ODESA NATIONAL MEDICAL UNIVERSITY Department of Internal Medicine № 1 with the course of cardiovascular diseases

METHODIC RECOMMENDATIONS FOR PRACTICAL CLASSES

Topic "Iodine deficiency disorders of the thyroid gland. Nodular forms of goiter. Thyroid cancer. Classification, symptoms, diagnosis, treatment. Diseases of the "

Course IV Faculty: international Specialty :222 -"Medicine"

The lecture was discussed on the methodical meeting of the department 27.08.2020 Protocol № 1 Head of the department Prof, Yu.I. Karpenko

Odesa I. Actuality of the topic. A goiter is an enlargement of the thyroid gland. The presence of goiter does not correlate with thyroid function, i.e., patients may be euthyroid, hypothyroid, or hyperthyroid. Thyroid cancer is a thyroid neoplasm that is malignant. It can be treated with radioactive iodine or surgical resection of the thyroid gland. Chemotherapy or radiotherapy may also be used.

II. The purpose of the lecture: 1. To determine the etiologic factors and pathogenesis of nodular forms of goiter. To practice palpation of the thyroid gland. 2. To aquaint students with the classification of nodular forms of goiter. 3. To make a plan of examination of patients with nodular forms of goiter. 4. To analyze the results of laboratory and instrumental studies, which are used for the diagnosis of nodular forms ofgoiter. 5. To make a treatment plan for patients with goiter. 6. To know etiology and pathogenesis of cancer of thyroid gland and diseases of parathyroid gland 7. To know clinical forms of cancer of thyroid gland and diseases of parathyroid gland 8. To know classifications of cancer of thyroid gland and diseases of parathyroid gland 9. To know clinical picture of cancer of thyroid gland and diseases of parathyroid gland 10. To know laboratory criterions 11. To know methods of cancer of thyroid gland and diseases of parathyroid gland treatment To realize the goal of study, basic knowledge is necessary: 1. Peculiarities of anatomy and physiology of endocrine system 2. Anamnesis of endocrine patients 3. Objective investigation 4. Methods of instrumental and laboratory diagnosis 5. Differential diagnosis of iodine deficiencydiseasesofthyroidgland with other endocrine diseases 6. Diagnosis

III. A task for the self-preparation of a student for a lesson Information for raising the level of basic knowledge can be found in the following textbooks: Training: 1. Davidson’s “Principles of Practice of Medicine” 22th edition, 2014. 2. Harrison’s “Principles of internal medicine”, 19th edition, 2015 Additional:

1. AACE/ACE/AME Medical Guidelines for Clinical Practice for the Diagnosis and Management of Thyroid Nodules – 2016 Update - © 2016 2. Hyperthyroidism and Other Causes of Thyrotoxicosis: Management Guidelines of the American Thyroid Association and American Association of Clinical Endocrinologists - © 2011 3. AACE/AAES Medical/Surgical Guidelines for Clinical Practice for Management of Thyroid Carcinoma © 2001 IV. Questions: 1. Etiology and pathogenesis of goiter 2. Clinical picture of goiter 3. Peculiarities of goiter flow in children, men, old people and with central forms of thyrotoxicosis 4. Clinics of thyroid crisis 5. Methods of goiter treatment 6. Methods of endocrine, autoimmune, ophtalmopathy treatment 7. Clinical manifestations of angio- and neuropathies 8. Etiology and pathogenesis of cancer of thyroid gland and diseases of parathyroid gland 9. Clinical forms of cancer of thyroid gland and diseases of parathyroid gland 10. Classifications of cancer of thyroid gland and diseases of parathyroid gland 11. Clinical picture of cancer of thyroid gland and diseases of parathyroid gland 12. Laboratory criterions 13. Methods of cancer of thyroid gland and diseases of parathyroid gland treatment

V. Plan of self-study: # Consequence of actions Indications 1 Diagnosis of goiter Plan of patient examination 2 Basic clinical and instrumental laboratory data of Criterions of goiter, diagnosis, goiter tests 3 Practical actions in clinics Clinical diagnosis, prescribe medicine

Task for self-study: References, tables, schemes of treatment

VI. The content of the topic: Primary hypothyroidism:

Primary hypothyroidism is the most common one (95% of patients) and develops due to disease in the thyroid; thyroid-stimulating hormone (TSH) is increased. The most common cause is autoimmune. It usually results from Hashimoto's thyroiditis and is often associated with a firm goiter or, later in the disease process, with a shrunken fibrotic thyroid with little or no function. The second most common cause is post-therapeutic hypothyroidism, especially after radioactive iodine therapy or surgery for hyperthyroidism or goiter. Hypothyroidism during overtreatment with propylthiouracil, methimazole, and iodide abates after therapy is stopped.

Most patients with non-Hashimoto's goiters are euthyroid or have hyperthyroidism, but goitrous hypothyroidism may occur in endemic goiter. Iodine deficiency decreases thyroid hormonogenesis. In response, TSH is released, which causes the thyroid to enlarge and trap iodine avidly; thus, goiter results. If iodine deficiency is severe, the patient becomes hypothyroid, a rare occurrence in the majority of developed countries since the advent of iodized salt.

Iodine deficiency can cause congenital hypothyroidism. In severely iodine-deficient regions worldwide, congenital hypothyroidism (previously termed endemic cretinism) is a major cause of intellectual disability.

Rare inherited enzymatic defects can alter the synthesis of thyroid hormone and cause goitrous hypothyroidism. Hypothyroidism may occur in patients taking lithium, perhaps because lithium inhibits hormone release by the thyroid. Hypothyroidism may also occur in patients taking amiodarone or other iodine-containing drugs, and in patients taking interferon alfa. Hypothyroidism can result from radiation therapy for cancer of the larynx or Hodgkin lymphoma. The incidence of permanent hypothyroidism after radiation therapy is high, and thyroid function (through measurement of serum TSH) should be evaluated at 6- to 12- months intervals.

Symptoms and Signs

Symptoms and signs of primary hypothyroidism are often subtle and insidious. Symptoms may include cold intolerance, constipation, forgetfulness, and personality changes. Modest weight gain is largely the result of fluid retention and decreased metabolism. Paresthesias of the hands and feet are common, often due to carpal-tarsal tunnel syndrome caused by deposition of proteinaceous ground substance in the ligaments around the wrist and ankle. Women with hypothyroidism may develop menorrhagia or secondary amenorrhea.

The facial expression is dull; the voice is hoarse and speech is slow; facial puffiness and periorbital swelling occur due to infiltration with the mucopolysaccharides hyaluronic acid and chondroitin sulfate; eyelids droop because of decreased adrenergic drive; hair is sparse, coarse, and dry; and the skin is coarse, dry, scaly, and thick. The relaxation phase of deep tendon reflexes is slowed. Hypothermia is common. Dementia or frank psychosis (myxedema madness) may occur.

Carotenemia is common, particularly notable on the palms and soles, caused by deposition of carotene in the lipid-rich epidermal layers. Deposition of proteinaceous ground substance in the tongue may cause macroglossia. A decrease in both thyroid hormone and adrenergic stimulation causes bradycardia. The heart may appear to be enlarged on examination and imaging, partly because of dilation but chiefly because of pericardial effusion. Pleural or abdominal effusions also may be noted. The pericardial and pleural effusions develop slowly and only rarely cause respiratory or hemodynamic distress.

Elderly patients have significantly fewer symptoms than do younger adults, and complaints are often subtle and vague. Many elderly patients with hypothyroidism present with nonspecific geriatric syndromes—confusion, anorexia, weight loss, falling, incontinence, and decreased mobility. Musculoskeletal symptoms (especially arthralgias) occur often, but arthritis is rare. Muscular aches and weakness, often mimicking polymyalgia rheumatica or polymyositis, and an elevated CK level may occur. In the elderly, hypothyroidism may mimic dementia or parkinsonism.

Definition of "goiter" The clinical term "nodular goiter" combines focal thyroid lesions, which have different pathomorphological structure - the cysts, nodes, benign and malignant tumors of the thyroid gland. Tumors of the thyroid gland in most cases are of epithelial origin - an adenoma and adenocarcinoma. Endemic goiter – is a disease that occurs in certain biogeochemical geographic areas with iodine deficiency in the environment, and is characterized by enlargement of the thyroid gland. Sporadic goiter is persistent increase of thyroid gland among residents of areas without iodine deficiency (a physiological providing of iodine). Goiter is an enlargement of the thyroid gland of third degree or higher. The increase of thyroid gland of 2nd degree is called thyroid hyperplasia, but in the presence of node this variant is also called goiter. WHO classification of endemic goiter: Group 0. No goiter. Group 1. Goiter is determined by palpation. The thyroid gland is clearly visible when head is turned back and neck is elongated. Group 2. Goiter is determined visually. Group 3. Goiter is seen at a distance, grows up to large sizes, mechanicaly makes breathing difficult. By the form of increased thyroid gland, the presence or absence of nodes: - Nodular goiter (characterized by tumorlike growth of thyroid tissue, often is round in shape, mainly it has elastic consistency, other sections of thyroid gland usually are not palpable); - Diffuse goiter (characterized by an even increase of the thyroid gland in the absence of local consolidations); - Mixed, or diffuse nodular goiter (union of the diffuse hyperplasia and node). Diseases that are accompanied by thyrotoxicosis.

Thyroid cancer is a thyroid neoplasm that is malignant. It can be treated with radioactive iodine or surgical resection of the thyroid gland. Chemotherapy or radiotherapy may also be used. Symptoms Micrograph of a lymph node with papillary thyroid carcinoma. Most often the first symptom of thyroid cancer is a nodule in the thyroid region of the neck. However, many adults have small nodules in their thyroids, but typically under 5% of these nodules are found to be malignant. Sometimes the first sign is an enlarged lymph node. Later symptoms that can be present are pain in the anterior region of the neck and changes in voice. Thyroid cancer is usually found in a euthyroid patient, but symptoms of hyperthyroidism or hypothyroidism may be associated with a large or metastatic well-differentiated tumor. Thyroid nodules are of particular concern when they are found in those under the age of 20. The presentation of benign nodules at this age is less likely, and thus the potential for malignancy is far greater. Diagnosis After a thyroid nodule is found during a physical examination, a referral to an endocrinologist, a thyroidologist or otolaryngologist may occur. Most commonly an ultrasound is performed to confirm the presence of a nodule, and assess the status of the whole gland. Measurement of thyroid stimulating hormone and anti-thyroid antibodies will help decide if there is a functional thyroid disease such as Hashimoto's thyroiditis present, a known cause of a benign nodular goiter. Classification Thyroid cancers can be classified according to their histopathological characteristics. The following variants can be distinguished (distribution over various subtypes may show regional variation): - Papillary thyroid cancer (75% to 85% of cases) - often in young females - excellent prognosis - Follicular thyroid cancer (10% to 20% of cases) - Medullary thyroid cancer (5% to 8% of cases)- cancer of the parafollicular cells, part of MEN-2. - Anaplastic thyroid cancer (Less than 5%). It is not responsive to treatment and can cause pressure symptoms. Others - Lymphoma - Squamous cell carcinoma, sarcoma The follicular and papillary types together can be classified as "differentiated thyroid cancer". These types have a more favorable prognosis than the medullary and undifferentiated types. Papillary microcarcinoma is a subset of papillary thyroid cancer defined as measuring less than or equal to 1 cm. The highest incidence of papillary thyroid microcarcinoma in autopsy series was reported by Harach et al. in 1985, who found 36 of 101 consecutive autopsies were found to have an incidental microcarcinoma. Michael Pakdaman et al. report the highest incidence in a retrospective surgical series at 49.9% of 860 cases. Management strategies for incidental papillary microcarcinoma on ultrasound (and confirmed on FNAB) range from total thyroidectomy with radioactive iodine ablation to observation alone. Harach et al. suggest using the term "occult papillary tumor" to avoid giving patients distress over having cancer.It was Woolner et al. who first arbitrarily coined the term "occult papillary carcinoma" in 1960, to describe papillary carcinomas ≤ 1.5 cm in diameter. Etiology From the 1940s to 1960s, external, low-dose radiation to the head and neck during infancy and childhood was used to treat many benign diseases. This type of therapy has been shown to predispose persons to thyroid cancer. The younger the patient was at time of exposure, the higher the risk of developing cancer. Another cause may be due to high-dose irradiation to the head and neck. Patients with Hodgkin lymphoma treated with mantlefield irradiation have an increased risk of developing thyroid cancer, although hypothyroidism is more likely. Treatment Thyroid cancer may require surgery. Common surgeries include thyroidectomy, lobectomy, and tracheostomy. Radioactive Iodine-131 is used in patients with papillary or follicular thyroid cancer for ablation of residual thyroid tissue after surgery and for the treatment of thyroid cancer. Patients with medullary, anaplastic, and most Hurthle cell cancers do not benefit from this therapy. External irradiation may be used when the cancer is unresectable, when it recurs after resection, or to relieve pain from bone metastasis.

Parathyroid glands are small glands of the endocrine system which are located in the neck behind the thyroid. Parathyroid glands control the calcium in our bodies--how much calcium is in our bones, and how much calcium is in our blood. Calcium is the most important element in our bodies (we use it to control many systems), so calcium is regulated very carefully. Parathyroid glands control the calcium.

Parathyroid glands (we all have 4 of them) are normally the size of a grain of rice. Occasionally they can be as large as a pea and still be normal.

The Role of Calcium in the Human Body... and how the Parathyroid Glands Control All Calcium Levels in our Bodies.

First a word about CALCIUM and what it does in our bodies. We use many elements in our bodies to perform all the different functions of life. Calcium is essential to life, and is used primarily for three things:

1. To provide the electrical energy for our nervous system. The most important thing that calcium does in the human body is provide the means for electrical impulses to travel along nerves. Calcium is what the nervous system of our body uses to conduct electricity. This is why the most common symptoms of parathyroid disease and high calcium levels are related to the nervous system (depression, weakness, tiredness, etc, etc). Much more about symptoms of parathyroid disease on another page. 2. To provide the electrical energy for our muscular system. Just like the nerves in our bodies, our muscles use changes in calcium levels inside the cells to provide the energy to contract. When the calcium levels are not correct, people can feel weak and have muscle cramps. 3. To provide strength to our skeletal system. Everyone knows that calcium is used to make our bones strong, but this is really only half the story. The bones themselves serve as the storage system that we use to make sure we will always have a good supply of calcium. Just like a bank vault where we constantly make deposits and withdrawals, we are constantly putting calcium into our bones, and constantly taking calcium out of our bones... all in small amounts... with the sole purpose of keeping our calcium levels in the blood at the correct level. Remember, the most important role of calcium is to provide for the proper functioning of our nervous system--not to provide strength to our bones--that is secondary.

Thus, calcium is the most closely regulated element in our bodies. In fact, calcium is the ONLY element / mineral that has its own regulatory system (the parathyroid glands). There are no other glands in our bodies that regulate any other element. Why? Because its our nervous system that separates us from all other plant and animal life--and calcium provides the electrical system for our nervous system. When our calcium levels get elevated (almost always due to a bad parathyroid gland), then we can have changes in our personality (typically noticed by our loved ones) and many other nervous-system symptoms (depression, etc). So, parathyroid disease is not just about osteoporosis and kidney stones, it is primarily about us feeling "normal" and enjoying life.

The Role of the Parathyroid Glands -- to Regulate Calcium.

The ONLY purpose of the parathyroid glands is to regulate the calcium level in our bodies within a very narrow range so that the nervous and muscular systems can function properly. This is all they do. They measure the amount of calcium in the blood every minute of every day... and if the calcium levels go down a little bit, the parathyroid glands recognize it and make (PTH) which goes to the bones and takes some calcium out (makes a withdrawal from the calcium vault) and puts it into the blood. When the calcium in the blood is high enough, then the parathyroids shut down and stop making PTH.

The single major disease of parathyroid glands is over-activity of one or more of the parathyroids which make too much parathyroid hormone causing a potentially serious calcium imbalance (too high calcium in the blood). This is called and this is the disease that this entire web site is about.

Hyperparathyroidism is overactivity of the parathyroid glands resulting in excess production of parathyroid hormone (PTH). The parathyroid hormone regulates calcium and phosphate levels and helps to maintain these levels. Excessive PTH secretion may be due to problems in the glands themselves, in which case it is referred to as primary hyperparathryroidism and which leads to hypercalcemia (raised calcium levels). It may also occur in response to low calcium levels, as encountered in various situations such as vitamin D deficiency or ; this is referred to as secondary hyperparathyroidism. In all cases, the raised PTH levels are harmful to bone, and treatment is often needed. Recent evidence suggests that Vitamin D deficiency/insufficiency plays a role in the development of hyperparathyroidism. Lithium is associated with an increased incidence of hyperparathyroidism. Classification Primary hyperparathyroidism Primary hyperparathyroidism results from a hyperfunction of the parathyroid glands themselves. There is oversecretion of PTH due to adenoma, hyperplasia or, rarely, carcinoma of the parathyroid glands. Secondary hyperparathyroidism Secondary hyperparathyroidism is the reaction of the parathyroid glands to a hypocalcemia caused by something other than a parathyroid pathology, e.g. chronic renal failure. Tertiary hyperparathyroidism Tertiary hyperparathyroidism result from hyperplasia of the parathyroid glands and a loss of response to serum calcium levels. This disorder is most often seen in patients with chronic renal failure. Symptoms and signs Asymptomatic hyperparathyroidism Many patients presenting with hyperparathyroidism will have no signs or symptoms, with diagnosis being made on further investigation after a coincidental finding of hypercalcemia. It is, however, reported that many patients will report that they feel better after treatment for hyperparathyroidism. Symptomatic hyperparathyroidism Of those patients who do present with symptoms, they are commonly associated with the effects of an increased level of calcium. Since calcium is involved in trans-synaptic communication in the nervous system, high blood calcium levels have a direct effect on the nervous system. Thus, most of the symptoms of parathyroid disease are "neurological" in origin. Common manifestations of hyperparathyroidism include weakness and fatigue, depression, bone pain, muscle soreness (myalgias), decreased appetite, feelings of and vomiting, constipation, polyuria, polydipsia, cognitive impairment, kidney stones and osteoporosis. Surgical removal of a parathyroid tumor will eliminate the symptoms in most patients. The Mnemonic; "Moans, Groans, Stones, Bones and Psychic Overtones" roughly sums it up. Osteoporosis Osteoporosis associated with hyperparathyroidism is caused by the high parathyroid hormone secreted by overactive parathyroid gland(s). Excess parathyroid hormone (PTH) acts indirectly on osteoclasts as they lack a PTH receptor. Instead, PTH stimulates osteoblasts, which in turn increases their expression of RANKL. RANKL is then able to bind osteoclasts which stimulates their activation which ultimately leads to the removal of calcium from the bones. Thus, the high calcium in the blood comes from the bones. Removing the offending parathyroid gland will restore normal bone density over several years. Laboratory tests Serum calcium In cases of primary hyperparathyroidism or tertiary hyperparathyroidism heightened PTH leads to increased serum calcium (hypercalcemia) due to: - increased bone resorption, allowing flow of calcium from bone to blood - reduced renal clearance of calcium - increased intestinal calcium absorption By contrast, in secondary hyperparathyroidism effectiveness of PTH is reduced. Serum phosphate In primary hyperparathyroidism, serum phosphate levels are abnormally low as a result of decreased renal tubular phosphate reabsorption. However, this is only present in about 50% of cases. This contrasts with secondary hyperparathyroidism, in which serum phosphate levels are generally elevated because of renal disease. Alkaline phosphatase Alkaline phosphatase levels are not elevated in all types of hyperparathyroidism. Kumar and Clark 6th edition states that alkaline phosphatase levels do not increase in primary hyperparathyroidism but may increase in secondary hyperparathyroidism. Etiology Primary hyperparathyroidism The most common cause is a benign that loses its sensitivity to circulating calcium levels. Usually, only one of the four parathyroid glands is affected. A less common cause is from multiple endocrine neoplasia (MEN). Secondary hyperparathyroidism Secondary hyperparathyroidism is due to excessive secretion of parathyroid hormone (PTH) by the parathyroid glands in response to hypocalcemia (low bloodcalcium levels) and/or hyperphosphatemia(high bloodphosphate levels), usually due to chronic renal failure. The bone disease in secondary parathyroidism along with renal failure is termed renal osteodystrophy. Patients with bipolar disorder who are receiving long-term lithium treatment are at increased risk for hyperparathyroidism. Elevated calcium levels are found in 15% to 20% of patients who have been taking lithium long-term. However, only a few of these patients have significantly elevated levels of parathyroid hormone and clinical symptoms of hyperparathyroidism. Lithium-associated hyperparathyroidism is usually caused by a single parathyroid adenoma. Tertiary hyperparathyroidism Tertiary hyperparathyroidism, quartary and quintary hyperparathyroidism are rare forms that are caused by long lasting disorders of the calcium feedback control system. In cases of long-standing secondary hyperparathyroidism, the hypertrophiedparathyroid glands can become autonomously functioning and continue to secrete PTH independent of whether the original stimuli to secrete PTH are still present. Diagnosis The gold standard of diagnosis is the Parathyroid immunoassay. Once an elevated Parathyroid hormone has been confirmed, goal of diagnosis is to determine whether the hyperparathyroidism is primary or secondary in origin by obtaining a serum calcium level: PTH serumcalcium likelytype primaryhyperparathyroid high high ism secondaryhyperparathyro high lowornormal idism Tertiary hyperparathyroidism has a high PTH and a high serum calcium. It is differentiated from primary hyperparathyroidism by a history of chronic kidney failure and secondary hyperparathyroidism. Treatment and monitoring Endocrinologists diagnose diseases affecting glands and should be consulted for hyperparathyroidism. Treatment for the three different types of hyperparathyroidism vary. Generally treatment is first and foremost directed at hypercalcemia; if symptomatic, patients are sent for surgery to remove the parathyroid tumor (parathyroid adenoma) or parathyroid gland (see hypercalcemia). Most experts now believe that almost all patients with hyperparathyroidism should be evaluated for surgery. If hyperparathyroidism is caused by a tumor, it will almost always progress as the tumor grows. Testing for hyperparathryroidism: - Calcium level - Bone density - Vitamin D - Phosphorus

In medicine (endocrinology), is decreased function of the parathyroid glands, leading to decreased levels of parathyroid hormone (PTH). The consequence, hypocalcaemia, is a serious medical condition. Signs and symptoms - Tingling lips, fingers, and toes - Muscle cramps - Pain in the face, legs, and feet - Abdominal pain - Dry hair - Brittle nails - Dry, scaly skin - Cataracts - Weakened tooth enamel (in children) - Muscle spasms called tetany (can lead to spasms of the larynx, causing breathing difficulties) - Convulsions (seizures) - Tetanic contractions - Additional symptoms that may be associated with this disease include: - Painful menstruation - Hand or foot spasms - Decreased consciousness - Delayed or absent tooth formation - Calcification of the basal ganglia due to increased phosphorus levels driving calcium into the brain tissue. In contrast to hyperparathyroidism (hyperfunction of the parathyroids), hypoparathyroidism does not have consequences for bone. Diagnosis Diagnosis is by measurement of calcium, serum albumin (for correction) and PTH in blood. PTH degrades rapidly at ambient temperatures and the blood sample therefore has to be transported to the laboratory on ice. If necessary, measuring cAMP (cyclic AMP) in the urine after an intravenous dose of PTH can help in the distinction between hypoparathyroidism and other causes. Differential diagnoses are: - (normal PTH levels but tissue insensitivity to the hormone, associated with mental retardation and skeletal deformities) and pseudopseudohypoparathyroidism (sic). - Vitamin D deficiency or hereditary insensitivity to this vitamin (X-linked dominant). - Malabsorption - Kidney disease - Medication: steroids, diuretics, some antiepileptics. Other tests include ECG for abnormal heart rhythms, and measurement of blood magnesium levels. Causes Hypoparathyroidism can have a number of divergent causes: Removal of or trauma to the parathyroid glands in thyroid surgery (thyroidectomy) or other neck surgeries is a recognized cause. It is now uncommon, as surgeons generally can spare them during procedures after identifying them. In a small percentage of cases, however, they can become traumatized during surgery and/or their blood supply can be compromised. When this happens the parathyroids may cease functioning for a while or stop altogether. Autoimmune invasion and destruction is the most common non-surgical cause. It can occur as part of autoimmune polyendocrine syndromes. Hemochromatosis can lead to iron accumulation and consequent dysfunction of a number of endocrine organs, including the parathyroids. Absence or dysfunction of the parathyroid glands is one of the components of chromosome 22q11 microdeletion syndrome (other names: DiGeorge syndrome, Schprintzen syndrome, velocardiofacial syndrome). Magnesium deficiency DiGeorge syndrome, a disease in which hypoparathyroidism can occur due to a total absence of the parathyroid glands at birth. Familial hypoparathyroidism occurs with other endocrine diseases, such as adrenal insufficiency, in a syndrome called type I polyglandular autoimmune syndrome (PGA I). Some very rare diseases Idiopathic (of unknown cause), occasionally familial Treatment Severe hypocalcemia, a potentially life-threatening condition, is treated as soon as possible with intravenouscalcium (e.g. as calcium gluconate). Generally, a central venous catheter is recommended, as the calcium can irritate peripheral veins and cause phlebitis. Long-term treatment of hypoparathyroidism is with calcium and vitamin D3 supplementation (D1 is ineffective in the absence of renal conversion). Teriparatide, a synthetic form of PTH (presently registered for osteoporosis) might become the treatment of choice for PTH supplementation, although further studies are awaited. In the event of a life-threatening attack of low calcium levels or tetany (prolonged muscle contractions), calcium is administered by intravenous (IV) infusion. Precautions are taken to prevent seizures or larynx spasms. The heart is monitored for abnormal rhythms until the person is stable. When the life-threatening attack has been controlled, treatment continues with medicine taken by mouth as often as four times a day. Possible Complications - Tetany can lead to a blocked airway, requiring a tracheotomy. - Stunted growth, malformed teeth, and slow mental development can occur if hypoparathyroidism develops in childhood. - Overtreatment with vitamin D and calcium can cause hypercalcemia (high blood calcium) and sometimes interfere with kidney function. - There is an increased risk of pernicious anemia, Addison's disease, cataract development, and Parkinson's disease.

The methodological recommendation is made by ass. RyabininaA.G.. Reviewer: doc. Potapchuk A.V.