Endocrine
1880 CE, Sweden (Ivar Sandström's anatomical description of parathyroid glands in humans)
Hyperparathyroidism was among the last of the major endocrine conditions to be identified, partly because the parathyroid glands themselves were not discovered until the nineteenth century and their function remained obscure for decades afterward. The condition's skeletal and systemic manifestations had been described under various names long before their underlying cause was traced to these tiny glands. The early twentieth century saw an extraordinary series of clinical and surgical discoveries that transformed understanding of calcium regulation and glandular disease.
Historical Narrative
The parathyroid glands were entirely unknown to ancient and medieval medicine, and the condition arising from their overactivity was therefore never conceptualized as a distinct entity in earlier eras. Skeletal deformities associated with what is now understood as long-standing hyperparathyroidism — bones that became soft, bent, and prone to fracture — were documented across centuries under terms including osteomalacia and osteitis fibrosa cystica, conditions attributed variously to nutritional deficiency, humoral imbalance, or constitutional weakness.
The parathyroid glands were first formally described in 1852 by Sir Richard Owen, the British comparative anatomist, who noted small yellowish bodies near the thyroid in his dissection of an Indian rhinoceros. In 1880, Swedish medical student Ivar Sandström provided the first systematic description of these structures in humans, naming them 'glandulae parathyroideae.' Sandström's discovery attracted little immediate clinical attention, and the function of these glands remained a puzzle for subsequent decades.
The critical importance of the parathyroid glands became apparent through a series of surgical accidents in the late nineteenth century. Surgeons removing thyroid glands for goiter began observing that patients sometimes died postoperatively from severe muscle spasms and convulsions — a condition then called tetany. Eugène Gley in France and others demonstrated experimentally in the 1890s that this postoperative tetany resulted from the inadvertent removal of the parathyroid glands alongside the thyroid, establishing that these small structures were essential to life, though precisely what they controlled remained unknown.
The Scottish physiologist John MacCallum and his colleague Carl Voegtlin demonstrated in 1909 that parathyroid removal in animals caused a dramatic fall in blood calcium, and that calcium administration could reverse the resulting convulsions. This breakthrough linked the parathyroid glands directly to calcium regulation for the first time and reframed tetany as a disorder of mineral metabolism rather than simple nerve irritability.
The clinical recognition of hyperparathyroidism — excess parathyroid activity rather than deficiency — came through a celebrated case in Vienna. In 1925, surgeon Felix Mandl operated on a tram conductor named Albert Jahne who had suffered years of progressive bone disease and multiple fractures consistent with osteitis fibrosa cystica. Mandl removed an enlarged parathyroid gland and the patient experienced dramatic initial improvement, marking the first successful surgical treatment of what was identified as parathyroid overactivity. The case galvanized European and American interest in parathyroid disease.
In the United States, physician Fuller Albright at Massachusetts General Hospital became the dominant figure in parathyroid research through the 1930s and 1940s. Albright and his collaborators described the clinical spectrum of hyperparathyroidism in extensive detail, linked it to kidney stone formation and abnormal calcium deposits throughout the body, and worked to distinguish primary overactivity of the gland from secondary forms arising in response to other disease states. Albright's integration of clinical observation with careful biochemical measurement set a new standard for endocrine investigation.
Jacob Erdheim, working in Vienna in the early twentieth century, contributed important pathological observations linking enlarged parathyroid glands to the bone disease seen in affected patients, helping to establish the gland as the anatomical seat of the disorder rather than the bones or kidneys themselves.
Key Historical Figures
Historical narrative only — this page describes how Hyperparathyroidism was understood historically. It is not medical advice and does not describe current diagnosis or treatment. Sourced from verified medical history references (NIH, Encyclopaedia Britannica, and standard medical history texts). See our medical disclaimer.