Purpura, arthritis and abdominal pain are known as the "classic triad" of Henoch–Schönlein purpura. Purpura occur in all cases, joint pains and arthritis in 80%, and abdominal pain in 62%. Some include gastrointestinal hemorrhage as a fourth criterion; this occurs in 33% of cases, sometimes, but not necessarily always, due to intussusception. The purpura typically appear on the legs and buttocks, but may also be seen on the arms, face and trunk. The abdominal pain is colicky in character, and may be accompanied by nausea, vomiting, constipation or diarrhea. There may be blood or mucus in the stools. The joints involved tend to be the ankles, knees, and elbows, but arthritis in the hands and feet is possible; the arthritis is nonerosive and hence causes no permanent deformity. Forty percent have evidence of kidney involvement, mainly in the form of hematuria (blood in the urine), but only a quarter will have this in sufficient quantities to be noticeable without laboratory tests. Problems in other organs, such as the central nervous system (brain and spinal cord) and lungs may occur, but is much less common than in the skin, bowel and kidneys.

Of the 40% of patients who develop kidney involvement, almost all have evidence (visible or on urinalysis) of blood in the urine. More than half also have proteinuria (protein in the urine), which in one eighth is severe enough to cause nephrotic syndrome (generalised swelling due to low protein content of the blood). While abnormalities on urinalysis may continue for a long time, only 1% of all HSP patients develop chronic kidney disease. Hypertension (high blood pressure) may occur. Protein loss and high blood pressure, as well as the features on biopsy of the kidney if performed, may predict progression to advanced kidney disease. Adults are more likely than children to develop advanced kidney disease.

Henoch–Schönlein purpura (HSP), also known as IgA vasculitis, anaphylactoid purpura, purpura rheumatica, and Schönlein–Henoch purpura, is a disease of the skin, mucous membranes, and sometimes other organs that most commonly affects children. In the skin, the disease causes palpable purpura (small, raised areas of bleeding underneath the skin), often with joint pain and abdominal pain. With kidney involvement, there may be a loss of small amounts of blood and protein in the urine (hematuria and proteinuria), but this usually goes unnoticed; in a small proportion of cases, the kidney involvement proceeds to chronic kidney disease. HSP is often preceded by an infection, such as a throat infection.

HSP is a systemic vasculitis (inflammation of blood vessels) and is characterized by deposition of immune complexes containing the antibody immunoglobulin A (IgA); the exact cause for this phenomenon is unknown. In children it usually resolves within several weeks and requires no treatment apart from symptom control, but may relapse in a third of cases and cause irreversible kidney damage in about one in a hundred cases. In adults the prognosis is different than in children. The average duration of cutaneous lesions is 27.9 months. And for many it tends to be relapsing-remitting over a long period of time rather than self-limiting and there tend to be more complications.

Patients usually present with systemic symptoms with single or multiorgan dysfunction. Common (and nonspecific) complaints include fatigue, weakness, fever, arthralgias, abdominal pain, hypertension, renal insufficiency, and neurologic dysfunction. The following symptoms should raise a strong suspicion of a vasculitis:

- Mononeuritis multiplex. Also known as asymmetric polyneuropathy, in a non-diabetic this is suggestive of vasculitis.

- Palpable purpura. If patients have this in isolation, it is most likely due to cutaneous leukocytoclastic vasculitis. If the purpura is in combination with systemic organ involvement, it is most likely to be Henoch-Schonlein purpura or microscopic polyarteritis.

- Pulmonary-renal syndrome. Individuals who are coughing up blood and have kidney involvement are likely to have granulomatosis with polyangiitis, microscopic polyangiitis, or anti-GBM disease (Goodpasture's syndrome).

Hypersensitivity vasculitis (allergic vasculitis). Usually due to a hypersensitivity reaction to a known drug. Drugs most commonly implicated are penicillin, sulphonamides and thiazide diuretics. There is presence of skin vaculitis with palpable petechiae or purpura. Biopsy of these lesions reveal inflammation of the small vessels, termed leukocytoclastic vasculitis, which is most prominent in postcapillary venules. At least 3 out of 5 criteria yields sensitivity and specificity of 71 and 84%:

- age > 16

- use of possible triggering drug in relation to symptoms

- palpable purpura

- maculopapular rash

- skin biopsy showing neutrophils around vessel

IgA vasculitis (IgAV; formerly known as Henoch-Schonlein purpura). Systemic vasculitis due to tissue deposition of IgA-containing immune complexes. Biopsy of lesions shows inflammation of small vessels. It is considered a form of hypersensitivity vasculitis but is distinguished by prominent deposits of IgA. This is the most common vasculitis in children. Presence of 3 or more criteria yielded sensitivity of 87% while less than 2 criteria yielded hypersensitivity vasculitis in 74%:

- palpable purpura (usually of buttocks & legs)

- bowel angina

- GI bleed

- hematuria

- onset < 20 years

- no new medications

Essential cryoglobulinemic vasculitis. Most often due to hepatitis C infection, immune complexes of cryoglobulins --- proteins that consists of immunoglobulins and complement and precipitate in the cold while dissolving upon rewarming --- are deposited in walls of capillaries, venules, or arterioles. Therefore, complement will be low with histology showing vessel inflammation with immune deposits.

Amyloid purpura usually occurs above the nipple-line and is found in the webbing of the neck and in the face and eyelids.

Amyloid purpura is a condition marked by bleeding under the skin (purpura) in some individuals with amyloidosis. Its cause is unknown, but coagulation defects caused by amyloid are thought to contribute.

In most cases skin lesions do not cause symptoms, however itching, burning, or pain may occur.

Frequently reported symptoms include mild fever, muscle pain, joint pain, or an overall feeling of discomfort. Additional symptoms depend on the cause of the vasculitis and if other organ systems are involved. For example, if the vasculitis is a manifestation of Henoch-Schönlein purpura, individuals may also experience abdominal pain or blood in the urine.

Initially red to pink, flat spots (formally, "macules") and raised bumps (formally, "papules") may be seen on the skin.

Once fully developed, the classic appearance is "non-blanching, palpable purpura". This appears as deep red to purple spots that feel raised to the touch. Purpura refers to the red-purple discolored spots, while palpable implies that these spots can be felt as raised from the surrounding skin. Additionally, when gently pressed, the color does not fade to a lighter color ("non-blanching"). The red-purple color of the lesions is due to the inflammation in the blood vessels causing red blood cells to escape into the dermis skin layer.

Small fluid-filled blisters (or "vesicles"), pus-filled bumps resembling a pimple (or "pustules"), or shallow ulcers may also develop but are less common.

The location of skin lesions varies but are most commonly found symmetrically below the waist, primarily on the buttocks and legs. Other distributions include localized areas on the upper body or over several areas of the body.

With treatment, the lesions typically resolve in weeks to months and leave behind flat spots that are darker than the surrounding skin. (see "Postinflammatory hyperpigmentation" on "Hyperpigmentation")

A portion of cases may be persistent or recurrent. This tends to occur when the vasculitis is associated with chronic conditions such as connective tissue diseases.

Possible symptoms include:

- General symptoms: Fever, weight loss

- Skin: Palpable purpura, livedo reticularis

- Muscles and joints: Myalgia or myositis, arthralgia or arthritis

- Nervous system: Mononeuritis multiplex, headache, stroke, tinnitus, reduced visual acuity, acute visual loss

- Heart and arteries: Myocardial infarction, hypertension, gangrene

- Respiratory tract: Nose bleeds, bloody cough, lung infiltrates

- GI tract: Abdominal pain, bloody stool, perforations

- Kidneys: Glomerulonephritis

Signs and symptoms due to the cryoglobulins of type I disease reflect the hyperviscosity and deposition of cryoglobulins within the blood vessels which reduce or stop blood perfusion to tissues. These events occur particularly in cases where blood cryoglobulin levels of monoclonal IgM are high in patients with IgM MGUS, smoldering Waldenström's macroglobulinemia, or Waldenström's macroglobulinemia and in uncommon cases where the levels of monoclonal IgA, IgG, free κ light chains, or free λ light chains are extremely high in patients with non-IgM MGUS, non-IgM smoldering multiple myeloma, or multiple myeloma. The interruption of blood flow to neurological tissues can cause symptoms of confusion, headache, hearing loss, and peripheral neuropathy. Interruption of blood flow to other tissues in type I disease can cause cutaneous manifestations of purpura, acrocyanosis, necrosis, ulcers, and livedo reticularis; spontaneous nose bleeds, joint pain, membranoproliferative glomerulonephritis; and cardiovascular disturbances such as shortness of breath, hypoxemia, and congestive heart failure.

The signs and symptoms in the increasingly rare cases of cryoglobulinemic disease that cannot be attributed to an underlying disease generally resemble those of patients suffering Type II and III (i.e. mixed) cryoglobulinemic disease.

Drug-induced purpura is a skin condition that may be related to platelet destruction, vessel fragility, interference with platelet function, or vasculitis.

By tradition, the term idiopathic thrombocytopenic purpura is used when the cause is idiopathic. However, most cases are now considered to be immune-mediated.

Another form is thrombotic thrombocytopenic purpura.

Thrombocytopenic purpura are purpura associated with a reduction in circulating blood platelets which can result from a variety of causes, such as kaposi sarcoma.

Treat the underlying disease . Eg for wegner's treatment is steroids and cyclophosphamide.

The clinical presentation of TMA, although dependent on the type, typically includes: fever, microangiopathic hemolytic anemia (see schistocytes in a blood smear), renal failure, thrombocytopenia and neurological manifestations. Generally, renal complications are particularly predominant with Shiga-toxin-associated hemolytic uremic syndrome (STx-HUS) and atypical HUS, whereas neurologic complications are more likely with TTP. Individuals with milder forms of TTP may have recurrent symptomatic episodes, including seizures and vision loss. With more threatening cases of TMA, and also as the condition progresses without treatment, multi-organ failure or injury is also possible, as the hyaline thrombi can spread to and affect the brain, kidneys, heart, liver, and other major organs.

Vasculitis can be classified by the cause, the location, the type of vessel or the size of vessel.

- "Underlying cause". For example, the cause of syphilitic aortitis is infectious (aortitis simply refers to inflammation of the aorta, which is an artery.) However, the causes of many forms of vasculitis are poorly understood. There is usually an immune component, but the trigger is often not identified. In these cases, the antibody found is sometimes used in classification, as in ANCA-associated vasculitides.

- "Location of the affected vessels". For example, ICD-10 classifies "vasculitis limited to skin" with skin conditions (under "L"), and "necrotizing vasculopathies" (corresponding to systemic vasculitis) with musculoskeletal system and connective tissue conditions (under "M"). Arteritis/phlebitis on their own are classified with circulatory conditions (under "I").

- "Type or size of the blood vessels" that they predominantly affect. Apart from the arteritis/phlebitis distinction mentioned above, vasculitis is often classified by the caliber of the vessel affected. However, there can be some variation in the size of the vessels affected.

According to the size of the vessel affected, vasculitis can be classified into:

- Large vessel: Polymyalgia rheumatica, Takayasu's arteritis, Temporal arteritis

- Medium vessel: Buerger's disease, Kawasaki disease, Polyarteritis nodosa

- Small vessel: Behçet's syndrome, Eosinophilic granulomatosis with polyangiitis, Cutaneous vasculitis, Henoch–Schönlein purpura, Microscopic polyannulomatosis ConditionofSome disorders have vasculitis as their main feature. The major types are given in the table below:

Takayasu's arteritis, polyarteritis nodosa and giant cell arteritis mainly involve arteries and are thus sometimes classed specifically under arteritis.

Furthermore, there are many conditions that have vasculitis as an accompanying or atypical feature, including:

- Rheumatic diseases, such as rheumatoid arthritis, systemic lupus erythematosus, and dermatomyositis

- Cancer, such as lymphomas

- Infections, such as hepatitis C

- Exposure to chemicals and drugs, such as amphetamines, cocaine, and anthrax vaccines which contain the Anthrax Protective Antigen as the primary ingredient.

In pediatric patients varicella inflammation may be followed by vasculitis of intracranial vessels. This condition is called post varicella angiopathy and this may be responsible for arterial ischaemic strokes in children.

Several of these vasculitides are associated with antineutrophil cytoplasmic antibodies. These are:

- Granulomatosis with polyangiitis (formerly known as Wegener's granulomatosis)

- Eosinophilic granulomatosis with polyangiitis (formerly known as Churg-Strauss syndrome)

- Microscopic polyangiitis

Meltzer’s triad describes the classical symptoms suggesting the diagnosis of cryoglobulinaemia of polyclonal CGs seen in essential-, viral-, or connective tissue disease-associated cryoglobulinaemia. The triad consists of:

- palpable purpura

- arthralgia (joint pain)

- weakness.

Purpura fulminans is an acute, often fatal, thrombotic disorder which manifests as blood spots, bruising and discolouration of the skin resulting from coagulation in small blood vessels within the skin and rapidly leads to skin necrosis and disseminated intravascular coagulation.

Palpable purpura is a condition where purpura, which constitutes visible non-blanching hemorrhages, are raised and able to be touched or felt upon palpation. It indicates some sort of vasculitis secondary to a serious disease.

Thrombotic microangiopathy (TMA) is a pathology that results in thrombosis in capillaries and arterioles, due to an endothelial injury. It may be seen in association with thrombocytopenia, anemia, purpura and renal failure.

The classic TMAs are hemolytic uremic syndrome and thrombotic thrombocytopenic purpura. Other conditions with TMA include atypical hemolytic uremic syndrome, disseminated intravascular coagulation, scleroderma renal crisis, malignant hypertension,

antiphospholipid antibody syndrome, and drug toxicities, e.g. calcineurin inhibitor toxicity.

Rheumatoid vasculitis is skin condition that is a typical feature of rheumatoid arthritis, presenting as peripheral vascular lesions that are localized purpura, cutaneous ulceration, and gangrene of the distal parts of the extremities.

Early purpura fulminans lesions look similar to traumatic skin bleeds or purpuric rashes, such as immune thrombocytopenic purpura or thrombotic thrombocytopenic purpura; however, purpura fulminans will rapidly progress to necrosis whereas other purpuric rashes do not. In most cases, differential diagnoses may be distinguished from purpura fulminans by other clinical and laboratory findings.

The initial appearance of purpura fulminans lesions is of well-demarcated erythematous lesions which progress rapidly to develop irregular central areas of blue-black haemorrhagic necrosis. Advancing areas of necrosis are often surrounded by a thin border of erythema that fades into adjacent unaffected skin. Haemorrhage into the necrotic skin causes purpura fulminans lesions to become painful, dark and raised, sometimes with vesicle or blister (bulla) formation.

The distribution of purpura fulminans lesions may be different according to the underlying pathogenesis. Purpura fulminans in severe sepsis typically develops in the distal extremities and progresses proximally or appears as a generalised or diffuse rash affecting the whole body surface. In cases of severe inheritable protein C deficiency, purpura fulminans with disseminated intravascular coagulation manifests within a few hours or days after birth.

Purpura are a common and nonspecific medical sign; however, the underlying mechanism commonly involves one of:

- Platelet disorders (thrombocytopenic purpura)

- Primary thrombocytopenic purpura

- Secondary thrombocytopenic purpura

- Post-transfusion purpura

- Vascular disorders (nonthrombocytopenic purpura)

- Microvascular injury, as seen in senile (old age) purpura, when blood vessels are more easily damaged

- Hypertensive states

- Deficient vascular support

- Vasculitis, as in the case of Henoch–Schönlein purpura

- Coagulation disorders

- Disseminated intravascular coagulation (DIC)

- Scurvy (vitamin C deficiency) - defect in collagen synthesis due to lack of hydroxylation of procollagen results in weakened capillary walls and cells

- Meningococcemia

- Cocaine use with concomitant use of the one-time chemotherapy drug and now veterinary deworming agent levamisole can cause purpura of the ears, face, trunk, or extremities, sometimes needing reconstructive surgery. Levamisole is purportedly a common cutting agent.

- Decomposition of blood vessels including purpura is a symptom of acute radiation poisoning in excess of 2 Grays of radiation exposure. This is an uncommon cause in general, but is commonly seen in victims of nuclear disaster.

Cases of psychogenic purpura are also described in the medical literature, some claimed to be due to "autoerythrocyte sensitization". Other studies suggest the local (cutaneous) activity of tissue plasminogen activator can be increased in psychogenic purpura, leading to substantial amounts of localized plasmin activity, rapid degradation of fibrin clots, and resultant bleeding. Petechial rash is also characteristic of a rickettsial infection.

Cryoglobulinemic purpura is a skin condition characterized by purpura and occurring most frequently in multiple myeloma and macroglobulinemia.