Secondary TTP is diagnosed when the patient's history mentions one of the known features associated with TTP. It comprises about 40% of all cases of TTP. Predisposing factors are:

- Cancer

- Bone marrow transplantation

- Pregnancy

- Medication use:

- Antiviral drugs (acyclovir)

- Certain chemotherapy medications such as gemcitabine and mitomycin C

- Quinine

- Oxymorphone

- Quetiapine

- Bevacizumab

- Sunitinib

- Platelet aggregation inhibitors (ticlopidine, clopidogrel, and prasugrel)

- Immunosuppressants (ciclosporin, mitomycin, tacrolimus/FK506, interferon-α)

- Hormone altering drugs (estrogens, contraceptives, hormone replacement therapy)

- HIV-1 infection

The mechanism of secondary TTP is poorly understood, as ADAMTS13 activity is generally not as depressed as in idiopathic TTP, and inhibitors cannot be detected. Probable etiology may involve, at least in some cases, endothelial damage, although the formation of thrombi resulting in vessel occlusion may not be essential in the pathogenesis of secondary TTP. These factors may also be considered a form of secondary aHUS; patients presenting with these features are, therefore, potential candidates for anticomplement therapy.

The mortality rate is around 95% for untreated cases, but the prognosis is reasonably favorable (80–90% survival) for patients with idiopathic TTP diagnosed and treated early with plasmapheresis.

Patients with cold agglutinin disease should include good sources of folic acid, such as fresh fruits and vegetables, in their diet. Activities for these individuals should be less strenuous than those for healthy people, particularly for patients with anemia. Jogging in the cold could be very hazardous because of the added windchill factor.

A hematologist-oncologist working in collaboration with a blood banker is helpful in complicated cases of cold agglutinin disease.

Careful planning and coordination with multiple personnel are needed if patients are to undergo a procedure during which their body temperature could fall.

Since the first description of cryoglobulinemia in association with the clinical triad of skin purpura, joint pain, and weakness by Meltzer et al in 1967, the percentage of cryoglobulinemic diseases described as essential cryoglobulinemia or idiopathic cryoglobulinemia, that is cryoglobulinemic disease that is unassociated with an underlying disorder, has fallen. Currently most cases of this disease are found to be associated with premalignant, malignant, infectious, or autoimmune disorders that are the known or presumed causes for the production of cryoglobulins. This form of non-essential or non-idiopathic cryoglobulinemic disease is classically grouped into three types according to the Brouet classification. The classification distinguishes three subtypes of cryoglobulinemic diseases based on two factors, the class of immunoglobulins in the cryoglobulin and the association of the cryoglobulinemic disease with other disorder. The following table lists these three types of cryoglobulenmic disease, characterized on the monoclonal immunoglobulin(s) comprising the involved cryoglobulin, percentage of total cryoglobulinemic disease cases, and class of disorders associated for each type.

The monoclonal or polyclonal IgM proteins involved in Types II and III cryoglobulinemic disease have rheumatoid factor activity. That is, they bind to polyclonal immunoglobulins, activate the blood Complement system, and thereby form tissue deposits that contain IgM, IgG (or, rarely, IgA), and components of the complement system, including in particular complement component 4. The vascular deposition of these types of cryoglobulin-containing immune complexes and complement can cause a clinical syndrome of cutaneous small-vessel vasculitis characterized by systemic vasculitis and inflammation termed cryoglobulinemic vasculitis. Accordingly type II and type III cryoglobulonemic disease is often grouped together and referred to as mixed cryoglobulinemia or mixed cryoglobulinemic disease. The monoclonal IgM involved in Type I cryoglobulinemic diseases lacks rheumatoid factor activity.

More recent high resolution protein electrophoresis methods have detected a small monoclonal immunoglobulin component in type III cryoglobulins and/or a micro-heterogeneous composition of oligo-clonal (i.e. more than one monoclonal) immunoglobulin components or immunoglobulins with structures that do not fit into any classifications in the cryoglobulins of ~10% of type II and III disease cases. It has been proposed that these cases be termed an intermediate type II-III variant of cryoglobulinemic disease and that some of the type III cases associated with the expression of low levels of a one or more isotypes of circulating monoclonal immunoglobulin(s) are in transition to type II disease.

Cryoglobulinemia, cryoglobulinaemia, or cryoglobulinemic disease, is a medical condition in which the blood contains large amounts of cryoglobulins – proteins (mostly immunoglobulins themselves) that become insoluble at reduced temperatures. This should be contrasted with cold agglutinins, which cause agglutination of red blood cells.

Cryoglobulins typically precipitate at temperatures below normal body temperatureand will dissolve again if the blood is heated. The precipitated clump can block blood vessels and cause toes and fingers to become gangrenous. While this disease is commonly referred to as cryoglobulinemia in the medical literature, it is better termed cryoglobulinemic disease for two reasons: 1) cryoglobulinemia is also used to indicate the circulation of (usually low levels of) cryoglobulins in the absence of any symptoms or disease and 2) healthy individuals can develop transient asymptomatic cryoglobulinemia following certain infections.

In contrast to these benign instances of circulating cryoglobulins, cryoglobulinemic disease involves the signs and symptoms of precipitating cryoglobulins and is commonly associated with various pre-malignant, malignant, infectious, or autoimmune diseases that are the underlying cause for production of the cryoglobulins.

Macrovascular disease is a disease of any large ("macro") blood vessels in the body. It is a disease of the large blood vessels, including the coronary arteries, the aorta, and the sizable arteries in the brain and in the limbs.

This sometimes occurs when a person has had diabetes for an extended period of time. Fat and blood clots build up in the large blood vessels and stick to the vessel walls.

Three common macrovascular diseases are coronary disease (in the heart), cerebrovascular disease (in the brain), and peripheral vascular disease (in the limbs)

Macrovascular disease (macroangiopathy) refers to atherosclerosis. Atherosclerosis is a form of arteriosclerosis (thickening and hardening of arterial walls), characterized by plaque deposits of lipids, fibrous connective tissue, calcium, and other blood substances. Atherosclerosis, by definition, affects only medium and large arteries (excluding arterioles).

Macrovascular disease is associated with the development of coronary artery disease, peripheral vascular disease, brain attack (stroke), and increased risk of infection. Type 2 diabetes is more closely associated with macrovascular diseases than type 1 diabetes. Peripheral vascular disease and increased risk of infection have important implications in the care of the acutely ill patient.

Overall, hemoglobin C disease is one of the more benign hemoglobinopathies. Mild-to-moderate reduction in RBC lifespan may accompany from mild hemolytic anemia. Individuals with hemoglobin C disease have sporadic episodes of musculoskeletal (joint) pain. People with hemoglobin C disease can expect to lead a normal life.

Hemoglobin C gene is found in 2-3% of US African-Americans while 8% of US African \-Americans have hemoglobin S (Sickle) gene. Thus Hemoglobin SC disease is significantly more common than Hemoglobin CC disease. Hemoglobin C is found in areas of West Africa, such as Nigeria, where Yorubas live.

About 1 out of every 40 African-Americans has hemoglobin C trait. The trait also affects people whose ancestors came from Italy, Greece, Africa, Latin America, and the Caribbean region. However, it is possible for a person of any race or nationality to have hemoglobin C trait. In terms of geographic distribution, the hemoglobin C allele is found at the highest frequencies in West Africa, where it has been associated with protection against malaria. Hemoglobin C disease is present at birth, though some cases may not be diagnosed until adulthood. Both sexes, male and female, are affected equally.

Vascular disease is a class of diseases of the blood vessels – the arteries and veins of the circulatory system of the body. It is a subgroup of cardiovascular disease. Disorders in this vast network of blood vessels, can cause a range of health problems which can be severe or prove fatal.

There are several types of vascular disease, (which is a subgroup of cardiovascular disease), the signs and symptoms depend on which type, among them are:

- Erythromelalgia - a rare peripheral vascular disease where syndromes includes burning pain, increased temperature, erythema and swelling, of mainly the hands and feet are affected.

- Peripheral artery disease – happens when atheromatous plaques build up in the arteries that supply blood to the arms and legs, plaque causes the arteries to narrow or become blocked.

- Renal artery stenosis - is the narrowing of renal arteries that carry blood to the kidneys from the aorta.

- Buerger's disease – is due to small blood vessels that inflame and swell, vessels then narrow or are blocked by blood clots.

- Raynaud's disease – a rare peripheral vascular disorder of constriction of the peripheral blood vessels, in the fingers and toes when the person is cold.

- Disseminated intravascular coagulation – a widespread activation of clotting in the smaller blood vessels.

- Cerebrovascular disease–a group of vascular diseases that affect brain function.

Minimal change disease is most common in very young children but can occur in older children and adults. It is by far the most common cause of nephrotic syndrome in children between the ages of 1 and 7, accounting for the majority (about 90%) of these diagnoses. Among teenagers who develop nephrotic syndrome, it is caused by minimal change disease about half the time. It can also occur in adults but accounts for less than 20% of adults diagnosed with nephrotic syndrome. Among children less than 10 years of age, boys seem to be more likely to develop minimal change disease than girls. Minimal change disease is being seen with increasing frequency in adults over the age of 80.

People with one or more autoimmune disorders are at increased risk of developing minimal change disease. Having minimal change disease also increases the chances of developing other autoimmune disorders.

Minimal change disease has been called by many other names in the medical literature, including minimal change nephropathy, minimal change nephrosis, minimal change nephrotic syndrome, minimal change glomerulopathy, foot process disease (referring to the foot processes of the podocytes), nil disease (referring to the lack of pathologic findings on light microscopy), nil lesions, lipid nephrosis, and lipoid nephrosis.

With Behçet's disease as an intercurrent disease in pregnancy, the pregnancy does not have an adverse effect on the course of Behçet's disease and may possibly ameliorate its course. Still, there is a substantial variability in clinical course between patients and even for different pregnancies in the same patient. Also, the other way around, Behçet's disease confers an increased risk of pregnancy complications, miscarriage and Cesarean section.

Behçet's can cause male infertility, either as a result of the condition itself or of a side effect of concomitant medication such as Colchicine, which is known to lower sperm count.

Life expectancy with Fabry disease for males was 58.2 years, compared with 74.7 years in the general population, and for females 75.4 years compared with 80.0 years in the general population, according to registry data from 2001 to 2008. The most common cause of death was cardiovascular disease, and most of those had received kidney replacements.

Urticaria is a vascular reaction of the skin characterized by the appearance of wheals, which are firm, elevated swelling of the skin. Angioedema, which can occur alone or with

urticaria, is characterized by a well-defined, edematous swelling that involves subcutaneous tissues, abdominal organs, or upper airway.

- Acquired C1 esterase inhibitor deficiency

- Acute urticaria

- Adrenergic urticaria

- Anaphylaxis

- Aquagenic urticaria

- Cholinergic urticaria

- Chronic urticaria (ordinary urticaria)

- Cold urticaria

- Dermatographism (dermographism)

- Episodic angioedema with eosinophilia (Gleich's syndrome)

- Exercise urticaria (exercise-induced urticaria)

- Galvanic urticaria

- Heat urticaria

- Hereditary angioedema (Quincke's edema)

- Localized heat contact urticaria

- Mast cell-independent urticaria

- Physical urticaria

- Primary cold contact urticaria

- Pressure urticaria (delayed pressure urticaria)

- Reflex cold urticaria

- Schnitzler syndrome

- Secondary cold contact urticaria

- Solar urticaria

- Systemic capillary leak syndrome

- Urticarial allergic eruption

- Urticaria-like follicular mucinosis

- Vibratory angioedema

The syndrome is rare in the United States, Africa and South America, but is common in the Middle East and Asia, suggesting a possible cause endemic to those tropical areas. A theory suggested that past exposure to lethal infectious agents might have fixed the genetic susceptibility factors to Behçet's disease in those area. It is not associated with cancer, and links with tissue-types (which are under investigation) are not certain. It also does not follow the usual pattern for autoimmune diseases. However, one study has revealed a possible connection to food allergies, particularly to dairy products. An estimated 15,000 to 20,000 Americans have been diagnosed with this disease. In the UK, it is estimated to have about 1 case for every 100,000 people. Globally, males are affected more frequently than females. In the United States, more females are affected than males.

In an epidemiologic study, 56 percent of patients with Behçet's disease developed ocular involvement at a mean age of 30. Ocular involvement was the first manifestation of Behçet's disease in 8.6 percent of patients. Ocular Behçet's disease with involvement of the optic nerve is rarely reported. Among patients with ocular Behçet's disease funduscopic findings of optic atrophy, and optic disc paleness have been identified with a frequency of 17.9 percent and 7.4 percent, respectively. Other fundoscopic findings include vascular sheathing (23.7%), retinal hemorrhage (9%), macular edema (11.3%), branch retinal vein occlusion (5.8%), and retinal edema (6.6%). However, optic atrophy was the most significant cause of visual impairment identified in 54 percent of patients with ocular Behçet's disease and permanent visual impairment.

The prevalence of this disease increases from North to South. It follows a more severe course in patients with an early age of onset particularly in patients with eye and gastrointestinal involvement.

Vascular-related cutaneous conditions result from dysfunction of the blood or blood vessels in the dermis, or lymphatics in the subcutaneous tissues.

- Aagenaes syndrome

- Acroangiodermatitis (acroangiodermatitis of Mali, Mali acroangiodermatitis, Pseudo-Kaposi's sarcoma)

- Acute hemorrhagic edema of infancy (acute hemorrhagic edema of childhood, Finkelstein's disease, infantile postinfectious iris-like purpura and edema, medallion-like purpura, purpura en cocarde avec oedema, Seidlmayer syndrome)

- Arterial insufficiency ulcer (ischemic ulcer)

- Arteriosclerosis obliterans

- Bier spots

- Blueberry muffin baby

- Bonnet–Dechaume–Blanc syndrome (Wyburn–Mason syndrome)

- Bullous lymphedema

- Bullous small vessel vasculitis (bullous variant of small vessel vasculitis)

- Calciphylaxis

- Caput succedaneum

- Cholesterol embolus (warfarin blue toe syndrome)

- Cobb syndrome

- Corona phlebectatica

- Cryofibrinogenemic purpura

- Cryoglobulinemic purpura

- Cryoglobulinemic vasculitis

- Cutaneous small-vessel vasculitis (cutaneous leukocytoclastic angiitis, cutaneous leukocytoclastic vasculitis, cutaneous necrotizing venulitis, hypersensitivity angiitis)

- Deep venous thrombosis

- Disseminated intravascular coagulation

- Doucas and Kapetanakis pigmented purpura

- Drug-induced purpura

- Drug-induced thrombocytopenic purpura

- Eczematid-like purpura of Doucas and Kapetanakis

- Epidemic dropsy

- Erythema elevatum diutinum

- Erythromelalgia (acromelalgia, erythermalgia)

- Factitial lymphedema (hysterical edema)

- Fibrinolysis syndrome (defibrinating syndrome, hypofibrinogenemia)

- Food-induced purpura

- Generalized essential telangiectasia (general essential telangiectasia)

- Giant-cell arteritis

- Gougerot–Blum syndrome (pigmented purpuric lichenoid dermatitis, pigmented purpuric lichenoid dermatitis of Gougerot and Blum)

- Harlequin color change

- Hematopoietic ulcer

- Hennekam syndrome (Hennekam lymphangiectasia-lymphedema syndrome, intestinal lymphagiectasia-lymphedema-mental retardation syndrome)

- Henoch–Schönlein purpura (anaphylactoid purpura, purpura rheumatica, Schönlein–Henoch purpura)

- Hereditary hemorrhagic telangiectasia (Osler's disease, Osler–Weber–Rendu disease)

- Idiopathic thrombocytopenic purpura (autoimmune thrombocytopenic purpura, Werlhof's disease)

- IgA vasculitis

- Kawasaki's disease (mucocutaneous lymph node syndrome)

- Levamisole-induced vasculitis

- Lichen aureus (lichen purpuricus)

- Livedo racemosa

- Livedo reticularis

- Livedoid dermatitis (embolia cutis medicamentosa, Nicolau syndrome)

- Livedoid vasculopathy (atrophie blanche, livedo reticularis with summer ulceration, livedoid vasculitis, PURPLE syndrome, segmental hyalinizing vasculitis)

- Lymphedema praecox

- Lymphedema–distichiasis syndrome

- Maffucci syndrome

- Majocchi's disease (purpura annularis telangiectodes, purpura annularis telangiectodes of Majocchi)

- Malignant atrophic papulosis (Degos' disease)

- Marshall–White syndrome

- Meige lymphedema

- Microscopic polyangiitis (microscopic polyarteritis, microscopic polyarteritis nodosa)

- Mondor's disease (Mondor's syndrome of superficial thrombophlebitis)

- Neuropathic ulcer (mal perforans)

- Njolstad syndrome

- Nonne–Milroy–Meige syndrome (hereditary lymphedema, Milroy disease)

- Obstructive purpura

- Orthostatic purpura (stasis purpura)

- Painful bruising syndrome (autoerythrocyte sensitization, Gardner–Diamond syndrome, psychogenic purpura)

- Parkes Weber syndrome

- Paroxysmal hand hematoma (Achenbach syndrome)

- Paroxysmal nocturnal hemoglobinuria

- Polyarteritis nodosa (panarteritis nodosa, periarteritis nodosa)

- Postcardiotomy syndrome

- Perinatal gangrene of the buttock

- Pigmentary purpuric eruptions (progressive pigmentary dermatosis, progressive pigmenting purpura, purpura pigmentosa chronica)

- Postinflammatory lymphedema

- Postmastectomy lymphangiosarcoma (Stewart–Treves syndrome)

- Purpura fulminans (purpura gangrenosa)

- Purpura secondary to clotting disorders

- Purpuric agave dermatitis

- Raynaud phenomenon

- Raynaud's disease (primary Raynaud's phenomenon)

- Reactive angioendotheliomatosis

- Schamberg's disease (progressive pigmentary dermatosis of Schamberg, purpura pigmentosa progressiva, Schamberg's purpura)

- Secondary lymphedema

- Septic thrombophlebitis

- Sinusoidal hemangioma

- Sneddon's syndrome (idiopathic livedo reticularis with cerebrovascular accidents)

- Solar purpura (actinic purpura, senile purpura)

- Stasis dermatitis (congestion eczema, gravitational dermatitis, gravitational eczema, stasis eczema, varicose eczema)

- Superficial thrombophlebitis

- Takayasu arteritis (aortic arch syndrome, pulseless disease)

- Temporal arteritis (cranial arteritis, Horton's disease)

- Thromboangiitis obliterans (Buerger's disease)

- Thrombotic thrombocytopenic purpura (Moschcowitz syndrome)

- Traumatic purpura

- Trousseau's syndrome

- Unilateral nevoid telangiectasia (nevoid telangiectasia)

- Urticarial vasculitis (chronic urticaria as a manifestation of venulitis, hypocomplementemic urticarial vasculitis syndrome, hypocomplementemic vasculitis, unusual lupus-like syndrome)

- Venous insufficiency ulceration

- Waldenström hyperglobulinemic purpura (purpura hyperglobulinemica)

- Waldenström macroglobulinemia

- Wegener granulomatosis

- Yellow nail syndrome (primary lymphedema associated with yellow nails and pleural effusion)

Fabry disease is estimated to occur in one in 40,000 to one in 120,000 live births.

There are no currently known causes of this disease. There are studies currently proposing several theories of the causes which include inflammation of the adipose tissue, nervous system malfunction and endocrine malfunction. None of the theories that are currently proposed have been found viable. Since little is known about Dercum's disease, there are currently no known modes of prevention. Some hypotheses state that maintaining a healthy weight and diet can help prevent Dercum's although it has not been proven.

Dercum's disease can affect people of any gender and of any age. The majority of cases are linked to women between the ages of 45 and 60, who are overweight and postmenopausal. Due to the difficulty of diagnosis of this disease, many cases are underreported or misdiagnosed and it is difficult to understand what part of the population is affected by it the most.

Urbach–Wiethe disease is very rare; there are fewer than 300 reported cases in medical literature. Although Urbach–Wiethe disease can be found worldwide, almost a quarter of reported diagnoses are in South Africa. Many of these are in patients of Dutch, German, and Khoisan ancestry. This high frequency is thought to be due to the founder effect. Due to its recessive genetic cause and the ability to be a carrier of the disease without symptoms, Urbach–Wiethe disease often runs in families. In some regions of South Africa, up to one in 12 individuals may be carriers of the disease. Most of the case studies involving Urbach–Wiethe disease patients involve only one to three cases and these cases are often in the same family. Due to its low incidence, it is difficult to find a large enough number of cases to adequately study the disease.

These differ according to the type of chronic liver disease.

- Excessive alcohol use

- Obesity

- Metabolic syndrome including raised blood lipids

- Health care professionals who are exposed to body fluids and infected blood

- Sharing infected needle and syringes

- Having unprotected sex and multiple sex partners

- Working with toxic chemicals without wearing safety clothes

- Certain prescription medications

The causes of Kyrle disease are unclear and can be idiopathic. The only correlation that has shown light is the frequent association with an underlying disorder, such as, diabetes mellitus, chronic renal failure, hyperlipoproteinemia, hepatic abnormalities, and congestive heart failure. However, there had been cases where Kyrle disease was seen without any conjunction with the previous mentioned disorders. Due to the causes of Kyrle disease is unknown, the best way to prevent the disease is to prevent the disorders that are usually reported in conjunction with it.

Morbidity and mortality range from both extremes as the significance correlate with the underlying systemic disease.

The disease is regarded as extremely rare, with an incidence (new number of cases per year) of one case per million people. The patients are predominantly male (86% in a survey of American patients), although in some countries the rate of women receiving a diagnosis of Whipple's disease has increased in recent years. It occurs predominantly in those of Caucasian ethnicity, suggesting a genetic predisposition in that population.

"T. whipplei" appears to be an environmental organism that is commonly present in the gasterointestinal tract but remains asymptomatic. Several lines of evidence suggest that some defect—inherited or acquired—in immunity is required for it to become pathogenic. The possible immunological defect may be specific for "T. whipplei", since the disease is not associated with a substantially increased risk of other infections.

The disease is usually diagnosed in middle age (median 49 years). Studies from Germany have shown that age at diagnosis has been rising since the 1960s.