Hyperparathyroidism

HYPERPARATHYROIDISM, HYPOPARATHYROIDISM, conditions of the organism that are the result of increased (hyper-) or diminished (hypo-) internal secretory activity of the parathyroid glands (see Parathyroid glands); to hypoparathyroidism belongs the entire complex of symptoms that develops after experimental removal of all (apoparathyroidism) or several parathyroid glands in animals, after damage or excision of them during thyroidectomy in humans, and a number of analogous clinical symptoms occurring in latent and overt tetany (spasmophilia). One should distinguish between acute and chronic parathyroid insufficiency. In the acute form, the clinical picture is dominated by symptoms of sharply increased neuromuscular excitability. Sometimes they are found only upon the application of electrical (Erb's phenomenon - muscle contractions upon breaking-cathodal irritation at a current strength of 5-10 milliamperes) or mechanical (Chvostek's and Trousseau's phenomena) provocation; in more severe cases, spontaneous clonic-tonic convulsions in the extremities, in the masticatory (trismus) and neck muscles, and generalized convulsions are observed. Convulsions can lead to death due to laryngospasm (often in children), tonic convulsions of the respiratory musculature, or due to poisoning by metabolic products formed during convulsions. Convulsive phenomena are also found in some cases in the smooth musculature (e.g., pylorospasm, attacks of bronchial asthma). Chronic hypoparathyroidism is characterized by rare and weak manifestations of increased neuromuscular excitability (latent hypoparathyroidism), trophic disorders come to the forefront - loss of hair, brittleness of nails, typical dental lesions (according to Iselin - the same changes in all bone tissue), cataracts, clouding of the cornea, depigmentation of the iris, degenerative changes in the liver and kidneys, disturbance of temperature regulation. In the chronic form, due to the general disturbance of trophicity, regenerative processes proceed poorly, the body's resistance to infection is lowered. Chronic hypoparathyroidism under the influence of a superimposed infection, changes in climatic conditions (early spring), diet (meat), etc., can pass into the acute convulsive form. The immediate cause of both acute and chronic hypoparathyroidism should be recognized as the impoverishment of the organism with calcium, resulting from insufficient activity of the parathyroid glands. The parathyroid glands regulate calcium metabolism and its condition in the body (for more details on this - see Parathyroid glands). Correspondingly to this, pathognomonic for hypoparathyroidism is hypocalcemia (decreased calcium content in the blood). Simultaneously in the blood an increase in the content of inorganic phosphorus, a tendency to alkalosis (during the convulsive period often - acidosis) is found. The impoverishment with calcium, which has a sedative, inhibitory effect on neuromuscular activity, should explain the increased excitability in acute forms. However, hypocalcemia does not always lead to convulsions (Perel'man), neuromuscular excitability is obviously regulated by a number of other factors (hormones, metabolic products, alimentary and infectious toxins), the addition of which in some cases can cause the transition from latent non-convulsive form to acute convulsive form. To the clinical manifestations of hypoparathyroidism, besides the mentioned tetany and spasmophilia (infantile tetany), were also attributed (Lundborg) hereditary myotonia, myoclonia, Parkinson's disease and professional 'workers' tetany'. However, one cannot attribute all cases of increased excitability to hypoparathyroidism. The presence of a large number of cases of spasmophilia without hypocalcemia allows, besides the latter 4 forms, to deny the role of parathyroid insufficiency in the genesis of some cases of spasmophilia. Here we are dealing with other causes (nervous, alimentary, etc.). One cannot deny the constitutional predisposing significance of hypoparathyroidism for these diseases, as well as for some forms of eclampsia of pregnancy and epilepsy, since a lack of calcium of course contributes to all convulsive manifestations. If the genesis of hypoparathyroidism appears to be clarified in many respects, then the situation with hyperparathyroidism was much worse up to the very last time. The difficulty of the question lay in the failure of attempts to experimentally induce hyperparathyroidism by the administration of various preparations of parathyroid gland or by transplantation of it. - Only since the time Collip obtained an active extract from the parathyroid glands does this question become firmly established. However, for now we have only data regarding acute experimental intoxication upon subcutaneous (most effective), intravenous and peroral administration of large doses of Collip's preparation. It causes in dogs hypercalcemia, reaching its maximum in 5-9 hours; after approximately the same period with medium doses the calcium concentration in the blood again reaches normal level, blood viscosity increases, hypochloremia and an increase in the concentration of phosphorus and residual nitrogen of the blood are found. If the calcium concentration in the blood (in dogs) rises above 15 mg%, then prostration, vomiting, bloody diarrhea and sometimes convulsions appear. Usually poisoning ends in death, but Collip stipulates that a single administration of the extract, no matter how high the hypercalcemia, does not lead to death. It is curious that the administration of the preparation per os in the highest doses is unable to bring hypercalcemia to toxic limits. With this is limited the reliable data regarding experimental hyperparathyroidism. It is necessary to point out the insufficiently substantiated attempts to attribute etiological and pathogenetic significance to hyperparathyroidism in myasthenia (Lundborg) and ankylosing arthritis (Oppel).