Keshan disease is a congestive cardiomyopathy caused by a combination of dietary deficiency of selenium and the presence of a mutated strain of Coxsackievirus, named after Keshan County of Heilongjiang province, Northeast China, where symptoms were first noted. These symptoms were later found prevalent in a wide belt extending from northeast to southwest China, all due to selenium-deficient soil. The disease peaked in 1960–1970, killing thousands of people.Often fatal, the disease affects children and women of child-bearing age, characterized by heart failure and pulmonary edema. Over decades, supplementation with selenium reduced this condition.It had been linked to the coxsackie B virus. Current research suggests that the lack of selenium results in a more virulent strain of the coxsackievirus becoming the dominant viral species present in the population of virus, but the mechanism of this selection event is unclear.Keshan disease can also lead to higher rates of cancer, cardiovascular disease, hypertension, and strokes. In addition, an individual can experience eczema, psoriasis, arthritis, cataracts, alcoholism, and infections. Signs and symptoms
Cardiac arrythmias,dizziness,fast breathing,shortness of breath(PULMONARY EDEMA)

Diagnosis
Prevention
It is hard to consider Keshan disease extremely preventable because the only way to ensure that the individual is getting enough selenium would be to test the soil in the area. However, one way that selenium intake can be improved is to increase intake of foods that are rich with selenium. Examples include Brazil nuts, onions, canned tuna, beef, cod, turkey, chicken breast, enriched pasta, egg, cottage cheese, oatmeal, white or brown rice, and garlic.
Blood and urine samples are collected for evaluation of kidney and liver function and determination of the presence of a monoclonal protein. Imaging studies such as echocardiography and an ultrasound of the abdomen will be performed. A CT scan, magnetic resonance imaging (MRI) or positron emission tomography (PET) may also be indicated. In patients with LCDD, a biopsy of the affected organ will show deposited light chains. A bone marrow biopsy will be done in order to rule out multiple myeloma. Treatment
Decreasing production of the organ-damaging light chains is the treatment goal. Options include chemotherapy using bortezomib, autologous stem cell transplantation, immunomodulatory drugs, and kidney transplant.There is no standard treatment for LCDD. High-dose melphalan in conjunction with autologous stem cell transplantation has been used in some patients. A regimen of bortezomib and dexamethasone has also been examined. Prognosis
The median time to progression to end stage renal disease is 2.7 years. After 5 years, about 37% of patients with LCDD are alive and do not have end stage renal disease. References
External links
National Institutes of Health Genetic and Rare Diseases Information Center
Emedicine