For instance, OHL with HIV/AIDS is a predictor of bad prognosis, (i.e. severe immunosuppression and advanced disease). Epidemiology
Hairy leukoplakia is one of the most common oral manifestations of HIV/AIDS, along with oral candidiasis. It is the most common HIV/AIDS related condition caused by EBV, although EBV associated lymphomas may also occur. OHL mainly occurs in adult males, less commonly in adult females and rarely in children. The incidence rises as the CD4 count falls, and the appearance of OHL may signify progression of HIV to AIDS. A study from 2001 reported a significant decrease in the incidence of some oral manifestations of AIDS (including OHL and necrotizing ulcerative periodontitis), which was attributed to the use of HAART, whilst the incidence of other HIV-associated oral lesions did not alter significantly. History
Oral hairy leukoplakia was discovered by Deborah Greenspan and John S. Greenspan, and in 1985 they identified a connection between it and Epstein-Barr virus (EBV). Oral hairy leukoplakia was first described by Greenspan et al. in 1984, a few years after the start of the AIDS epidemic. A link with OHL was not initially reported as scientific understanding of HIV/AIDS was just beginning to develop at that time. It was subsequently thought to occur only in HIV-infected, homosexual males, however, this is now known to not always be the case. Research directions
It has been suggested that OHL be renamed according to its causative factor as “EBV leucoplakia”. References


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Primary Budd–Chiari syndrome (75%): thrombosis of the hepatic vein
Hepatic vein thrombosis is associated with the following in decreasing order of frequency:Polycythemia vera
Pregnancy
Postpartum state
Use of oral contraceptives
Paroxysmal nocturnal hemoglobinuria
Hepatocellular carcinoma
Lupus anticoagulantsSecondary Budd–Chiari syndrome (25%): compression of the hepatic vein by an outside structure (e.g. a tumor)Budd–Chiari syndrome is also seen in tuberculosis, congenital venous webs and occasionally in inferior vena caval stenosis. Often, the patient is known to have a tendency towards thrombosis, although Budd–Chiari syndrome can also be the first symptom of such a tendency. Examples of genetic tendencies include protein C deficiency, protein S deficiency, the Factor V Leiden mutation, hereditary anti-thrombin deficiency and prothrombin mutation G20210A. An important non-genetic risk factor is the use of estrogen-containing (combined) forms of hormonal contraception. Other risk factors include the antiphospholipid syndrome, aspergillosis, Behçets disease, dacarbazine, pregnancy, and trauma.Many patients have Budd–Chiari syndrome as a complication of polycythemia vera (myeloproliferative disease of red blood cells). People who have paroxysmal nocturnal hemoglobinuria (PNH) appear to be especially at risk for Budd–Chiari syndrome, more than other forms of thrombophilia: up to 39% develop venous thromboses, and 12% may acquire Budd-Chiari.A related condition is veno-occlusive disease, which occurs in recipients of bone marrow transplants as a complication of their medication. Although its mechanism is similar, it is not considered a form of Budd–Chiari syndrome.Other toxicologic causes of veno-occlusive disease include plant & herbal sources of pyrrolizidine alkaloids such as Borage, Boneset, Coltsfoot, Tu-san-chi, Comfrey, Heliotrope (sunflower seeds), Gordolobo, Germander, and Chaparral.