemic vascular disorders, such as strokes, due to underlying genetic cause

- Idiopathic livedo reticularis – the most common form of livedo reticularis, completely benign condition of unknown cause affecting mostly young women during the winter: It is a lacy purple appearance of skin in extremities due to sluggish venous blood flow. It may be mild, but ulceration may occur later in the summer.

- Secondary livedo reticularis:

- Vasculitis autoimmune conditions:

- Livedoid vasculitis – with painful ulceration occurring in the lower legs

- Polyarteritis nodosa

- Systemic lupus erythematosus

- Dermatomyositis

- Rheumatoid arthritis

- Lymphoma

- Pancreatitis

- Chronic pancreatitis

- Tuberculosis

- Drug-related:

- Adderall (side effect)

- Amantadine (side effect)

- Bromocriptine (side effect)

- Beta IFN treatment, "i.e." in multiple sclerosis

- Livedo reticularis associated with rasagiline

- Methylphenidate and dextroamphetamine-induced peripheral vasculopathy

- Gefitinib

- Obstruction of capillaries:

- Cryoglobulinaemia – proteins in the blood that clump together in cold conditions

- Antiphospholipid syndrome due to small blood clots

- Hypercalcaemia (raised blood calcium levels which may be deposited in the capillaries)

- Haematological disorders of polycythaemia rubra vera or thrombocytosis (excessive red cells or platelets)

- Infections (syphilis, tuberculosis, Lyme disease)

- Associated with acute renal failure due to cholesterol emboli status after cardiac catheterization

- Arteriosclerosis (cholesterol emboli) and homocystinuria (due to Chromosome 21 autosomal recessive Cystathionine beta synthase deficiency)

- Intra-arterial injection (especially in drug addicts)

- Ehlers-Danlos syndrome – connective tissue disorder, often with many secondary conditions, may be present in all types

- Pheochromocytoma

- Livedoid vasculopathy and its association with factor V Leiden mutation

- FILS syndrome (polymerase ε1 mutation in a human syndrome with facial dysmorphism, immunodeficiency, livedo, and short stature)

- Primary hyperoxaluria, oxalosis (oxalate vasculopathy)

- Cytomegalovirus infection (very rare clinical form, presenting with persistent fever and livedo reticularis on the extremities and cutaneous necrotizing vasculitis of the toes)

- Generalized livedo reticularis induced by silicone implants for soft tissue augmentation

- As a rare skin finding in children with Down syndrome

- Idiopathic livedo reticularis with polyclonal IgM hypergammopathy

- CO angiography (rare, reported case)

- A less common skin lesion of Churg-Strauss syndrome

- Erythema nodosum-like cutaneous lesions of sarcoidosis showing livedoid changes in a patient with sarcoidosis and Sjögren's syndrome

- Livedo vasculopathy associated with IgM antiphosphatidylserine-prothrombin complex antibody

- Livedo vasculopathy associated with plasminogen activator inhibitor-1 promoter homozygosity and prothrombin G20210A heterozygosity

- As a first sign of metastatic breast carcinoma (very rare)

- Livedo reticularis associated with renal cell carcinoma (rare)

- Buerger's disease (as an initial symptom)

- As a rare manifestation of Graves hyperthyroidism

- Associated with pernicious anaemia

- Moyamoya disease (a rare, chronic cerebrovascular occlusive disease of unknown cause, characterized by progressive stenosis of the arteries of the circle of Willis leading to an abnormal capillary network and resultant ischemic strokes or cerebral hemorrhages)

- Associated with the use of a midline catheter

- Familial primary cryofibrinogenemia.

The epidemiology of Idiopathic sclerosing mesenteritis disease is extremely rare and has only been diagnosed in about an estimated 300 patients worldwide to date (as of 2014), it is probably under diagnosed.

It can occur in children.

IOI or orbital pseudotumor is the second most common cause of exophthalmos following Grave’s orbitopathy and the third most common orbital disorder following thyroid orbitopathy and lymphoproliferative disease accounting for 5–17.6% of orbital disorders, There is no age, sex, or race predilection, but it is most frequently seen in middle-aged individuals. Pediatric cases account for about 17% of all cases of IOI.

Bronchomalacia can best be described as a birth defect of the bronchus in the respiratory tract. Congenital malacia of the large airways is one of the few causes of irreversible airways obstruction in children, with symptoms varying from recurrent wheeze and recurrent lower airways infections to severe dyspnea and respiratory insufficiency. It may also be acquired later in life due to chronic or recurring inflammation resulting from infection or other airway disease.

The exact cause of IOI is unknown, but infectious and immune-mediated mechanisms have been proposed. Several studies have described cases where onset of orbital pseudotumor was seen simultaneously or several weeks after upper respiratory infections. Another study by Wirostko et al. proposes that organisms resembling Mollicutes cause orbital inflammation by destroying the cytoplasmic organelles of parasitized cells.

Orbital pseudotumor has also been observed in association with Crohn’s disease, systemic lupus erythematosus, rheumatoid arthritis, diabetes mellitus, myasthenia gravis, and ankylosing spondylitis all of which strengthen the basis of IOI being an immune-mediated disease. Response to corticosteroid treatment and immunosuppressive agents also support this idea.

Trauma has also been seen to precede some cases of orbital pseudotumor. However, one study by Mottow-Lippe, Jakobiec, and Smith suggests that the release of circulating antigens caused by local vascular permeability triggers an inflammatory cascade in the affected tissues.

Although these mechanisms have been postulated as possible causes of IOI, their exact nature and relationships to the condition still remain unclear.

The overwhelming majority of neutrophilic eccrine hidradenitis (NEH) is seen in people with cancer, especially leukaemia, who receive chemotherapy with a cytotoxic drug. These include: Bleomycin, chlorambucil, cyclophosphamide, cytarabine, doxorubicin, lomustine, mitoxantrone, topotecan, and vincristine.

NEH was first described in 1982 in a patient with acute myeloid leukaemia (AML) who had received cytarabine as chemotherapy.

Cancer itself, infections, and other medicinal drugs also can lead to NEH. NEH has been reported in patients with cancer who have not received any form of chemotherapy (i.e., as a paraneoplastic syndrome), in patients with HIV and/or AIDS, and after the use of paracetamol (acetaminophen). Also the use of targeted agents can lead to NEH, e.g. imatinib, a tyrosine kinase inhibitor.

NEH has also been described without any known reason (idiopathic cases), including idiopathic cases in children.

The exact cause of NEH is unknown. In patients receiving chemotherapy, it has been postulated that a high concentration of the cytotoxic drug in sweat has a direct toxic effect on the eccrine glands.

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

Pulmonary fibrosis may be a secondary effect of other diseases. Most of these are classified as interstitial lung diseases. Examples include autoimmune disorders, viral infections and bacterial infection like tuberculosis which may cause fibrotic changes in both lungs upper or lower lobes and other microscopic injuries to the lung. However, pulmonary fibrosis can also appear without any known cause. In this case, it is termed "idiopathic". Most idiopathic cases are diagnosed as "idiopathic pulmonary fibrosis". This is a diagnosis of exclusion of a characteristic set of histologic/pathologic features known as usual interstitial pneumonia (UIP). In either case, there is a growing body of evidence which points to a genetic predisposition in a subset of patients. For example, a mutation in surfactant protein C (SP-C) has been found to exist in some families with a history of pulmonary fibrosis.

Diseases and conditions that may cause pulmonary fibrosis as a secondary effect include:

- Inhalation of environmental and occupational pollutants, such as metals in asbestosis, silicosis and exposure to certain gases. Coal miners, ship workers and sand blasters among others are at higher risk.

- Hypersensitivity pneumonitis, most often resulting from inhaling dust contaminated with bacterial, fungal, or animal products.

- Cigarette smoking can increase the risk or make the illness worse.

- Some typical connective tissue diseases such as rheumatoid arthritis, SLE and scleroderma

- Other diseases that involve connective tissue, such as sarcoidosis and granulomatosis with polyangiitis.

- Infections

- Certain medications, e.g. amiodarone, bleomycin (pingyangmycin), busulfan, methotrexate, apomorphine, and nitrofurantoin

- Radiation therapy to the chest