Tertiary hyperparathyroidism is a condition involving the overproduction of the hormone, parathyroid hormone, produced by the parathyroid glands. The parathyroid glands are involved in monitoring and regulating blood calcium levels and respond by either producing or ceasing to produce parathyroid hormone. Anatomically, these glands are located in the neck, para-lateral to the thyroid gland, which does not have any influence in the production of parathyroid hormone. Parathyroid hormone is released by the parathyroid glands in response to low blood calcium circulation. Persistent low levels of circulating calcium are thought to be the catalyst in the progressive development of adenoma, in the parathyroid glands resulting in primary hyperparathyroidism. While primary hyperparathyroidism is the most common form of this condition, secondary and tertiary are thought to result due to chronic kidney disease (CKD). Estimates of CKD prevalence in the global community range from 11 to 13% which translate to a large portion of the global population at risk of developing tertiary hyperparathyroidism. Tertiary hyperparathyroidism was first described in the late 1960s and had been misdiagnosed as primary prior to this. Unlike primary hyperparathyroidism, the tertiary form presents as a progressive stage of resolved secondary hyperparathyroidism with biochemical hallmarks that include elevated calcium ion levels in the blood, hypercalcemia, along with autonomous production of parathyroid hormone and adenoma in all four parathyroid glands. Upon diagnosis treatment of tertiary hyperparathyroidism usually leads to a surgical intervention. Presentation
Symptoms in tertiary hyperparathyroidism are generally those seen in relation to elevated blood calcium levels.
Earl de Grey who presented four reports on British soldiers with these symptoms between 1864 and 1868, and attributed them to the heavy weight of military equipment being carried in knapsacks which were tightly strapped to the chest in a manner which constricted the action of the heart. Also in 1864, Henry Harthorme observed soldiers in the American Civil War who had similar symptoms which were attributed to “long-continued overexertion, with deficiency of rest and often nourishment”, and indefinite heart complaints were attributed to lack of sleep and bad food. In 1870 Arthur Bowen Myers of the Coldstream Guards also regarded the accoutrements as the cause of the trouble, which he called neurocirculatory asthenia and cardiovascular neurosis.J. M. Da Costas study of 300 soldiers reported similar findings in 1871 and added that the condition often developed and persisted after a bout of fever or diarrhoea. He also noted that the pulse was always greatly and rapidly influenced by position, such as stooping or reclining. A typical case involved a man who was on active duty for several months or more and contracted an annoying bout of diarrhoea or fever, and then, after a short stay in hospital, returned to active service. The soldier soon found that he could not keep up with his comrades in the exertions of a soldiers life as previously, because he would get out of breath, and would get dizzy, and have palpitations and pains in his chest, yet upon examination some time later he appeared generally healthy.