With thyroid pathology, increased (hyperthyroidism) or decreased (hypothyroidism) production of thyroid hormones is observed.
Hyperthyroidism occurs in diseases such as diffuse toxic goiter, toxic nodular goiter, thyroid adenoma, as well as when taking thyroid hormones, thyroid cancer. The combination of rheumatic diseases with thyroid pathology primarily refers to Hashimoto’s thyroiditis and diffuse toxic goiter, in the genesis of which autoimmune mechanisms are important. In both diseases, antibodies to thyroglobulin and to the microsomal fraction of the thyroid gland, rheumatoid factor and antinuclear antibodies are detected. The most common combination of autoimmune thyroid disease with rheumatoid arthritis. The range of musculoskeletal manifestations of hyperthyroidism includes myopathy, systemic osteoporosis, periarthritis, acropathy. (7)
Thyrotoxic myopathy (TM)
As an independent nosological form, highlighted in 1938. Currently, TM is rarely diagnosed, which is largely due to the existing opinion that weakness in thyrotoxicosis is always caused by general asthenia, and not by skeletal muscle damage. There are also objective reasons that hinder the diagnosis of TM: relatively mild damage to individual muscles; absence (with rare exceptions) of paralysis; masking myopathy with symptoms of thyrotoxicosis. So, patients with TM, as a rule, do not complain of muscle weakness, and explain the existing motor difficulties with other reasons (weight loss, nervous fatigue, age, “salt deposition”, etc.). The diagnosis is also difficult because the muscles often have a “healthy” appearance due to the absence of their atrophy, therefore, the neuromuscular system is not studied and myopathy is not recognized. Although in a special clinical study it is detected in 61-81.5%, and in electromyography, according to various authors, in 92.6-100% of patients with thyrotoxicosis. Tests to objectify muscle weakness in clinical practice are getting up from a squatting position and from a low stool, from a supine position, etc. (4).
In most patients, symptoms of myopathy develop during the first 6-7 months from the onset of symptoms of thyrotoxicosis. The severity of myopathy does not depend on the severity and duration of thyrotoxicosis, the degree of enlargement of the thyroid gland, and the severity of eye symptoms (4).
Most often in TM, the ileo-lumbar, gluteus maximus, palmar interosseous and vermiform muscles, neck flexors and biceps of the shoulders are involved in the process. Detection of the weakness of these muscles can serve as one of the important diagnostic criteria for TM.
Opinions about the ratio of the frequency (and degree) of muscle weakness and atrophy in patients with TM in the literature are contradictory. Some researchers believe that muscle weakness is invariably accompanied by their atrophy (5). Others that muscle atrophy occurs many times more often than their weakness (5.14). This question was studied in detail by Kozakov V.M. et al. taking into account the anatomical regions and muscle groups (5). In the muscles of the shoulder girdle (trapezius, anterior dentate), shoulder girdle (supra- and infraspinatus), shoulders (triceps), hips (quadriceps and adductors) atrophy is more often detected than weakness. In other muscle groups (facial, flexor of the neck, interosseous and worm-shaped, straight and oblique abdomen, large gluteal, iliac-lumbar), on the contrary, weakness is detected more often than atrophy.
Another feature of TM is excessive skin folding over the affected muscles. Most often this is observed in the region of the triceps muscle of the shoulder and the quadriceps of the thigh. It is these muscles, which seem to be the most atrophied, that invariably retain full strength. Apparently, the disappearance of subcutaneous fat and creates a false impression of severe muscle atrophy.
In the clinical picture of the disease under study, other peculiar features were noted: frequent damage to the facial muscles (frontal and circular eyes) of mild to moderate degrees, the preservation or increase of deep reflexes, the absence of muscle pseudohypertrophies and terminal atrophies, tendon and muscle retractions, pathological deformations of individual body segments ( 5).
For the diagnosis of neuromuscular disease, in addition to knowing the frequency of weakness and atrophy of individual muscles, the topography (formula) of muscle lesions is important. Kozakov V.M. and Sovt. localization of muscle weakness was studied depending on the severity of myopathy (5). Patients with mild myopathy initially showed weakness of the iliopsoas muscles (93.4%), gluteus maximus (70.3%), interosseous and vermiform muscles of the hands (69%) and / or neck flexors (54%). As the progression of myopathy, the muscles of the shoulders (biceps, deltoid), hips (adductors and the posterior group) and the shoulder girdle (trapezius, anterior dentate, supraspinatus, and muscles) were successively involved.
It is widely believed that with TM (as with other myopathies), muscles of the shoulder and pelvic girdles and proximal limbs are mainly affected; cases of involvement of the distal parts, the own muscles of the hands were rarely described. Kozakov V.M. et al. the frequency of detecting tenar and hypotenar muscle weaknesses has been specially studied in comparison with the frequency of detecting weakness of the palmar interosseous and vermiform muscles of the hands (5). The muscles of the first group were rarely involved (in 1.9% of patients). Muscle weakness of the second group was encountered quite often (in 74.1% of patients).
Thus, at the earliest phase, TM can be recognized by the following criteria:
1) The “formula” for the spread of muscle weakness with the capture of the iliopsoas, gluteus maximus, interosseous palmar and worm muscles of the hands and / or neck flexors;
2) Atrophy of the triceps muscles of the shoulders and the quadriceps muscles of the thighs without reducing their strength;
3) Excessive skin folding over these muscles. The diagnosis is confirmed by a thyroid function test.
It should be noted that TM, according to the clinic and morphological changes in the muscles, as well as electromyography, is a phenocopy of a number of hereditary and non-inherited neuromuscular diseases, which requires an appropriate differential diagnosis. It is extremely important to distinguish this exogenous myopathy from similar diseases, since adequate and timely treatment in most cases leads to an almost complete regression of TM. In the absence of a specific treatment for TM, muscle weakness increases progressively, the patient ceases to move independently. In rare cases, acute thyrotoxic myopathy develops (3.7). The disease is manifested by generalized flaccid paralysis and paresis, accompanied by impaired swallowing and breathing. Pathological muscle fatigue is observed. These symptoms can last from several minutes to several hours and even days. In their pathogenesis, a certain role is given to reducing the concentration of potassium in the blood, which requires the immediate determination of its concentration in the blood. Taking potassium preparations sometimes leads to interruption of these symptoms and prevents the appearance of new ones (7). Cases of death from TM are described.
The group of diseases with which TM has to be differentiated is determined by its severity (4). Severe forms with severe muscle atrophy must be distinguished from myodystrophy, carcinomatous myopathy, proximal spinal muscular atrophy and diabetic proximal amyotrophy; with the addition of bulbar disorders – from polymyositis, myotonic dystrophy and myasthenia gravis. Mild forms in which muscle weakness dominates should be differentiated from polymyositis, Addison’s disease, and steroid myopathy.
Phenotypic similarity of TM with a hip variant of myodystrophy is found (4). However, in patients with myodystrophy, complaints of muscle weakness and motor impairments caused by it are leading, while in thyroid patients “thyrotoxic complaints” prevail. In addition, the hereditary form of myodystrophy develops slowly (over a number of years). In both diseases, the ileo-lumbar and gluteus maximus muscles are involved in the process early. However, in patients with TM, as a rule, weakness of the palmar interosseous and vermiform muscles and (or) flexors of the neck is simultaneously revealed; in patients with myodystrophy, the function of these muscles is preserved even in the late stage of the disease. There are differences in the further generalization of muscle lesions. With a hereditary form of myodystrophy, weakness of the quadriceps muscles of the thighs and the middle gluteus muscles, as well as the muscles of the interscapular region, occurs early. Patients often fall (weakness of the quadriceps muscles), when walking, they roll over from side to side (“duck gait” – weakness of the middle gluteus muscles), raising arms above the head is difficult (weakness of the trapezius and anterior dentate muscles). Due to a significant imbalance in muscle balance, various persistent skeletal deformations are formed (increased lumbar lordosis, shift of the shoulder girdles down and inward, “sunken chest”, “pterygo-shaped shoulder blades”). In patients with TM described violations are not found. In patients with myodystrophy, muscle weakness usually follows atrophy (with the exception of pseudo-hypertrophied muscles). In TM, “weak” muscles often maintain normal volume, while atrophied muscles retain muscle power to a large extent. It should be added that deep reflexes in patients with myodystrophy early decrease and disappear, while in patients with TM they remain normal or increase. In addition, in patients with myodystrophy, the phenomenon of excessive folding of the skin over the affected muscle does not happen even with the complete disappearance of the muscle abdomen.
In a number of patients with TM, along with the weakness of the proximal and distal muscles, bulbar muscle damage is detected. In such cases, it is necessary to differentiate TM not only with myodystrophy (oculopharyngeal form), but with proximal spinal muscular atrophy (PSMA), which begins with damage to the muscles of the pelvic girdle and hips, subsequently the process extends to the shoulder girdle and shoulders; in the later phase, the muscles of the distal arms and legs, and the 5,7,9-12th nuclei of the cranial nerves are affected (4). Mild dysphagia, dysarthria occurs , fasciculations in the muscles of the face, tongue, limbs and trunk are observed . In contrast to TM, with PSMA along with weakness, atrophy of the facial and masticatory muscles and tongue is detected. Atrophy and weakness of the thigh muscles occur early. The defeat of the distal extremities is more severe: atrophy and weakness of the small muscles of the hands (especially tenar and hypotenar), pronounced weakness of the flexors and extensors of the hands and feet is revealed.
The differential diagnosis of TM and idiopathic polymyositis causes great difficulties (6). Clinical similarities between these diseases were found: pronounced general weight loss and increasing muscle weakness, early involvement of the neck and pelvic flexor muscles in the process, the prevalence of muscle weakness over the degree of atrophy; creatinuria. However, with polymyositis, unlike TM, muscle weakness is more common; Along with proximal, distal extremities are often involved in the process. The flexors and extensors of the hands and feet may be affected early and severely. Unlike TM, atrophied muscles are always weakened, there is never excessive folding in the area of the affected muscle. In muscle biopsies with polymyositis, there are signs of myofibril necrosis, phagocytosis, regeneration with mononuclear infiltration, which is not found in TM. However, along with inflammation of the striated muscles, the development of polymyositis and other idiopathic inflammatory myopathies is often characterized by vivid systemic manifestations, such as fever, Raynaud’s phenomenon, skin lesions in the form of Gottron papules over interphalangeal and metacarpophalangeal joints, redness, hyperpigmentation, hyperperation , flaking, and cracking on the palms (so-called “hands mechanics”), polymorphous rash, panniculitis, cutaneous vasculitis, inflammatory non-erosive arthritis and arthralgia, res Single failure due to interstitial pulmonary fibrosis which sometimes leads to pulmonary hypertension; myocarditis, manifested by severe violations of rhythm and conduction, sometimes leading to congestive heart failure, damage to the gastrointestinal tract.
Of great diagnostic importance is the study of thyroid function. If using conventional methods it is not possible to accurately establish the diagnosis, and clinical data support TM, ex juvantibus methylthiouracil should be prescribed, followed by determination of the urine creatinine level (4). With thyrotoxicosis, its large doses (80 g / day) cause a significant decrease or disappearance of creatinuria within a few days. The lack of regression of myopathy with the achievement of euthyroidism testifies in favor of polymyositis.
Clinical signs of muscle lesions that occur with steroid therapy may resemble those with TM (4). Weakness and atrophy of the muscles of the pelvic girdle and hips develop. All patients by the time of muscle lesions, as a rule, have the features of Itsenko-Cushing’s syndrome. Muscular atrophy is more pronounced than with TM. Along with a change in the muscles of the pelvic girdle, significant atrophy and muscle weakness of the forearms and hands are revealed. On the electromyogram, mixed changes (myogenic and neurogenic) are determined. Myopathy regressed after drug withdrawal.
Pathological muscle weakness and fatigue are characteristic signs of severe myasthenia gravis (4). Muscle weakness in TM is constant in nature and captures certain muscles. With myasthenia gravis, muscle weakness is more generalized, increases with the slightest physical exertion to the extent that it is impossible to perform physical work. This causes fluctuations in the severity of various symptoms throughout the day. Ptosis, diplopia, restriction of the movement of the eyeballs up and out, dysarthria, dysphagia, amimia are also characteristic. TM can also be complicated by weakness of the bulbar muscles, but weaknesses of the external eye muscles, as well as “sagging” of the lower jaw due to the pronounced weakness of the chewing muscles proper, are not observed. In patients with TM, unlike myasthenia gravis, administration of anticholinesterase drugs is not accompanied by an increase in muscle strength, and the potential amplitude does not restore to normal.
In the treatment of TM, the most favorable results were obtained using the combined method: taking thyrostatic drugs followed by subtotal thyroidectomy. The results were worse with the appointment of only a conservative method of treatment. However, with both methods, the signs of myopathy regressed slowly, for many months after the removal of thyrotoxicosis. These data, taking into account the results of histological, histochemical, electroneuromyographic studies of skeletal muscles in patients and experimental animals with TM, have raised the question of the pathogenetic treatment of myopathy itself (5). Based on theoretical assumptions about the involvement of cyclic nucleotides in the pathogenesis of muscle weakness in TM, the use of drugs that increase the level of c-AMP in skeletal muscle (allopurinol, aminophylline) should be considered indicated. To normalize calcium metabolism – sodium oxalate; drugs that improve skeletal muscle metabolism – vitamin B12, – tocopherol, anabolic hormones. After removal of thyrotoxicosis, repeated courses of pathogenetic treatment of myopathy are quite justified.
Hyperthyroidism leads to an increase in bone metabolism due to an increase in the number of osteoclasts and resorption surfaces, as well as a violation of the ratio of resorption and bone-forming spaces. Increased resorption is the cause of hypercalcemia, which occurs in almost 50% of patients with thyrotoxicosis, while PTH and 1.25 (OH) 2D3 levels are reduced and intestinal absorption of calcium is reduced. However, increased bone formation does not compensate for the sharp increase in bone resorption. As a result, bone mass decreases in the proximal femur and spine. It should be noted that with an excess of thyroid hormones, women during menopause are most susceptible to osteoporosis, patients with long-term treatment with endogenous thyrotoxicosis and people receiving thyroid hormones in suppressive doses (more than 150 μg thyroxine per day) after surgery for thyroid cancer. Osteopenia is primarily detected in bones with a predominantly cortical type of structure. Disorders of bone metabolism are manifested in an increase in both bone formation (osteocalcin and alkaline phosphatase activity) and resorption (fasting hypercalciuria and increased urinary hydroxyproline excretion). Identified changes are directly dependent on the duration and activity of the disease and tend to normalize with persistent remission of the disease. A number of recent studies have shown that reduced bone mineral density in patients with thyrotoxicosis can recover after reaching euthyroid status (9).
With hyperthyroidism, periarthritis of the shoulder joints is most often observed (7). Damage to the periarticular tissues of the knee, hip, metacarpophalangeal, and interphalangeal joints is less common. Radiologically revealed thickening of the capsule of the joints. Periarthritis in hyperthyroidism is usually resistant to corticosteroid homone therapy and disappears with the appointment of thyreostatic drugs. Acropathy in hyperthyroidism is characterized by a change in the shape of the distal phalanges of the fingers, such as “drum sticks”, stiffness in the joints, swelling of the soft tissues of the hands and feet without signs of inflammation. Most often, changes are noted in the area of the metacarpophalangeal, proximal interphalangeal and metatarsophalangeal joints. X-ray revealed periosteal changes of bone diaphysis, having the appearance of soap bubbles, which distinguishes their perestostitis observed with hypertrophic osteoarthropathy, pachydermopereostosis, syphilis and hypervitaminosis A. The combination of acropathy with exophthalmos and pretibial myxedema in patients with diffuse toxic. Acropathy can occur with a duration of the disease from several weeks to 28 years. In some patients, it develops after relief of signs of hyperthyroidism. There is no effective treatment (7).
Hypotheriosis
A disease characterized by severe tissue edema due to extracellular deposition of proteoglycans, dramatically increasing the hydrophilicity of connective tissue. Hypothyroidism may be accompanied by the development of a number of rheumatic syndromes, in particular arthropathy and myopathy (7). Arthropathy is manifested by stiffness, swelling of the joints, sometimes the appearance of effusion in the joint cavity, which is non-inflammatory in nature. Typically, the absence of joint pain during palpation. Typically, the knee, wrist, small joints of the hands (metacarpophalangeal and proximal interphalangeal) and metatarsophalangeal joints are symmetrically affected. In some cases, destructive arthropathy is observed with localization of changes mainly in the proximal interphalangeal and less often in the distal interphalangeal joints. With the involvement of small joints of the hands and feet, it is often necessary to carry out a differential diagnosis with rheumatoid arthritis.
A number of patients may develop weakness of the ligamentous apparatus of the knee joints and a Baker cyst may form. In some cases, tenosynovitis of the flexor muscles of the hand is observed. A biopsy of the synovial membrane reveals its thickening without signs of inflammation, which is explained by the activating effect of TSH on synoviocyte adenylate cyclase. Crystals of calcium pyrophosphate are often found in the synovial fluid , usually not causing the development of pseudogout attacks, which is explained by a decrease in the functional activity of neutrophilic leukocytes (7). The appointment of thyroid hormone replacement therapy can provoke the development of pseudogouty arthritis. Despite the frequent increase in serum uric acid levels in patients with hypothyroidism, uric acid crystals are usually not found in the synovial fluid. The development of acute gouty arthritis is also uncharacteristic, although in some cases tofuses are formed.
There is evidence of an increased frequency of ischemic bone necrosis. Described necrosis of the lunate, tuberosity of the tibia and femoral heads (7).
Without treatment, in patients with hypothyroidism, violations of calcium metabolism are detected: there is a tendency to a decrease in the level of calcium in the blood and its excretion in the urine, the level of PTH and 1.25 (OH) D3 increase. In patients, bone remodeling is slowed down – the rate of bone resorption and bone formation is reduced by a factor of 2–3. It is difficult to trace in dynamics the effect of hypothyroid status on the condition of the skeleton, since patients are immediately prescribed treatment with thyroid hormones, which increase the rate of bone remodeling. A number of works draw attention to an increase in the rate of bone loss. During the first year of thyroxine replacement therapy, acceleration of bone loss in the spine and femoral neck was noted (8.9). At the same time, there is evidence of a lack of bone loss in the radius after a three-year treatment with thyroid hormones (9,13). Rozhinsky L. Ya. Et al. 36 women of reproductive age with various types of hypothyroidism were examined (postoperative for diffuse toxic goiter or nodule formation against autoimmune thyroiditis and congenital) (9). Women with untreated hypothyroidism showed signs of a decrease in both bone formation and bone resorption in the absence of signs of osteopenia in the spine and in the proximal femur. Patients on substitution therapy revealed elevated bone metabolism, most pronounced in congenital hypothyroidism, which may be due to the duration of therapy and the early (before the peak of bone mass) onset of the disease. In patients with postoperative hypothyroidism who underwent thyrotoxicosis, osteopenia of the proximal femur was detected. Thus, the development of osteopenia in hypothyroidism in premenopausal women is affected by the duration of thyroid therapy and the early age of its initiation.
Hypothyroid myopathy is characterized by muscle weakness and stiffness, mainly in the proximal arms and legs, painful cramps and pulling pains in the muscles, elevated serum creatine phosphokinase (CPK), and decreased tendon reflexes (2,3,7). There may be a violation of the function of the facial muscles (dysarthria). Muscle atrophy for hypothyroidism is not characteristic. A typical muscle disorder is myopathy with muscle hypertrophy (Hoffmann syndrome). In addition to weakness and stiffness, he is characterized by cramps, an increase in muscle volume and density. Muscular hypertrophy is associated with an increase in muscle fibers due to the deposition of proteoglycans in them. When prescribing thyroid hormone replacement therapy, muscle symptoms completely disappear.
Signs of damage to the peripheral nervous system occur in the vast majority of patients with hypothyroidism. They are manifested by numbness, paresthesia, pain in the distal extremities, often accompanied by malnutrition of the muscles of the hands and, occasionally, the muscles of the feet. Carpal canal syndrome is often observed, which develops due to compression of the median nerve by a bunch of flexors in the wrist joint due to edema and tissue tightening characteristic of hypothyroidism, which causes characteristic nocturnal paresthesia, which sometimes progresses to the loss of sensitivity and muscle weakness of the finger (2, 7). According to Steven G. Atcheson, carpal tunnel syndrome associated with hypothyroidism ranks first among the metabolic causes of this syndrome and occurred in 41 (13.8) of 297 patients with carpal tunnel syndrome, while in hyperthyroidism it was observed only in 1 (0.3) of these patients (10).
Hyperparathyroidism
First of all, it is characterized by excessive secretion of parathyroid hormone by an adenoma or hyperplastic tissue of the parathyroid glands, which leads to a sharp activation of bone metabolism with a predominance of resorption processes. The defeat of the skeletal system is manifested by pain in the bones, often the limbs, aggravated by movement, soreness during palpation of bones. Later, there are skeletal deformities, the so-called “duck” gait, broken bones of the extremities with the slightest trauma, and sometimes spontaneous. Generalized osteoporosis occurs, which is one of the main manifestations of hyperparathyroid osteodystrophy.
The classic manifestation of long-existing hyperparathyroidism is fibrocystic osteitis (osteodystrophy). It is based on the high activity of osteoclasts and lacunar resorption of bone elements with the subsequent development of fibrous tissue, the formation of cysts and giant “brown” tumors (reminiscent of osteoclastic bone). Cysts and giant tumors are located in the diaphysis of long tubular bones, ribs, lower jaw, bones of the wrist, pelvis, and skull. During percussion over the cysts of the skull, “watermelon sound” is determined (7). A peculiar kind of osteoporosis of the bones of the cranial vault – nostril, as if “eaten by moth”, can take the form of “frosted glass”, often resembles “lumps of wool” – pagetoid form of hyperparathyroidism (1). In contrast, with Paget’s disease in blood tests, the concentration of alkaline phosphatase increases at normal concentrations of calcium and phosphorus despite a 40-50-fold acceleration of metabolic processes in the bone (15). Clinically manifested by vague pain in the bones, sometimes palpated as tumors. After an ectomy, the parathyroid glands may become ossified. Gradually, curvature of long tubular bones (lower legs, thighs), and an increase in bending of the spine can occur (1.7). Today, the classic picture of fibrocystic osteitis is becoming less common, since the diagnosis of primary hyperparathyroidism is usually established at the stage of asymptomatic hypercalcemia (2).
An early radiological sign of hyperparathyroidism is subperiosteal resorption of bone tissue, which consists in subperiosteal resorption of bone substance, most often the middle and terminal phalanges of the fingers, mainly from their radial side (1,7). At the same time, the terminal phalanges seem to be “moth-eaten”, “sucked”. After removal of the parathyroid glands, resorption is suspended. Bone resorption is often accompanied by subperiosteal erosion in the middle phalanx, wrist bones, proximal tibia and femur, both ends of the clavicle, pubic and sacroiliac joints. With erosion in the small joints of the hands there may be arthralgia, swelling, morning stiffness, which requires a differential diagnosis with rheumatoid arthritis. There may be a breakthrough of the cyst in the joint cavity, which leads to the development of synovitis (usually knee). Hypermobility occurs less often due to weakness of the ligamentous apparatus and joint capsule, which may be accompanied by a separation of tendons (more often the quadriceps femoris tendon).
Chondrocalcinosis is detected in 35-50% of patients with long-term primary primary hyperthyroidism, accompanied by asymptomatic calcification of menisci, knee cartilage, wrist joints, intervertebral discs, triangular wrist cartilage, which can lead to carpal tunnel syndrome (2.7). After parathyroidectomy, acute pseudogout attacks can occur. With hyperparathyroidism, hyperuricemia also occurs with the development of gouty arthritis. Muscle damage is manifested by weakness of the proximal muscles without increasing the content of muscle enzymes in the blood serum, myalgia, atrophy. Symptoms usually disappear after parathyroidectomy.
Hypoparathyroidism
It exists in two forms: hypoparathyroidism and pseudohypoparathyroidism (Albright syndrome), in which PTH secretion does not suffer, but due to the insensitivity of target tissues to its action, the same biochemical and clinical disorders develop as with hypoparathyroidism (12). One of the few clinical differences between Albright syndrome and idiopathic hypoparathyroidism is a peculiar skeletal symptom complex: a round face, a short neck, a wide stocky trunk, stunted growth, shortening of metacarpal and metatarsal bones, and in some cases phalanxes of fingers; subcutaneous calcifications are found in the area of large joints; asymptomatic hyperuricemia is observed. The disease is familial in nature. A combination of a decrease in calcium and an increase in phosphorus in the blood serum, which is observed with hypoparathyroidism, Albright syndrome and resistance to PTH in patients with chronic renal failure, is characteristic. A particularly rare complication is myopathic syndrome, manifested by weakness of the proximal muscles of the limbs, a decrease in deep reflexes, an increase in blood CPK, in the absence of changes in electromyographic parameters (11). One of the manifestations of myopathy can be ptosis, tetanic convulsions, more often in the distal muscles of the limbs; painful cramping of the muscles of the chest or anterior abdominal wall, simulating acute diseases of the organs of the chest and abdominal cavity, arising mainly due to damage to the nervous system. As a result of treatment with vitamin D2, muscle weakness regresses, which is accompanied by a decrease in blood CPK levels (11).
With hypoparathyroidism, a spinal lesion is observed , resembling an idiopathic ankylosing skeleton hyperostosis, but in contrast, it is accompanied by stiffness and restriction of movements. X-ray detection of ossification of the ligaments of the spine with normal iliac-sacral joints (7). With hypoparathyroidism, osteosclerosis, periostosis of long tubular bones, premature calcification of the cartilage of the ribs, ribbon-like compaction of metaphyses, transverse metaphysical “growth lines”, calcification of soft tissues (cerebral plexuses, vascular wall, dura mater, basal ganglion) is observed .