Surgical options for tertiary hyperparathyroidism include subtotal parathyroidectomy (three and one half of total tissue) and total parathyroidectomy with autotransplatation of resected tissue. Outcomes from surgery are generally favourable and a return to normalised blood calcium levels and parathyroid function is seen. History
In 1962, Dr C.E Dent reported that autonomous hyperparathyroidism may result from malabsorption syndromes and chronic kidney disease. The term tertiary hyperparathyroidism was first used in 1963 by Dr Walter St. Gaur to describe a case reported on at Massachusetts General hospital. This case involved a patient who had presented with autonomous parathyroid adenoma causing hypercalcemia with a background of parathyroid hyperplasia. Further reports were recorded in 1964, 65 and 67 of suspected tertiary hyperparathyroidism.In 1968 Davies, Dent and Watson produced a historic case study where they reviewed 200 cases of previously diagnosed primary hyperparathyroidism and found the majority of these cases should be reclassified as tertiary. These were important findings as it allowed an understanding into distinguishing features of primary, secondary and tertiary hyperparathyroidism which then allows appropriate medical treatment.It is now understood that tertiary hyperparathyroidism is defined as the presence of hypercalcemia, hyperphosphatemia and parathyroid hormone due to terminally biased parathyroid-bone-kidney feedback loop. Although there is still conjecture as to whether tertiary hyperparathyroidism is also due to adenomatous growth or hyperplasia it is clear that tertiary hyperparathyroidism presents with some form of tissue enlargement in all four parathyroid glands. See also
Hyperparathyroidism
Primary hyperparathyroidism
Secondary hyperparathyroidism

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Ranolazine also exhibits its effects on the delayed rectifier current (hERG/IKr potassium channels), it readily stimulates myogenesis, it reduces a pro-oxidant inflammation/oxidative condition, and activates the calcium signaling pathway.Ranolazine prolongs the action potential duration, with corresponding QT interval prolongation on electrocardiography, blocks the INa current, and prevents calcium overload caused by the hyperactive INa current, thus it stabilizes the membrane and reducing excitability. History
Syntex Inc. originally began developing ranolazine in 1985 and 61 studies were completed from then until 1994. Afterwards, Phase 2 studies were done however it was found that the formulation did not result in adequate plasma concentrations of drug. It is due to this that the sustained-release (SR) formulation of ranolazine was created.Roche acquired Syntex in 1994 In 1996, CV Therapeutics licensed the North American and European rights to ranolazine from Syntex, a subsidiary of Roche, which had discovered the drug and had developed it through Phase II trials in angina. In 2006, CV Therapeutics acquired the remaining worldwide rights to ranolazine from Roche. In 2008 CV Therapeutics exclusively licensed rights for ranolazine in Europe and some other countries to Menarini. In 2009, Gilead acquired CV Therapeutics. In 2013 Gilead expanded the partnership with Menarini to include additional countries, including those in Asia. Society and culture
Legal status
Ranolazine was approved by the FDA in January 2006, for the treatment of patients with chronic angina as a second-line treatment in addition to other drugs. In 2007 the label was updated to make ranolazine a first-line treatment, alone or with other drugs.