Hyperparathyroidism: symptoms and treatment in women. Modern ideas about etiology, pathogenesis, clinical picture, diagnosis and treatment of primary hyperparathyroidism Primary hyperparathyroidism Clinical recommendations

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Hyperparathyroidism is a disease caused by endocrinological disorders that provoke an increase in the secretion of the hormones of the parachitoid glands. It is characterized by a significant violation of calcium and phosphorus exchange processes. As a result, the dice becomes fragile, the risk of their damage and fractures increases.

There are primary, secondary, as well as tertiary forms of the disease. Alimentary hyperparathyroidism occurs only in veterinary practice.

Let's talk on www.Site about how the hyperparathyroidism is manifested by the treatment of it, what is his reasons, what are the recommendations of disease professionals - about all this and our today's conversation will go:

Causes, Symptoms of Disease

Primary hyperparathyroidism (Recklinghausen disease):

The reasons

The most common cause of this form is considered the presence of the solitary adenoma of the parachitoid gland or, otherwise, parastromates. It is less likely to cause multiple adenoma to the occurrence of the primary form. More often - cancer of parachitoid gland. This form of the disease is more often diagnosed in adults, but sometimes it can occur in children and the elderly.

It should be noted that the primary hyperparathyroidism is observed in syndromes of multiple endocrine neoplasia.

How the primary hyperparathyroidism (symptoms) is manifested

Disease may not manifest itself for a long time, as it develops asymptomatic. This is typical for the initial stage when the calcium level is increased slightly. With the development of the disease, characteristic symptoms appear. Heavy complications may develop, for example, hypercalcemic crisis.

However, this form is most often manifested by the following symptomatics:

Bone-tissue changes: bone fragility increases, frequent fractures occur. Sometimes there may be a decrease in the growth of the patient;

Urolled, renal disease;

Elevated level of ionized calcium, pronounced calciumuria, manifestations of severe hypercalcemia;

Visceral complications of the primary form of hyperparathyroidism: fibrous periostitis, nephroalcinosis;

Secondary and tertiary hyperparathyroidism

Secondary hyperfunction and hyperplasia of parachitoid glands occurring against the background of long hypocalcemia, hyperphosphatemia is called secondary hyperparathyroidism.

For tertiary, the development of the adenoma of the parachitoid glands, which proceeds against the background of the secondary hyperparathyroidism for a long time is characteristic.

Causes of secondary hyperparathyroidism

The main causes of the secondary form of pathology are chronic renal failure, as well as some diseases of the digestive system.

How do tertiary and secondary hyperparathyroidism (symptoms) manifest?

The clinical signs of the secondary and tertiary form are similar to the symptoms of the main disease. Most often, chronic renal failure (CPN) is found.

Specific features include:

Soreness of bones;

Muscle weakness, arthralgia;

Frequent damage, fractures, bone deformations;

A characteristic symptom may also be the calcification of the arteries. This state provokes ischemic changes. It is manifested by the formation of periarticular calcinates on hand and legs.

Calcification of conjunctivations is also possible. With a combination of this pathology with recurrent conjunctivitis, a state occurs that specialists are denoted as a red-eye syndrome.

How is the tertiary and secondary hyperparathyroidism (treatment) corrected?

Therapy of the secondary and tertiary form of hyperparathyroidism is quite complicated. In severe cases, hemodialysis is prescribed, the kidney transplantation is carried out, which extends the life of the patient about 10-15 years.

When prescribing drug treatment, the drug rocaltrol is used. At the same time, carefully controls the calcium allocated with urine. Vitamin D metabolites are prescribed, for example, calcitriol, phosphates binding aluminum preparations are used.

With a very high level of calcium, as well as in the presence of pronounced symptoms, the patient must be hospitalized, after which treatment is carried out under hospital. If there are high brittleness of bone tissue, it shows a strict bed mode, therapeutic nutrition.

If the calcium level is raised slightly, characteristic symptoms are absent or expressed insignificantly, urgent medical intervention is not required. The patient can lead an ordinary life without restrictions. On the recommendation of the doctor, the patient may be shown the healing nutrition. Its principles are always developed individually.

In order to prevent hyperparathyroidism, the chronic diseases of the kidneys, the digestive system should be treated on time. More to go, play sports, practicing with solar and air baths. It is very important to avoid stressful states. Be healthy!

Primary hyperparathyroidism (PGPT) is a disease, the development of which is associated with excessive secretion of the parathyroid hormone (PTH) and as a result of this, with an increase in the content of calcium in the blood serum. PGPT is one of the causes of hypercalcemia - metabolic disorders manifested by an increase in the level of calcium in blood serum and accompanied by a varying degree of severity by a clinical picture. In addition to the PGPT hypercalcemia, malignant neoplasms are accompanied (osteolatic metastases of malignant tumors in the bone); pseudo-opporathyroidism; Family isolated hyperparathyroidism; Tertiary hyperparathyroidism; thyrotoxicosis; chronic adrenal insufficiency; Feochromocytoma; Vipoma; blood system diseases (leukemia, lymphoma, myeloma disease, lymphogranulomatosis); Medical hypercalcemia; bone fractures; long immobility; Acute renal failure and family hypocalciuric hypercalcemia.

Epidemiology PGPT

PGPT is the most common cause of hypercalcemia. The frequency of occurrence of PGPT is approximately 25-28 cases per 100,000 population. The prevalence of PGPT is 0.05-0.1%, while in women it occurs 4 times more often than in men. Approximately half of all cases of the disease fall on the age group from 40 to 60 years, the peak of morbidity is 60-70 years. Thus, in the group of women older than 50 years, the prevalence of hyperparathyroidism is 1-2%. Over the past 50 years, the clinical picture of this disease has undergone significant changes. In the countries of Western Europe and North America, by 1965, the manifestic forms of PGPT prevailed: 60% - kidney pathology, 25% of the bone system and only 2% is the asymptomatic form of PGPT. By 1975, about 50% of kidney forms, 15% of bone and 20% of asymptomic or low-power; By 1990, 18% was the pathology of the kidneys, bone manifestations decreased to 2%, and the proportion of asymptomatic and soft forms of PGPT increased to 80%. In Russia, until 2000, the asymptomic and soft forms of PGPT were practically not treated and did not have been treated, while manifestic, often heavy forms of PGPT were diagnosed in 85-90% of cases. According to preliminary data obtained in the separation of neuroendocrinology and osteopathies of the Federal State Unitary Enterprise ENZ RosMedtechnology, among 340 patients observed about the PGPT, the proportion of manifest forms is comparable to the shares of small-mixed. Thus, a tendency towards an increase in the specific gravity of soft and asymptomatic forms of PGPT and in Russia is traced.

Etiology and pathogenesis of PGPT

The PGPT is due to adenoma or hyperplasia and, less likely, the carcinoma of the Pori-shaped glands (SCC). In most cases, solitary paratromes (80-89%) are detected, less often - multiple adenoma (2-3%), hyperplasia (2-6%) and Cancer ADC (0.5-3%). Hyperparathyroidism, accompanied by a hyperplasia of the alex or multiple adenomas, as a rule, is combined with hereditary syndromes: multiple endocrine neoplasia of the 1st type (Main-1), hyperparathyparatrosis syndrome with a tumor of the lower jaw, family isolated hyperparathyroidism and family hypercalcium. As for sporadic forms, in addition to age and gender, the irradiation of the neck area with a diagnostic or therapeutic goal is a significant risk factor.

Adenoma Associty is usually benign. In accordance with the modern data, the development of adenoma ADCH is associated with two types of mutations: I type - Mutation in mitotic control and type II - mutation of the finite control mechanism of PTH Calcium secretion. The monoclonal tumors are attributed to both the adenoma observed in the Meng-1, sporadic (incomarestic) hyperplasia and the secondary or tertiary hyperplasia of the Associty in chronic renal failure (CPN) and Uremia.

In other cases, under the influence of various factors (low calcium or calcitriol), there is a population of rapidly proliferating cells, which can cause hyperplasia or hyperplastic adenoma. In such cases, polyclonal adenoma is developing.

A specific role in the mutation of the gene encoding PTH belongs to a specific PRAD1-gene belonging to the proto-curved and localized chromosome 11Q13 on which the gene encoding PTH is also localized - 11p15. Subsequently, it was proved that oncogen Prad1 refers to cycles - cellular cycle regulators. Cyclin A is involved in the regulation of the S-phase, and Cycline B - in the regulation of the C2-M-phase of the cell cycle. The PRAD1 protein gene, or cyclin D1, is excessively expressed in the adenoma of the SCC.

In recent years, it has been established that, in addition to the above factors for the formation of tumors of the SCC, this contributes to microsatellite instability. Microsatellites are short tandem repeats in polymorphic DNA sites (usually sa-repetitions). Variations between tandem repeated nucleotides in tumors, but not in normal tissue is called microsatellite instability. Microsatellite instability L. A. LOEB determined as a marker of a mutagenic phenotype with cancer. Confirmation of this concept is a study conducted by M. Sarquis et al., In which it was first shown that a sporadic large adenoma of the Associty, removed from the girl at the age of 8.5 years, contained instability of 4 dinucleotide markers in three different loci 1st, 10 And the 11th chromosome.

It is suggested that the violation of the physiological action of vitamin D is one of the factors predisposing to the development of adenoma ADN. This assumption was confirmed by the study by T. Carling et al., Which believe that the level of mRNA receptor to vitamin D was significantly reduced with adenoma or hyperplasia of the ... 42 ± 2.8 and 44.0 ± 4.0%, respectively) compared to Its content in normal gentle. The reduced expression of the vitamin D receptor gene is probably worsens 1.25 (s) 2D3-mediated control of parathyroidic functions, and it has a value in the pathogenesis not only the secondary hyperparathyroidism at CPN, but also PGPT.

Clinical picture of PGPT

Clinically PGPT can manifest itself as a asymptomatic form, a soft shape, a clinically manifesting form without complications and a clinically manifesting form with the development of complications.

The development of clinical manifestations of PGPT is due to hypercalcemia, which is a consequence of PTG hypersection. With asymptomatic form, hypercalcemia, as a rule, moderate, and clinical manifestations are nonspecific.

Hypercalcemia is manifested by numerous symptoms and signs of the disease that can be submitted by the following groups:

1) manifestations of systemic nature (general weakness, dehydration, calcification of horny shell, soft and other tissues);
2) violations of the CNS activities (decline in the concentration of attention, depression, psychosis, changes in consciousness - from twilight consciousness to coma);
3) the pathology of the musculoskeletal system (osteoporosis, hyperparathyroid osteodistrophy, fractures, proximal myopathy);
4) disorders of the function of the gastrointestinal tract (nausea, vomiting, anorexia, constipation, abdominal pain in pancreatitis and peptic ulcers);
5) disorders of the kidney function (polyuria, polydipsee, isoostenuria, reduction of glomerular filtration, renal disease, nephrollociety);
6) Violations of the function of the cardiovascular system (hypertension, the shortening of the Qt interval, increasing sensitivity to Digitalis preparations).

There are several clinical (manifest) forms of PGPT:

• bone - osteoporotic, fibrous-cystic osteite, pedaloidal;
• burcepathic - with preferably damage to the kidneys, gastrointestinal tract, cardiovascular system;
• mixed.

The damage to the bone system is one of the permanent symptoms of hyperparathyroidism. Bone losses in the peripheral skeleton are first revealed in the end departments of tubular bones due to the prevalence of spongy bone here. Endostal resorption plays a dominant role in PGPT. The result of this process is to expand the bone marrow channel with the thinning of the cortical layer. It was previously believed that one of the most frequent lesions of the bone system in hyperparathyroidism is a generalized fibrous-cystic osteite, which was observed more than 50% of patients. In recent years, due to the earlier diagnosis of the disease, these lesions of bone tissue are revealed less often (10-15%). Cysts and giant tumors are arranged, as a rule, in long tubular bones and are detected during radiography. Cysts are also found in the bones of wrists, ribs, bones pelvis. Gigantaeer tumors on radiographs have a mesh structure and a characteristic view of bee honeycombs. With histological examination of bone lesions, a decrease in the trabecual number is revealed, an increase in multi-core osteoclasts and a substitution of cellular and bone marginal elements with a fibrovascular cloth. The osteoporotic variant is characterized by a progressive decrease in the bone mass in a unit of bone volume with respect to the normal indicator in individuals of the appropriate gender and age, disruption of bone microarchitectonics, leading to increased bone fragility and increasing the risk of fractures from minimal injury and even without such. At PGPT, a diffuse reduction of bone mineral density (IPC) is often fixed, which is difficult to distinguish from age or postmenopausal osteoporosis. It is believed that more frequent detection of osteoporosis is associated with the earlier diagnosis of hyperparathyroidism, when the processes characteristic of fibrous-cystic osteite were not fully formed. These data reflect the influence of low PTH concentration, which causes diffuse osteolysis, and not localized osteoclastic proliferation. Along with this, individual patients identify the characteristic subperiodal resorption of bone tissue, which is most often localized in the phalanges of the fingers of the brush. In this case, resorption prevails over oste formation, which is reflected in the change in levels of bone resorption markers.

In most cases, patients with PGPT occur in the spinal bones, characterized by varying degrees of osteoporosis from a slight deformation of the vertebrae to the characteristic "fish vertebral", sometimes with fractures of the vertebral bodies. In these cases, patients indicate a decrease in growth during the disease. Many patients have complaints against back pain, increasing after exercise, with a long stay in the same position (standing or sitting). Often, when the PGPT is observed the lesion of the joints - chondroalcinosis (calcium phosphatehydrate crystals).

Visceral shape with a predominant kidney damage is found in more than 60% of cases of primary manifestic hyperparathyraratroposis, sometimes kidney damage can be the only manifestation and more often in the form of urolithiasis. In 13-15% of cases, single stones are detected, in 25-30% - multiple and in 30-32% of cases - concrections in both kidneys. In cases of visceral manifestations of hyperparathyroidism, for example, in the form of urolithiasis, the surgical removal of the stone does not lead to recovery, the concrections may be formed in another kidney, and often in the operated one. However, the forecast of the urolithiasis after removing the adenoma is favorable, if CPN has not developed. Conductors in the kidneys with hyperparathyroidism consist of oxalate or calcium phosphate.

With a visceral form with a predominant lesion of the Cardiovascular system, the PGPT is accompanied by hypertension, calcification of coronary arteries and heart valves, left ventricular hypertrophy and the deposition of calcium salts in the heart muscle and others. The deposition of calcium salts in the heart muscle can cause myocardial necrosis with a clinic of acute myocardial infarction. In a prospective study by T. Stefenelli et al. It was established that PTH PER SE plays an important role in maintaining myocardial hypertrophy. After parathyroidectomy and normalization of the level of calcium in the blood serum for 41 months, the authors observed the regression of hypertrophy of the partition, the back wall and left ventricle by 6-21%.

Gastrointestinal symptoms are detected by half of patients with PGPT. Patients impose complaints against anorexia, constipation, nausea, flatulence, weight loss. The peptic ulcers of the stomach and / or duodenum are found in 10-15% of cases, pancreatitis - at 7-12%, less often pancreaticalculcosis and pancreaticity. The development of the gastric ulcers in hypercalcemia is associated with an increase in gastroin and hydrochloric acid, which returns to the norm after removing the adenoma of the resolution. The course of the gastric ulcer with PGPT is characterized by a more pronounced clinical picture (frequent exacerbations with strong pain syndrome, perforations are possible) than with a stomach peppercan disease due to other factors.

In addition to the above-described symptoms in PGPT, it is observed in rare cases, skin necrosis due to the deposition of calcium salts, the calcification of the ears of the sinks, the rod keratitis (linear keratopathy), developing due to the deposition of calcium salts in the corneal of the cornea of \u200b\u200bthe eye.

One of the serious complications of PGPT is hypercalcemic crisis. An increase in calcium content above 3.49-3.99 mmol / l (14-16 mg / 100 ml) leads to the development of signs of intoxication, characteristic of hypercalcemia.

Hypercalcemic crisis is a severe complication of PGPT arising against the background of fractures, infectious diseases, pregnancy, immobilization, intake antacids (calcium carbonate). It develops suddenly, while nauseous, indomitable vomiting, thirst, acute abdominal pain, pain in muscles and joints, high fever, convulsions, confusion, stupor, coma. Mortality in hypercalcemic crisis reaches 60%. Against the background of Anuuria, cardiovascular failure appears. If hypercalcemia increases to 4.99 mmol / l (20 mg / 100 ml), then the activities of the CNS with the braking of the function of the respiratory and vascular centers are oppressed and an irreversible shock is developing.

Diagnostics and Differential PGPT

The diagnosis of hyperparathyroidism is based on anamnesis data, patient complaints, clinical picture (peptic ulcer of the stomach, urolithiasis, pancreatitis, chondroalcinosis, bone changes - osteoporosis, bone cysts) and the results of laboratory studies.

Laboratory research

During the laboratory research, the cardinal sign in suspected of the PGPT is an increase in the level of PTH, which in most cases is accompanied by hypercalcemia. The permanent sign of hyperparathyroidism is hypercalcemia; Hypophosphatemia is less constant than the increase in calcium in serum. The content of alkaline phosphatase in the blood serum is increased. Less often occurs hypomagnesiamia. Along with this, the excretion of calcium, phosphorus with urine.

In some patients with elevated PTH level, the concentration of general calcium in serum is normal. This state is called a normocalcemic variant of PGPT.

Causes of the normocalcemic version of the PGPT:

• renal failure (violation of Calcium tubular reabsorption);
• calcium absorption disorder in the intestine;
• avitaminosis D.

To distinguish the hyperparathyroidism with vitamin D from the isolated Avitaminosis d, vitamin D is carried out. Against the background of vitamin D replacement therapy in patients with hyperparathyroidism, hypercalcemia occurs, and in patients with insulated avitaminosis D is restored by normocalcemia. Transient normocalcemia can occur in the early stages of the development of PGPT. In order to confirm the diagnosis of hyperparathyroidism in patients with recurrent urolithiasis and normocalcemia, a provocative test with thiazide diuretics is carried out.

For bone and mixed PGPT forms, a significant increase in bone metabolism is characterized with an increase in the frequency of activation and the predominance of resorption processes. In the manifest form of the PGPT, the average osteokalcin level exceeded the normative values \u200b\u200bof 2.6-20 times, and a reliable correlation between alkaline phosphatase activity and PTH (R \u003d 0.53, P< 0,01), между уровнем остеокальцина и ПТГ (r = 0,68, p < 0,01). У больных ПГПТ отмечается повышение общей щелочной фосфатазы крови, остеокальцина крови и оксипролина мочи, а также дезоксипиридинолина мочи и тартратрезистентной кислой фосфатазы крови . В исследовании пациентов с ПГПТ были выявлены статистически значимые корреляции между дезоксипиридинолином мочи и сывороточной костной щелочной фосфатазой, а также остеокальцином сыворотки. Кроме того, отрицательные корреляции высокой степени были выявлены между дезоксипиридинолином мочи и минеральной плотностью костной ткани как в позвоночнике, так и в лучевой кости .

The effect of PTH on the products of osteoprothyterine (HGG) and the Ligand of the NF-KAPPAB receptor of the NF-KAPPAB (RANKL) is not fully installed. It has been demonstrated that PTH reduces the GDG products and increases RANKL products. It was noted that in front of the surgical treatment of hyperparathyroidism Rankl and osteoprothyterine correlated with serum osteocalcin. The ratio of Rankl / osteoprothyterin decreased after surgical treatment, which indicates the possibility of their use as markers of the state of bone tissue with PGPT.

Speaking about the role of the N-terminal Telopeptide, it should be noted that according to the researchers, the high level of this marker is a factor indicating the greatest effectiveness of surgical treatment.

The diagnosis of hyperparathyroidism is confirmed by determining the content of PTH in serum. Sensitive methods for determining PTH in the blood are developed: immunoradiometric (IRMA) and immunohemyluminometric (ICMA). Thus, the bases for the diagnosis of PGPT is a resistant hypercalcemia and an increase in the level of PTH in serum.

Instrumental research

To detect bone changes, it is conducted by radiography of tubular bones, pelvic bones, the chest and lumbar spine, osteodensitometry of lumbar vertebrae, proximal departments of the thigh, radiation bone.

Finding out the nature of hypercalcemia and the diagnosis of hyperparathyroidism should be carried out comprehensively, including studies in order to determine the localization of adenoma or hyperplasia: ultrasound examination (ultrasound), arteriography, scintigraphy, selective veins, , magnetic resonance tomography (MRI).

Ultrasound Joints. The sensitivity of the method is from 34% to 95%, specificity reaches up to 99%. The results of the study depend on the experience of a specialist in ultrasound diagnostics, the mass of the mind (with a mass of gland less than 500 mg, sensitivity is significantly reduced to 30%). The method is not informative with atypical localization of the resistant - behind the sternum, in the possession of the space.

Scintigraphy. As a rule, it is performed with Tallium 201TL, pephotos 99 MTS technicia, which accumulate in the thyroid gland and in increased resistant. One of the latest methods is scintigraphy using Tehnetrile-99Ts (99MTC-SESSIBI-scintigraphy) - the complex Technetium 99m and methoxyisobutylinitrile. Compared to 201t, scintigraphy with techneteril-99ts is characterized by a significantly lower radial load and more accessibility, the sensitivity of the method reaches 91%. It should be noted that if there are gigantaic tumors in the bones, which are with heavy forms of PGPT and are detected x-ray, the accumulation of 99MTC in the lesions of the damage to these bones can give a false positive result of topical diagnostics, which should be borne in mind when evaluating the SCINTIGRATIGRATIGRATIGRATIGRATIGRAY data to compare The results of the X-ray study of the corresponding skeleton department.

CT allows you to reveal the adenoma of a decrease in 0.2-0.3 cm. The sensitivity of the method is from 34% to 87%. The disadvantages of the method are the load in the form of ionizing radiation.

Some authors consider MRI with one of the most effective methods of visualization of the Assignment, but due to the high cost and time spent time spent to obtain an image, it does not apply quite widely. It is believed that the gentlemen located in the tissues of the thyroid gland is much more difficult to differentiate with MRI than with an ultrasound, but, focusing on the latest data, we can assume that MRI is a fairly sensitive method (50-90%).

Invasive research methods include puncture of the Association under the control of ultrasound, selective arteriography, veins catheterization and taking from the blood from the gland to determine PTH. Invasive methods are used in the case of PGPT recurrence or after an unsuccessful audit of the ADD while maintaining the signs of PGPT.

However, sometimes, despite the use of all research methods, it is not possible to confirm the presence of adenoma, and the course of the disease does not allow continuing conservative therapy. In these cases, an operation is recommended during which all the Audit revision is conducted. More often (60-75%) adenoma is located in the lower detection, and the detection of the tumor in one of them, as a rule, eliminates the adenomose in the other gentlemen. Nevertheless, the revision of the rest of the glands is obligatory.

Treatment of primary hyperparathyroidism. Selection of therapy

The choice of the treatment method depends on the presence or absence of the adenoma of the ASH, on the degree of expression of hypercalcemia and the presence of complications, such as nephroalcinosis, ulcerative illness of the stomach, etc. If there is a confirmed tumor, hypercalcemia and complications are recommended operation. According to the consensus on the diagnosis and maintenance of patients with PGPT, surgical intervention is shown in the following cases:

1) the concentration of general calcium in the blood serum by 0.25 mmol / l (1 mg%) exceeds the rate set in this laboratory for this age group;
2) reducing the glass filtration rate by more than 30% compared with the norm established in this laboratory for this age group;
3) visceral manifestations of PGPT;
4) Daily excretion of calcium more than 400 mg;
5) Reducing the IPC of the cortic bones by more than 2.5 SD on the T-criterion;
6) Age less than 50 years.

Surgical treatment methods

As a rule, during operations on the SCC about the PGPT, there are revision of all four wells, since not always a preoperative topical diagnosis reveals multiple adenoma and hyperplasia, the adenoma of the extension.

According to J. N. Attie, from 1196 patients operated on for hyperparathyroidism, a single adenoma (including one patient with Men-2 syndrome) was discovered in 1079 patients; In 41 patients - two adenomas; 4 - three adenomas; In 23 - primary hyperplasia; In 30 - secondary hyperplasia; in 6 - tertiary hyperplasia; At 12 - Cancer Association and in 1 patient - in one degree of cancer and in the second - adenoma. Interestingly, out of 1158 patients operated on by the author on the PGPT, in 274 (23.7%) were simultaneously identified and thyroid diseases were identified: in 236 patients, changes in the tissues of the thyroid gland were benign and 38 - a papillar or follicular thyroid cancer was found. glands. Of the 38 patients with malignant tumors of the thyroid gland, 26 tumors were palpable before the operation; In 2 patients, they were found on the ultrasound and 10 - revealed randomly during surgery about the removal of the adenoma of the SCC.

In the case of diagnosis of PGPT during pregnancy, parathyroidectomy is permissible in the II trimester of pregnancy.

Specific peculiarities are characterized by operational tactics against the Cancer ADC. Cancer Associty, as a rule, slowly grows and rarely gives metastases. With full gland removal without damage to the capsule, the forecast is favorable. In some cases, cancer is more aggressive, and at the first operation, metastases in the lungs, liver and bones are found. It is not always possible to immediately determine that the primary tumor is precisely cancer; With histological examination of the non-invasive tumor, it is possible to detect an increase in the number of figures of mitosis and fibrosis of stroma gland. Cancer Associty is often diagnosed retrospectively. Hyperparathyroidism due to the cancer of the gentleman, it is often impossible to distinguish from other forms of PGPT. At the same time, it is known that Cancer Associty is often accompanied by severe hypercalcemia. Therefore, at the level of calcium in the blood, more than 3.5-3.7 mmol / l, the surgeon should be particularly attentive to prevent damage to the capsule when the affected gland is removed.

The frequency of complications and mortality in the surgical treatment of PGPT is not large, and recovery occurs in more than 90% of cases. With successful intervention, the postoperative period proceeds, as a rule, without complications. It is necessary 2 times a day to determine the content of calcium in the blood; With its rapid decline, calcium preparations are recommended. Permanent ECG controls.

The most common postoperative complications include: damage to the return gastriced nerve, transient or resistant hypocalcemia, very rarely hypomagnation, in patients suffering from heavy hypercalcemia, can develop "hungry bone syndrome".

Treatment of postoperative hypocalcemia ("hungry bone syndrome")

Most clinical symptoms of PGPT after successful operational intervention are exposed to reverse development. After the surgical treatment of PGPT, i.e., after eliminating PTG hyperproduction, there is a fairly rapid reverse development of clinical symptoms and biochemical indicators. After adequately conducted surgical treatment in some cases, hypocalcemia occurs, which requires the use of vitamin D or its active metabolites and calcium preparations. To eliminate the "hungry bones" syndrome in the bone form of the hyperparathyroidism in the postoperative period, calcium preparations are prescribed at a dose of 1500-3000 mg (by calcium-element) in combination with alpha calcidol (etylph, alpha d3-teva) by 1.5-3.0 μg per day and / or dihydroitachisterol (dihydrootahsterol, A.T. 10) at 20-60 drops per day. In the rate of normocalcemia, the dose is gradually decreasing to supporting: 1000 mg of calcium and 1-1.5 μg of alpha cellsidol by 0.5-2 years. In our practice, calcium-d3 is prescribed more often (in 1 chewing tablet 500 mg of calcium and 400 mg vitamin D3) in combination with alpha cellsidol. These drugs are well transferred, convenient to use and safe.

Treatment of patients with soft forms of PGPT

Patients older than 50 years with light hypercalcemia, normal or slightly reduced bone weight and normal or slightly disturbed kidney function can be treated conservatively. In these cases, it is recommended:

• increase fluid intake;
• limit the reception of sodium, protein and calcium;
• take diuretics;
• take preparations that reduce the resorption rate of bone tissue.

According to a 10-year-old prospective study of 120 patients with PGPT, subjected to or not exposed to surgical treatment, the authors concluded that there are no significant differences in biochemical indicators and indicators of bone mineral density in non-eaten patients with a small-mixed and asymptomatic hyperparathyroidism. However, a number of patients were revealed, in whose surveillance process there were indications for surgical treatment (the occurrence or progression of the urolithiasis, the negative dynamics of the bone mineral density, small-acting fractures). At the same time, if patients with PGPT deterioration of signs of the disease is not noted, it is possible to refrain from surgical treatment.

With the soft forms of PGPT with a moderate decrease in the IPC in women during menopause, it is recommended that estrogen or bisphosphonate preparations are recommended to prevent osteoporosis progression. In recent years, bisphosphonates are prescribed more often. The purpose of the appointment of bisphosphonates for long-term use is the correction of osteoporosis, and not a decrease in the level of PTH, but it is possible to reduce hypercalcemia. For therapy with bisphosphonates, paminery acid (pamineroneate medal), risadronate, alendronate are used. S. A. Reasner et al. Used to treat patients with osteoporosis and PGPT risadronate, which for 7 days normalized the level of calcium in serum while reducing not only alkaline phosphatase in the blood, but also the excretion of hydroxyproline, as well as an increase in calcium renal tubular reabsorption. Good results were also noted when using alendronate.

It should be emphasized that the effectiveness of the methods of treatment varies greatly depending on the pathogenetic variety of hypercalcemia and the individual sensitivity of the patient to a particular preparation. In medicinal tactics, the dynamics of laboratory indicators and the possibility of reducing hypercalcemia should be taken into account.

Conclusion

Thus, the above review of literature dedicated to etiologies, pathogenesis, diagnosis and treatment of PGPT, indicates both significant achievements and a number of unresolved problems in this area. Due to the presence of difficulties in the early diagnosis of PGPT, normocalcemic breakers of PGPT against the background of vitamin D deficiency, the absence of the widespread determination of calcium in the blood and urine in routine clinical practice, patients with soft or asymptomatic forms are poorly revealed. The question of testimony for surgical treatment, on conservative therapy of patients with a soft form of PGPT continues to be discussed. All this determines the need for further study of clinical manifestations of the disease and improve the methods of differential diagnosis and optimizing the treatment of patients with PGPT.

For literature, please contact the editor.

L. Ya. Rorinskaya, doctor of Medical Sciences
Enz Rosmedtehnologiy, Moscow

Hyperparathyroidism is a disease that is more susceptible to women than men, and it is 2-3 times more often. This disease belongs to the violations of the endocrine system, and is caused by excessive generation of parachitoid glands of the parathgamon (PTH). This hormone leads to the accumulation of calcium in the blood, which is why bone tissues suffer, as well as the kidneys. During the diagnosis of hyperparathyroidism, symptoms and treatment in women - information that is necessary for everyone who has disorders in the work of the thyroid gland, especially if the girl is in the risk group - aged 25 to 50 years.

The reasons

Healthy thyroid gland produces a normal number of pararathgamon, but when there are violations, the quantity can arise both to decrease and grow significantly. The work of the gland affect:

1. Tumors, appeared in the tissues of the thyroid or lymph nodes of the neck. In this case, disorders cause malignant and benign neoplasms.
2. Renal failurehaving passed into the chronic stage.
3. Hereditary autosomal dominant syndromewhich provokes tumors in one or more glasses of internal secretion. Sometimes diseases cause hyperplasia instead of a tumor.
4. Diseases associated with gastrointestinal tract.
5. Secondary hyperparathyroidism Against the background of vitamin D deficiency, one of rare cases of illness, it usually has a chronic form, which leads to changes in the tissues of internal organs. Most often, the violation in the work of the thyroid gland is not the only symptom.
6. Alimentary hyperparathyroidism - disease caused by poor nutrition. It may be present even with a diverse and balanced diet if the body does not absorb part of the beneficial substances.

Depending on the reasons that caused the disease, distinguish:

1. Primary hyperparathyroidism - the cause of violations are diseases of the thyroid gland. Most often it is hereditary violations that are diagnosed at an early age.
2. Secondary - it appears as an answer of the body for a long-term lack of calcium caused by poor food or disadvantage of vitamin D. Another cause of secondary hyperparathyroidism are bone tissue diseases or digestive organs, as well as the kidneys too quickly derive calcium from the body.
3. Tertiary - appears only with a long flow of secondary hyperparathyroidism, which, without proper treatment, provokes the appearance in the parachitoid glands of adenoma.

In addition to the present disease caused by disorders in the thyroid gland, there are pseudo-opporathyroidism caused by the production of a substance similar to the functions with a pararathgamon. There is such diseases due to malignant tumors producing this substance. At the same time, the neoplasms are affected by other glands in the body, and do not directly affect the secretion of the parathgamon.

Symptoms

Hyperparathyroidism, the symptoms of which are not specific in the early stages, and in some cases the disease passes without significant manifestations. Therefore, the violation is rarely diagnosed in a light form if there are no significant changes in the tissues of the thyroid.

In the early stages appear:

• Headache and deterioration of cognitive functions.
• Increased fatigue.
• Reducing the tone of the muscles, which leads to difficulties with movement, especially seriously the patient climbs the stairs, even on a small height.
• The deterioration in the emotional sphere, the emergence of signs of neurasthenia, and sometimes depressed. People with reduced immunity, as well as children and the elderly, mental disorders may appear, which cannot be explained by genetic predisposition or external influence.
• Changes on the color of the skin on the pale, and with a long disturbance, it acquires an earthy tint.
• The change in the gait, which becomes the "duck", due to the reduction of the tone of the pelvic muscles or changes in the bone structure of the hip.

At the later stage, disorders arise in bone tissue:

1. Osteoporotic - Developing reduction in bone mass, as well as violations of its structure.
2. Fibrozno-cystic osteite - Inflammation in the bones leading to the appearance of cystic tumors.

Due to the disorder of the bone structure, patients often have fractures, with ordinary movements that are not traumatic. So, a person can break his hand or leg, being in bed. With this stage of the disease, pain occurs without a clear localization, and most often they are characterized as "bone lomit". Fractures that appeared in this stage deliver less painful sensations than a healthy person, but at the same time they worse heal, and more often accompanied by complications. Broken bones are often incorrect, because of which the deformation of the limbs occurs.

The problems with the bone structure cause not only fractures, but also changes in the spine, because of which a person can be lower than the growth or the posture will deteriorate sharply. A frequent occasion is a violation of the integrity of the teeth, at which they begin to stagger, due to violations in the alveolar bone and tissues. Often in such cases, even healthy native teeth begin to fall out.

Hyperparathyroidism, the symptoms of which are nonspecific, is called bombcopathic. He meets very rarely. This case of the disease is developing gradually, due to which difficulties arise with diagnostics. Initially, a person appears signs of intoxication, often repeated vomiting or diarrhea, elevated meteorism, as well as a decrease in appetite and a quick loss of body weight.

Ulzes that are accompanied by bleeding can appear in the gastrointestinal tract, while the treatment of the mucous membrane is ineffective, which is why frequent exacerbations and relapses occur. Perhaps the damage to the pancreas, liver or raging bubble. And also often register an increase in the amount of urine released more than the daily rate, which is why patients appear constant thirst, which is impossible to quench. In the development of the disease in kidney tissues, calcium salts are minimized, which causes their change, and with time and renal failure.

Diagnostics

Initially, the disease does not have specific symptoms, which is why it is difficult to diagnose. But there are a number of general analyzes that can show an increase in calcium content in the body:

1. The overall urine analysis - the liquid becomes more alkaline, while in it there are calcium salts, and the amount of phosphorus increases. Sometimes a protein occurs in the urine, which indicates inflammation in the kidneys. At the same time, the density of the discharge is reduced, but their number increases.
2. Biochemical blood test - allows you to find out the composition of the blood, to accurately determine the violation of proportions. With hyperparathyroidism, the number of general and ionized calcium in the blood is increased, and phosphorus is reduced.

Specific analyzes:

1. Chemiluminescent immunoassay - Fence of venous blood for determining the number of parathgamon.
2. Ultrasound thyroid gland - Allows you to determine changes in tissues, as well as detect disorders in lymph nodes.
3. Radiography, CT or MRI - Conduct both in the neck and limbs, if the patient complains of pain, unexpected fractures, or a change in mobility.
4. Scyntigraphy gland - It makes it possible to determine how well the parathyroid glands are located, as well as which fabrics are included in their composition, there are pathological changes, and as an organ functions.

In addition to general and specific analyzes, the doctor may appoint additional research to identify the cause of the disease. This is especially important if the disease is secondary.

Treatment

When a hyperparathyroidism is detected, treatment must be complex, it will depend on the root cause of the disease. Due to the fact that tumors or other disorders of the thyroid structure are often present, the combination of surgical intervention and drug therapy is optimal.

With the primary formulation of the diagnosis of hyperparathyroidism, the clinical recommendations of the doctors most often contain the removal of the tumor or parathyroid dysplasia. If the size of the changed tissues is small, the special endoscopic equipment is used, which reduces the intervention in the body, which has a beneficial effect on the rate of recovery.

In addition, doctors prescribe different measures to reduce calcium in the blood. For this, the sodium chloride solution can be administered intravenously, as well as assign a furosemide, potassium chloride and a solution of glucose 5%. But such measures are needed only with too high calcium content, which can provoke crisis. It increases the burden on the kidneys, so all medicines must be taken only under the supervision of the doctor to reduce the likelihood of pathological changes.

If the disease is caused by malignant tumors, then after their removal, a course of radiation or chemotherapy is carried out, selected individually, depending on the occurrence of the disease.

If the disease is diagnosed in the early stages, there are no serious chronic diseases in the body, the treatment prediction is quite favorable. When the disease began to strike bone tissue, but did not go too far, therapy takes 4 to 24 months. The defeat of the kidneys is considered a more severe case due to pathological changes in the organs.

In the disease, hyperparathyroidism, symptoms and treatment in women do not differ from those that are characteristic of men, but due to an unstable hormonal background, the gland of the internal secretion is more susceptible to changes. Therefore, having sexual women are important to follow the health of the thyroid gland and regularly check the amount of calcium in the blood.