Senile osteoporosis has been recently recognized as a geriatric syndrome with a particular pathophysiology. There are different classification of osteoporosis: primary, in which bone loss is a result of aging and secondary, in which bone loss occurs from various clinical and lifestyle factors. Primary, or involuntary osteoporosis, can further be classified into Type I or Type II. Type I refers to postmenopausal osteoporosis and is caused by the deficiency of estrogen. While senile osteoporosis is categorized as an involuntary, Type II, and primary osteoporosis, which affects both men and women over the age of 70 years. It is accompanied by vitamin D deficiency, bodys failure to absorb calcium, and increased parathyroid hormone.Research over the years has shown that senile osteoporosis is the product of a skeleton in an advanced stage of life and can be caused by a deficiency caused by calcium. However, physicians are also coming to the conclusion that multiple mechanisms in the development stages of the disease interact together resulting in an osteoporotic bone, regardless of age. Still, elderly people make up the fastest growing population in the world. As bone mass declines with age, the risk of fractures increases. Annual incidence of osteoporotic fractures is more than 1.5 million in the US and notably 20% of people die during the first year after a hip fracture.It costs the US health system around $17 billion annually, with the cost projecting to $50 billion by 2040.
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.