Blood on TMS in vitro. Epilepsy in children - Fr. Examples of the use of liquid chromatography in combination with tandem mass spectrometry in clinical assays

What is Tandem Mass Spectrometry

Tandem mass spectrometry (TMS) is one of the modern methods for the analysis of compounds, which is widely used for various scientific and practical purposes. This method allows the analysis of several hundred compounds in microquantities of biological material.

Where is this method applied?

In world healthcare practice, this method is used for mass screening of newborns for hereditary metabolic diseases (HMD). In a spot of dried blood, it is possible to determine amino acids (including phenylalanine) and acylcarnitines. The quantitative determination of these substances makes it possible to exclude several dozen hereditary diseases belonging to various classes of NBOs (disturbances in the metabolism of amino acids, organic acids, and defects in mitochondrial β-oxidation of fatty acids). According to foreign literature data, their total frequency is 1:2000 live newborns. Previously, the diagnosis of these disorders required a large amount of biological material, several studies (amino acid analysis, gas chromatography-mass spectrometry, determination of the spectrum of acylcarnitines), which required considerable time and material costs. TMS allows you to quantify all of these compounds in one run!

What diseases can be detected using this method?

Unfortunately, one universal, highly sensitive and specific test for the diagnosis of all known NBOs does not yet exist, but technologies aimed at identifying several tens and even hundreds of diseases in one analysis are already becoming a reality. TMS is one of these methods. This method makes it possible to detect with high reliability about 40 hereditary disorders of the metabolism of amino acids, organic acids, and defects in mitochondrial beta-oxidation of fatty acids. Most of these diseases appear during the neonatal period. The list of diseases that can be diagnosed using this technology is given in the analyzes section.

Why is it important to diagnose metabolic diseases as early as possible?

Many physicians mistakenly believe that NBOs are so rare that they should only be excluded as a last resort, and very often the correct diagnosis is made only at a later date or the disease is not diagnosed at all.

However, more than 150 forms of NBO are already known for which methods of effective therapy have been developed, and the life and health of the patient largely depends on how quickly and correctly the diagnosis is made. For 20 diseases that can be diagnosed using TMS, specific treatments have been developed. A timely diagnosis is a saved life and health of the patient!

Rules for collecting blood samples

Blood is collected on a standard filter card (#903) used to screen newborns for PKU. Blood can be either capillary (from the finger, heel), or venous. It is necessary to saturate the selected area on the filter well! The filter card must clearly indicate the full name, by whom and from where the patient was referred, date of birth and telephone number of the attending physician. The sample is dried for 2-3 hours in air. It is advisable to attach an extract from the medical history.

4, 1

1 Federal State Budgetary Institution Medical Genetic Research Center of the Russian Academy of Medical Sciences

2 SBEE HPE "Rostov State Medical University of the Ministry of Health of Russia"

3 GBUZ "Regional Clinical Hospital No. 1 named after Professor S.V. Ochapovsky" of the Health Department of the Krasnodar Territory

4 FGBU “Medical Genetic Research Center”

In order to justify the introduction of a mass screening of newborns for hereditary metabolic diseases (HME) by tandem mass spectrometry (MS/MS), a retrospective study of archival blood samples of children (n=86) who died in the first year of life was carried out. Changes in the profiles of amino acids and acylcarnitines were detected in 4 cases (4.7%). In one of them, a multiple increase in the concentration of leucine, isoleucine and valine, specific for the disease, was found. The clinical picture and the detection of a mutation in the first exon of the BCKDHB gene (с.98delG) in the heterozygous state indirectly confirmed the diagnosis of leucinosis. In the remaining three cases, the identified changes in the profile of amino acids and acylcarnitines are not of the same specific nature. In these cases, repeated blood tests by MS/MS, additional clinical and biochemical studies would be necessary. As a result of the study, the necessity of introducing the MS/MS method into neonatal screening programs for NBO for their timely diagnosis and treatment was confirmed.

retrospective diagnosis

tandem mass spectrometry

hereditary metabolic diseases

1. Krasnopolskaya K. D. Hereditary metabolic diseases. Reference manual for doctors. - M.: ROO "Center for Social Adaptation and Rehabilitation of Children" Fohat ", 2005. - 364 p.

2. Mikhailova S. V., Zakharova E. Yu., Petrukhin A. S. Neurometabolic diseases in children and adolescents. Diagnosis and approaches to treatment. - M.: "Literra", 2011. - 352 p.

3. Chace H. D. Rapid diagnosis of MCAD deficiency quantitative analysis of octanoylcarnitine and other acylcarnitines in newborn blood spots by tandem mass spectrometry / Chace H. D., Hillman S. L., Van Hove J. L. et al. // Clinical Chemistry. - 1997. - V. 43. - No. 11. - R. 2106-2113.

4. Nyhan L. W., Barshop B. A., Ozand P. T. Atlas of metabolic diseases. - Second edition. - London: Hodder Arnold, 2005. - 788 p.

5. Rashed M. S. Clinical application of tandem mass spectrometry: ten years of diagnosis and screening for inherited metabolic diseases // J. of Chrom. B. - 2001. - V. 758. - No. 27-48.

6. Sweetman L. Naming and counting disorders (counditions) included in newborn screening panels / Sweetman L., Millington D. S., Therrell B. L. et al. // Pediatrics. - 2006. - V. 117. - P. 308-314.

7. Van Hove J. L. Medium-chain acl-CoA dehydrogenase deficiency: diagnosis by acylcarnititne analysis in blood/Van Hove J. L., Zhang W., Kahler S. G. et al. // Am. J. Hum. Genet. - 1993. - V. 52. - P. 958-966.

Introduction

To date, more than 500 nosological forms of hereditary metabolic diseases (NBO) are known. The main part of NBO is extremely rare, but their total frequency in the population is 1:1000-1:5000. As a rule, NBOs manifest in the first year of life with nonspecific symptoms that clinically mask them as another, non-hereditary somatic pathology. At the same time, timely diagnosis of metabolic hereditary diseases is important, since for many of them effective methods of pathogenetic treatment have been developed and continue to be developed, without which the outcome of the disease often remains fatal. It is generally recognized that one of the most justified and effective approaches to the early detection of hereditary pathology is neonatal genetic screening. The development of the method of tandem mass spectrometry (MS/MS) with electrospray ionization made large-scale mass spectrometric screening applicable in the practice of mass screening at NBOs by the end of the 1990s. This highly sensitive micromethod makes it possible to simultaneously determine the concentrations of tens of amino acids and acylcarnitines in several microliters of blood, which are important for the diagnosis of NBO. The effectiveness of the MS/MS laboratory test made it possible to include it in the state programs of neonatal screening of newborns for aminoacidopathy, organic aciduria, and defects in mitochondrial β-oxidation of fatty acids in a number of countries. However, in the Russian Federation, the MS/MS method has not been introduced into the system of mass screening of newborns and is available for selective screening for NBO only in a few federal medical centers.

The purpose of this study was to scientifically substantiate the need to include MS/MS studies in regional programs of mass screening of newborns for the diagnosis of aminoacidopathy, organic aciduria, and defects in mitochondrial β-oxidation of fatty acids based on a retrospective mass spectrometric analysis of blood samples from sick children whose diseases ended. death in the first year of life.

Patients and research methods

This retrospective study included children (n=86, boys:girls ratio 48/38) who died in the first year of life (aged 5 days to 11 months of life) within one calendar year (2010) in the administrative territory of the Krasnodar Territory . The study included children with congenital malformations (n=29), infectious diseases - pneumonia, sepsis, bacterial meningoencephalitis (n=37), perinatal CNS damage (n=11), sudden death syndrome (n=6) and other diseases ( n=3). The control group consisted of 438 clinically healthy newborns (227 girls, 211 boys) aged 3-8 days. In this group, reference values ​​of concentrations of amino acids and acylcarnitines in capillary blood were determined in healthy children of the neonatal period.

The material for the study was archival peripheral blood samples on standard paper test forms obtained on the 3rd-8th day of life for standard neonatal screening. The concentration of amino acids and acylcarnitines (Table 1) in the blood was determined by tandem mass spectrometry (MS/MS) using an Agilent 6410 quadrupole tandem mass spectrometer (Agilent Technologies, USA) according to the certified method of CHROMSYSTEM No. V1 07 05 57136 001. The study was performed in the laboratory of medical genetics of the State Budgetary Educational Institution of Higher Professional Education "Rostov State Medical Institute of the Ministry of Health of Russia".

Table 1

Metabolites determined by MS/MS

	Metabolite	Symbol		Metabolite	Symbol
A mino acids
				3-methylcrotonylcarnthine
	Aspartic acid			3-hydroxyisovalerylcarnitine
	Glutamic acid			Hexanoylcarnitine
	Leucine + Isoleucine			Octanoylcarnitine
	Methionine			Octenoylcarnitine
	Phenylalanine			Decanoylcarnitine
				Decenoylcarnitine
				Dodecanoylcarnitine
				Myristilcarnitine
	citrulline			Tetradecenoylcarnitine
				Tetradecinoylcarnitine
				Hydroxymyristylcarntine
A c i l k a r n i t i n y				Palmitoylcarnitine
	free carnitine			Hexadecenoylcarnitine
	Acetylcarnitine			Hydroxyhexadecenoylcarnitine
	Propionylcarnitine			Hydroxypalmitoylcarnitine
	Malonylcarnitine			Stearoylcarnitine
	Butyrylcarntine			Oleoylcarnitine
	Methylmalonylcarnitine			Hydroxystearoylcarnitine
	Isovalerylcarntin			Hydroxyoleoilcarnitine
	Glutarylcarnitine			Hydroxylinoylcarnitine

Statistical processing of the obtained data was carried out using the Statistica 6.0 software package and Excel 2007 spreadsheets. To determine the descriptive numerical characteristics of the variables, standard methods of statistical analysis were used: calculation of the median, 0.5 and 99.5 percentiles.

For confirmatory molecular genetic diagnosis of leucinosis, DNA was isolated from dried blood spots using the DiatomDNAPrep kit (LLC Biocom, Russia). The selection of primers for PCR amplification was carried out for 10 exons of the BCKDHA and BCKDHB genes. Sequencing of PCR fragments to detect rare mutations was carried out according to the manufacturer's protocol on an ABIPrism 3500 genetic analyzer (Applied Biosystem, USA).

Research results and discussion

As a result of the study of the concentrations of amino acids and acylcarnitines in the peripheral blood of 438 clinically healthy newborn children, 0.5 and 99.5 percentile concentrations of the studied metabolites were determined, which were used by us later as reference values ​​(Table 2). Comparison of the concentrations of amino acids and acylcarnitines, determined in blood samples of 86 children who died in the first year of life, with reference values ​​of concentrations, showed that in 82 patients (95.3%) none of the studied parameters went beyond 0.5 and 99, 5 percentiles of the control group, which made it possible to abandon the working version of the presence of amino acid and carnitine metabolism disorders that were not verified in vivo. However, in 4 children (4.7%), the concentrations of some amino acids and acylcarnitines were several times higher than the upper limits of the reference interval of the control group (Table 2).

table 2

Results of a retrospective assessment of the concentrations of amino acids and acylcarnitines in newborns (n=4) with the level of individual metabolites outside the range of 0.5-99.5 percentiles

	Metabolites	Concentrations of individual metabolites (µmol/l)
		Reference values ​​of the control group (n= 438) in the range 0.5-99.5 percentiles	Individual patient values ​​(n=4) *
			Patient 1	Patient 2	Patient 3	Patient 4
A mino acids
			2503,868
						1457,474
A c i l k a r n i t i n y

* Note:

Patient 1 - boy KM (diagnosis: obstructive bronchiolitis), died at the age of 11 months;

Patient 2 - boy CF (diagnosis: pneumonia), died at the age of 1 month;

Patient 3 - girl PV (diagnosis: sepsis), died at the age of 12 days.

Patient 4, a PA girl (diagnosis: pneumonia), died at the age of 6 days.

In the first case, in a CM patient who died at the age of 11 months and was diagnosed with obstructive bronchiolitis, tandem mass spectrometry of amino acids and acylcarnitines in archival blood samples revealed changes in the content of leucine, isoleucine and valine, which are specific enough to indicate a high probability of congenital metabolic defect in the catabolism pathway of leucine and isoleucine. In the studied archival blood samples, an increase in the concentration of leucine and isoleucine by more than 9 times and valine - by more than 3 times compared to the reference values ​​was found, which suggests the diagnosis of "disease with the smell of maple syrup urine".

From the available clinical data in favor of leucinosis in a KM child, the following clinical manifestations testified: early refusal of breastfeeding, symptoms of neonatal encephalopathy, an increase in neurological symptoms - changes in muscle tone, convulsions, epilepsy, psychomotor retardation. The child often had severe respiratory tract infections, which caused bronchiolitis obliterans, which was the cause of death at the age of 11 months. We do not have information about whether the child had a specific smell of urine, but the increase in the concentration of metabolites typical for leucinosis and the characteristic clinical symptoms confirm our assumption. In addition, the results of a DNA diagnosis of leucinosis using archived blood samples support the diagnosis of maple syrup urine odor disease. Molecular genetic analysis revealed a c.98delG deletion in the first exon of the BCKDHB gene in the child in the heterozygous state. The same mutation was found in the mother's blood. Due to the limited number of archival blood samples of the child and the unavailability of the biological material of his father, the second mutation could not be found. However, a combination of clinical, biochemical and molecular genetic data support the diagnosis of leucinosis (or maple syrup urine odor disease, MIM ID 248600) in the case studied.

In the remaining three cases, the identified changes in the profile of amino acids and acylcarnitines are not of the same specific nature as in the previous case. It is impossible to assume certain NBOs based on MS/MS data, and even more so to assert with certainty, in these cases. For the differential diagnosis of aminoacidopathy and organic aciduria, repeated blood tests using the MS/MS method, additional clinical and biochemical studies would be necessary.

The degree of increase in disease-specific metabolites is variable and depends on many factors. The nature of the child's nutrition, taking certain medications should be taken into account when interpreting the results. Thus, taking drugs containing valproic acid or medium chain triglycerides leads to an increase in C6, C8 and C10, which makes it difficult to diagnose medium chain acyl-CoA dehydrogenase deficiency. The intake of carnitine-containing drugs can also lead to an increase in the concentrations of short- and medium-chain acylcarnitines. The content of long-chain acylcarnitines in plasma and whole blood is different, since they are associated with erythrocyte membranes, therefore, the hematocrit has a certain value. With some exceptions, a one and a half to twofold increase in concentration requires a second blood test. So, the levels of metabolites, pathognomonic for propionic and isovaleric aciduria, usually increase by more than 5 times, and even a slight change in the concentration of glutarylcarnitine requires not only a second blood test, but also an additional study of organic urine acids characteristic of type I glutaric aciduria.

Conclusion

A retrospective study of blood samples from young children who died from various causes, carried out by the MS/MS method, made it possible to suggest a hereditary metabolic pathology in a number of cases. In one of them, the diagnosis of the disease was confirmed by the smell of maple syrup urine (leucinosis). Timely diagnostic measures in such cases are an important component in the differential diagnosis of congenital metabolic errors. The study of the concentrations of amino acids and acylcarnitines in samples of biological fluids can be of diagnostic value in the analysis of cases of infant mortality. A posthumous diagnosis of a hereditary metabolic disease in a deceased child is an indication for medical genetic counseling of the family. It is necessary to widely implement the MS/MS method in neonatal screening as the main tool for detecting aminoacidopathy, organic acidemia, and defects in β-mitochondrial fatty acid oxidation in newborns for timely diagnosis and treatment of NBO.

Reviewers:

Polevichenko Elena Vladimirovna, Dr. med. Sci., Professor, Chief Researcher of the Department of Rehabilitation and Medical and Social Assistance of the Dmitry Rogachev Federal Research Center of Pediatric Hematology, Oncology and Immunology, Ministry of Health of Russia, Moscow.

Mikhailova Svetlana Vitalievna, Dr. med. Sci., Head of the Department of Medical Genetics, Federal State Budgetary Institution "Russian Children's Clinical Hospital of the Ministry of Health of Russia", Moscow.

Bibliographic link

Baydakova G.V., Antonets A.V., Golihina T.A., Matulevich S.A., Amelina S.S., Kutsev S.I., Kutsev S.I. RETROSPECTIVE DIAGNOSIS OF HEREDITARY METABOLIC DISEASES BY THE METHOD OF TANDEM MASS SPECTROMETRY // Modern problems of science and education. - 2013. - No. 2.;
URL: http://science-education.ru/ru/article/view?id=8953 (date of access: 12.12.2019). We bring to your attention the journals published by the publishing house "Academy of Natural History"

In the era of the New Age, with the flourishing of natural scientific thought, special attention began to be paid to "animal electricity". Inquisitive minds were excited by the experiments of Luigi Galvani, who made the frog's leg contract. Later, with the advent of the "voltaic pillar", anyone who considers himself a modern person and naturalist conducted similar experiments. The physical properties of muscle tissue were studied using current, and the experience in which a direct current pulse caused the muscles of a corpse to contract was considered the apotheosis of "likeness to the Creator".

With the development of electrical engineering and the advent of Faraday's experiments, new equipment appeared that made it possible to obtain magnetic fields using current, and vice versa. Thus, the idea was gradually born of using not directly an electric current, but a magnetic field to influence areas of the cerebral cortex. After all, a magnetic field generates an electric current, and already it causes various processes in the body. It was from this idea that a method called transcranial magnetotherapy was born. What is it, and how does science define it?

Definition

TKMS, or transcranial magnetic stimulation, is a method used in scientific and clinical practice, which allows, without pain and induction of electric current at a distance, to stimulate the cerebral cortex with a magnetic field, receiving various responses to short pulses of a magnetic field. This method is used both for the diagnosis and treatment of certain types of diseases.

The essence of the technique and mechanism of action

The device for electromagnetic stimulation of the brain is based on the principle of excitation of electromagnetic induction. The property of current passing through an inductor is known to give rise to a magnetic field. If we choose the characteristics of the current and the coil so that the magnetic field is strong and the eddy currents are minimal, then we will have the TKMS apparatus. The main sequence of events might be:

The device block generates pulses of high-amplitude currents, discharging the capacitor when a high-voltage signal is shorted. The capacitor has a high current and high voltage - these characteristics are very important for obtaining strong fields.

These currents are directed to a hand probe, on which a magnetic field generator is located - an inductor.

The probe moves very close to the scalp, so the generated magnetic field with a power of up to 4 Tesla is transmitted to the cerebral cortex.

Modern inductors are forced cooled because they still get very hot due to eddy currents. Do not touch the patient's body with them - you can get burned.

Four Tesla is a very impressive amount. Suffice it to say that this exceeds the power of a high-field MRI scanner, which gives 3 T each on a large ring of electromagnets. This value is comparable to the data of large dipole magnets of the Large Hadron Collider.

Stimulation can be carried out in different modes - single-phase, two-phase, and so on. It is possible to choose the type of inductor coil, which allow to give a differently focused magnetic field to different depths of the brain.

In the cortex, secondary processes are generated - the depolarization of neuron membranes and the generation of an electrical impulse. The TMS method allows, by moving the inductor, to achieve stimulation of different parts of the cortex and get a different response.

Transcranial magnetic stimulation requires interpretation of the results. A series of different impulses are sent to the patient, and the result is the identification of the minimum threshold of the motor response, its amplitude, delay time (latency) and other physiological indicators.

If the doctor acts on the cortex, then as a result the muscles of the trunk can contract according to the "motor homunculus", that is, in accordance with the cortical representation of the muscles of the motor zone. This is the MEP, or motor evoked potentials.

If, at the same time, sensors are applied to the desired muscle and electroneuromyography is performed, then it is possible to “ring out” the nervous tissue, taking into account the characteristics of the induced impulse.

Indications for the procedure

In addition to the function of research, the "artificial" impulse created by neurons can have a therapeutic effect in muscle diseases. In children with cerebral palsy, TKMS stimulates muscle development and has a positive effect on spasticity. Transcranial magnetic stimulation is used to diagnose and treat the following diseases:

• multiple sclerosis and other demyelinating diseases;
• cerebral atherosclerosis, diffuse vascular lesions of the brain;
• consequences of injuries and injuries of the brain and spinal cord;
• radiculopathies, myelopathy, lesions of the cranial nerves (Bell's palsy);
• Parkinson's disease and secondary parkinsonism;
• various dementias (Alzheimer's).

In addition, the method of transcranial magnetic stimulation can help in the diagnosis of speech disorders, problems associated with neurogenic bladder, angiocephalgia (migraine) and epilepsy.

A solid experience (mostly foreign) has been accumulated when this technique is used for depression, affective states and neuroses. TKMS also helps with obsessive-compulsive states (obsessive neurosis). Its course use contributes to the elimination of psychotic symptoms in exacerbations of schizophrenia, as well as in various hallucinations.

But such a method, which uses strong magnetic fields, cannot but have contraindications.

Contraindications

Despite the fact that TKMS is a non-invasive technique, strong magnetic fields are its effector. It must be remembered that, unlike MRI, where the entire human body is exposed to a powerful magnetic field, transcranial magnetotherapy generates it at a distance of several centimeters. There are a number of serious and even absolute contraindications to its implementation, for example, ferromagnetic materials inside the skull (implants), or hearing aids. A pacemaker is also a contraindication, but theoretical, since it can only accidentally be in the area of ​​\u200b\u200bthe magnetic field.

Currently, there are devices for deep brain stimulation, for example, in Parkinson's disease. In this case, the procedure is also contraindicated.

Clinical contraindications include:

• focal formations of the central nervous system that can cause an epileptic seizure;
• the appointment of funds that can increase the excitability of the cerebral cortex (and receive a synchronous discharge);
• traumatic brain injury with prolonged loss of consciousness;
• anamnestic - seizure or epilepsy, epiactivity on the encephalogram;
• increased intracranial pressure.

As can be seen from the above, the main danger is to get a synchronous hemispheric or total focus of excitation of cortical neurons, or an epileptic seizure.

About side effects

It would be naive to think that such a serious effect as the secondary induction of a neuron action potential by a strong magnetic field can proceed without any side effects. The most frequently occurring conditions include:

• stomach discomfort and nausea;
• fear of unexpected muscle contractions;
• redness of the skin;
• temporary loss of speech (with stimulation of Broca's area), often accompanied by violent laughter;
• pain in the muscles of the head and face;
• dizziness and fatigue;
• temporary hearing loss.

Also, the device is used very carefully when working with children. When stimulating the child's motor acts, it is difficult to expect complete control and relaxation from him. There is a danger that if a probe with a coil is accidentally passed near the heart, the device can cause a heart rhythm disturbance. Usually the magnetic field causes extrasystoles and no help is required. But in patients with atrial fibrillation, with thyrotoxicosis, this can lead to a worsening of the condition.

[06-225 ] Blood test for amino acids (32 indicators)

5645 rub.

Order

Amino acids are important organic substances in the structure of which there are carboxyl and amino groups. A comprehensive study that determines the content of amino acids and their derivatives in the blood makes it possible to identify congenital and acquired disorders of amino acid metabolism.

* Composition of the study:

1. Alanine (ALA)
2. Arginine (ARG)
3. Aspartic Acid (ASP)
4. Citrulline (CIT)
5. Glutamic acid (GLU)
6. Glycine (GLY)
7. Methionine (MET)
8. Ornithine (ORN)
9. Phenylalanine (PHE)
10. Tyrosine (TYR)
11. Valine (VAL)
12. Leucine (LEU)
13. Isoleucine (ILEU)
14. Hydroxyproline (HPRO)
15. Serine (SER)
16. Asparagine (ASN)
17. Glutamine (GLN)
18. Beta-alanine (BALA)
19. Taurine (TAU)
20. Histidine (HIS)
21. Threonine (THRE)
22. 1-methylhistidine (1MHIS)
23. 3-methylhistidine (3MHIS)
24. Alpha-aminobutyric acid (AABA)
25. Proline (PRO)
26. Cystathionine (CYST)
27. Lysine (LYS)
28. Cystine (CYS)
29. Cysteic acid (CYSA)

Russian synonyms

Screening for aminoacidopathy; amino acid profile.

SynonymsEnglish

Amino Acids Profile Plasma.

Methodresearch

High performance liquid chromatography.

What biomaterial can be used for research?

Venous blood.

How to properly prepare for research?

• Eliminate alcohol from the diet for 24 hours prior to the study.
• Do not eat for 8 hours before the study, you can drink clean non-carbonated water.
• Completely exclude the use of drugs within 24 hours before the study (as agreed with the doctor).
• Eliminate physical and emotional overstrain for 30 minutes before the study.
• Do not smoke for 30 minutes prior to the study.

General information about the study

Amino acids are organic substances containing carboxyl and amine groups. About 100 amino acids are known, but only 20 are involved in protein synthesis. These amino acids are called "proteinogenic" (standard) and, if possible, are classified into interchangeable and irreplaceable in the body. Essential amino acids include arginine, valine, histidine, isoleucine, leucine, lysine, methionine, threonine, tryptophan, phenylalanine. Non-essential amino acids are alanine, asparagine, aspartate, glycine, glutamate, glutamine, proline, serine, tyrosine, cysteine. Proteinogenic and non-standard amino acids, their metabolites are involved in various metabolic processes in the body. The defect of enzymes at various stages of the transformation of substances can lead to the accumulation of amino acids and their transformation products, and have a negative impact on the state of the body.

Amino acid metabolism disorders can be primary (congenital) or secondary (acquired). Primary aminoacidopathy is usually inherited autosomal recessively or X-linked and manifests itself in early childhood. Diseases develop due to a genetically determined deficiency of enzymes and / or transport proteins associated with the metabolism of certain amino acids. More than 30 variants of aminoacidopathy have been described in the literature. Clinical manifestations can range from mild benign disorders to severe metabolic acidosis or alkalosis, vomiting, mental retardation and growth, lethargy, coma, sudden neonatal death syndrome, osteomalacia, and osteoporosis. Secondary amino acid metabolism disorders may be associated with diseases of the liver, gastrointestinal tract (eg, ulcerative colitis, Crohn's disease), kidney (eg, Fanconi syndrome), malnutrition, or neoplasms. Early diagnosis and timely treatment can prevent the development and progression of symptoms of the disease.

This study allows you to comprehensively determine the concentration in the blood of standard and non-proteinogenic amino acids, their derivatives and assess the state of amino acid metabolism.

Alanine (ALA) can be synthesized in the human body from other amino acids. It is involved in the process of gluconeogenesis in the liver. According to some reports, an increased content of alanine in the blood is associated with an increase in blood pressure, body mass index,.

Arginine (ARG) depending on the age and functional state of the organism, it belongs to semi-essential amino acids. Due to the immaturity of enzyme systems, premature babies are not capable of its formation, therefore, they need an external source of this substance. An increase in the need for arginine occurs with stress, surgical treatment, and injuries. This amino acid is involved in cell division, wound healing, the release of hormones, the formation of nitric oxide and urea.

Aspartic acid (A.S.P.) can be formed from citrulline and ornithine and be a precursor of some other amino acids. aspartic acid and asparagine (ASN) participate in gluconeogenesis, the synthesis of purine bases, nitrogen metabolism, the function of ATP synthetase. In the nervous system, asparagine plays the role of a neurotransmitter.

citrulline (CIT) can be formed from ornithine or arginine and is an important component of the hepatic urea cycle (ornithine cycle). Citrulline is a constituent of filaggrin, histones, and plays a role in autoimmune inflammation in rheumatoid arthritis.

Glutamic acid (GLU) - a non-essential amino acid, which is of great importance in nitrogen metabolism. Free glutamic acid is used in the food industry as a flavor enhancer. glutamic acid and glutamate are important excitatory neurotransmitters in the nervous system. Decreased release of glutamate is noted in classical phenylketonuria.

Glycine (GLY) is a non-essential amino acid that can be formed from serine under the action of pyridoxine (vitamin B6). It takes part in the synthesis of proteins, porphyrins, purines and is an inhibitory mediator in the central nervous system.

Methionine (MET) - an essential amino acid, the maximum content of which is determined in eggs, sesame, cereals, meat, fish. It can form homocysteine. Methionine deficiency leads to the development of steatohepatitis,.

Ornithine (ORN) is not encoded by human DNA and is not included in protein synthesis. This amino acid is formed from arginine and plays a key role in the synthesis of urea and the excretion of ammonia from the body. Preparations containing ornithine are used to treat cirrhosis, asthenic syndrome.

Phenylalanine (PHE) - an essential amino acid, which is a precursor of tyrosine, catecholamines, melanin. A genetic defect in the metabolism of phenylalanine leads to the accumulation of the amino acid and its toxic products and the development of aminoacidopathy - phenylketonuria. The disease is associated with disorders of mental and physical development, convulsions.

Tyrosine (TYR) enters the body with food or is synthesized from phenylalanine. It is a precursor of neurotransmitters (dopamine, norepinephrine, adrenaline) and melanin pigment. With genetic disorders of tyrosine metabolism, tyrosinemia occurs, which is accompanied by damage to the liver, kidneys and peripheral neuropathy. An important differential diagnostic value is the absence of an increase in the level of tyrosine in the blood in phenylketonuria, in contrast to some other pathological conditions.

Valine (VAL), Leucine (LEU) and isoleucine (ILEU)- essential amino acids, which are important sources of energy in muscle cells. With fermentopathies that disrupt their metabolism and lead to the accumulation of these amino acids (especially leucine), "maple syrup disease" (leucinosis) occurs. The pathognomonic sign of this disease is the sweet smell of urine, which resembles maple syrup. Symptoms of aminoacidopathy begin early in life and include vomiting, dehydration, lethargy, hypotension, hypoglycemia, seizures and opisthotonus, ketoacidosis, and central nervous system abnormalities. The disease often ends fatally.

Hydroxyproline (HPRO) is formed during the hydroxylation of proline under the influence of vitamin C. This amino acid ensures the stability of collagen and is its main component. With a deficiency of vitamin C, the synthesis of hydroxyproline is disrupted, the stability of collagen decreases and damage to the mucous membranes occurs - symptoms of scurvy.

Serine (SER) is part of almost all proteins and is involved in the formation of active centers of many body enzymes (for example, trypsin, esterases) and the synthesis of other non-essential amino acids.

Glutamine (GLN) is a partially replaceable amino acid. The need for it increases significantly with injuries, some gastrointestinal diseases, intense physical exertion. It takes part in nitrogen metabolism, synthesis of purines, regulation of acid-base balance, performs a neurotransmitter function. This amino acid accelerates the healing and recovery processes after injuries and operations.

Gamma-aminobutyric acid (GABA) synthesized from glutamine and is the most important inhibitory neurotransmitter. GABA drugs are used to treat a variety of neurological disorders.

Beta-aminoisobutyric acid (BAIBA) is a metabolic product of thymine and valine. An increase in its level in the blood is observed with a deficiency of beta-aminoisobutyrate-pyruvate aminotransferase, starvation, lead poisoning, radiation sickness, and some neoplasms.

Alpha-aminobutyric acid (AABA)- a precursor of the synthesis of ophthalmic acid, which is an analogue of glutathione in the lens of the eye.

Beta-alanine (BALA), unlike alpha-alanine, it is not involved in the synthesis of proteins in the body. This amino acid is part of carnosine, which, as a buffer system, prevents the accumulation of acids in the muscles during physical exertion, reduces muscle pain after training, and accelerates recovery after injuries.

Histidine (HIS)- an essential amino acid, which is a precursor of histamine, is part of the active centers of many enzymes, is found in hemoglobin, and promotes tissue repair. A rare genetic defect in histidase causes histidinemia, which can present with hyperactivity, developmental delay, learning difficulties, and in some cases mental retardation.

Threonine (THRE)- an essential amino acid necessary for protein synthesis and the formation of other amino acids.

1-methylhistidine (1MHIS) is a derivative of anserine. The concentration of 1-methylhistidine in the blood and urine correlates with the consumption of meat food and increases with deficiency. An increase in the level of this metabolite occurs with a deficiency of carosinase in the blood and is observed in Parkinson's disease, multiple sclerosis.

3-methylhistidine (3MHIS) is a product of actin and myosin metabolism and reflects the level of protein breakdown in muscle tissue.

Proline (PRO) synthesized in the body from glutamate. Hyperprolinemia due to a genetic defect in enzymes or due to inadequate nutrition, increased levels of lactic acid in the blood, liver disease can lead to convulsions, mental fatigue and other neurological pathologies.

Lysine (LYS)- an essential amino acid that is involved in the formation of collagen and tissue repair, the function of the immune system, the synthesis of proteins, enzymes and hormones. Lack of glycine in the body leads to asthenia, memory loss and impaired reproductive functions.

Alpha-Aminoadipic Acid (AAA) is an intermediate product of lysine metabolism.

Cysteine ​​(CYS) is an essential amino acid for children, the elderly and those with nutritional deficiencies. In healthy people, this amino acid is synthesized from methionine. Cysteine ​​is a component of hair and nail keratins, is involved in the formation of collagen, is an antioxidant, a precursor of glutathione, and protects the liver from the damaging effects of alcohol metabolites. cystine is a dimeric cysteine ​​molecule. With a genetic defect in the transport of cystine in the renal tubules and intestinal walls, cystinuria occurs, which leads to the formation of stones in the kidneys, ureters and bladder.

Cystathionine (CYST) is an intermediate product of cysteine ​​metabolism during its synthesis from homocysteine. With hereditary deficiency of the enzyme cystathionase or acquired hypovitaminosis B 6, the level of cystathionine in the blood and urine increases. This condition is described as cystathioninuria, which proceeds benignly without obvious pathological signs, but in rare cases it can manifest itself as an intellectual deficiency.

Cysteic acid (CYSA) It is formed during the oxidation of cysteine ​​and is a precursor of taurine.

Taurine (TAU) is synthesized from cysteine ​​and, unlike amino acids, is a sulfonic acid containing a sulfo group instead of a carboxyl group. Taurine is part of bile, participates in the emulsification of fats, is an inhibitory neurotransmitter, improves reparative and energy processes, has cardiotonic and hypotensive properties.

In sports nutrition, amino acids and proteins are widely used and are used to increase muscle mass. In vegetarians, due to the lack of animal protein in the diet, there may be a deficiency of some essential amino acids. This study allows us to assess the adequacy of such types of nutrition and, if necessary, to correct them.

What is research used for?

• Diagnosis of hereditary and acquired diseases associated with impaired metabolism of amino acids;
• differential diagnosis of the causes of nitrogen metabolism disorders, removal of ammonia from the body;
• monitoring adherence to dietary therapy and the effectiveness of treatment;
• assessment of nutritional status and nutritional modification.

When is the study scheduled?

• If there is a suspicion of a violation of the metabolism of amino acids in children, including newborns (vomiting, diarrhea, metabolic acidosis, a special smell and color of diapers, impaired mental development);
• with hyperammonemia (an increase in the level of ammonia in the blood);
• with a burdened family history, the presence of congenital aminoacidopathy in relatives;
• when monitoring compliance with dietary recommendations, the effectiveness of treatment;
• when examining athletes (for example, bodybuilders) who use sports nutrition (proteins and amino acids);
• when examining vegetarians.

What do the results mean?

• Alanine (ALA):

• Arginine (ARG):

• Aspartic acid (ASP):

• Citrulline (CIT):

• Glutamic Acid (GLU):

• Glycine (GLY)

• Methionine (MET)

• Ornithine (ORN)

• Phenylalanine (PHE)

• Tyrosine (TYR)

• Valine (VAL)

• Leucine (LEU)

• Isoleucine (ILEU)

• Hydroxyproline (HPRO)

• Serine (SER)

• Asparagine (ASN)

• Alpha-aminoadipic acid (AAA)

• Glutamine (GLN)

• Beta-alanine (BALA): 0 - 5 µmol/L.
• Taurine (TAU)

• Histidine (HIS)

• Threonine (THRE)

• 1-methylhistidine (1MHIS)

• 3-methylhistidine (3MHIS)

• Gamma-aminobutyric acid (GABA)

• Beta-aminoisobutyric acid (BAIBA)

• Alpha-aminobutyric acid (AABA): 0 - 40 µmol/l.
• Proline (PRO)

• Cystathionine (CYST): 0 - 0.3 µmol/L.
• Lysine (LYS)

• Cystine (CYS)

• Cysteic acid (CYSA): 0.

Interpretation of the results is carried out taking into account age, nutritional habits, clinical condition and other laboratory data.

An increase in the overall level of amino acids in the blood is possible with:

• eclampsia;
• violation of tolerance to fructose;
• diabetic ketoacidosis;
• renal failure;
• Reye's syndrome.

A decrease in the overall level of amino acids in the blood can occur when:

• hyperfunction of the adrenal cortex;
• fever
• Hartnup's disease;
• chorea of ​​Huntington;
• inadequate nutrition, starvation (kwashiorkor);
• malabsorption syndrome in severe diseases of the gastrointestinal tract;
• hypovitaminosis;
• nephrotic syndrome;
• pappatachi fever (mosquito, phlebotomy);
• rheumatoid arthritis.

Primary aminoacidopathy

Raise arginine, glutamine- deficiency of arginase.

Raise arginine succinate, glutamine- deficiency of arginosuccinase.

Raise citrulline, glutamine- citrullinemia.

Raise cystine, ornithine, lysine- cystinuria.

Raise valine, leucine, isoleucine- maple syrup disease (leucinosis).

Raise phenylalanine- phenylketonuria.

Raise tyrosine- tyrosinemia.

Secondary aminoacidopathy

Raise glutamine- hyperammonemia.

Raise alanine- lactic acidosis (lactic acidosis).

Raise glycine- Organic aciduria.

Raise tyrosine- transient tyrosinemia in newborns.

Literature

• Part 8. Amino Acids. In: Scriver CR, Beaudet AL, Valle D, Sly WS, Childs B, Kinzler KW, Vogelstein B, eds. The Metabolic and Molecular Bases of Inherited Disease. 8th ed. New York, NY: McGraw-Hill, Inc.; 2001;1665-2105.
• Part IV. Disorders of amino acid metabolism and transport. Fernandes J, Saudubray J-M, Van den Berghe G, eds. Inborn Metabolic Diseases Diagnosis and Treatment. 3rd ed. New York, NY: Springer; 2000;169-273.
• Part 2. Disorders of amino acid metabolism. Nyhan WL, Barshop BA, Ozand PT, eds. Atlas of Metabolic Diseases. 2nd ed. New York, NY: Oxford University Press Inc; 2005;109-189.
• Blau N, Duran M, Blaskovics ME, Gibson KM, eds. Physician's Guide to the Laboratory Diagnosis of Metabolic Diseases. 2nd ed. New York, NY: Springer; 2003.
• Human Metabolome Database. Access mode: http://www.hmdb.ca/

During pregnancy, a woman has to take many laboratory tests, and after evaluating the results of one of them, she may find out that she has thick blood. Is this blood condition dangerous for the expectant mother and her baby? Why did this happen? What to do? Is it possible to do without medication? All these and many other questions will certainly arise in every woman who is faced with such a problem, and in our article we will answer each of them.

When detecting thick blood of a future mother, in no case should you panic. Often, this blood condition during childbearing is not dangerous and is easily corrected, but sometimes a woman will need to undergo a course of treatment that will be aimed at preventing certain risks.

What blood tests can indicate a blood clot?

If you suspect an increase in blood viscosity, the doctor will prescribe a blood test for clotting.

The causes of thick blood can be a variety of factors and diseases. In some cases, a woman may not even be aware of them.

In most cases, a pregnant woman finds out that she has thick blood at the next doctor's appointment after she has passed a general analysis. The doctor will definitely notice an increase in the level of blood cells and hematocrit and inform the woman about it. Sometimes a pregnant woman can learn about thick blood from a laboratory assistant who takes blood from a vein and notices that it is poorly absorbed into the syringe, clogging the needle lumen. Such a phenomenon should be reported to the doctor.

If the above signs of blood density are detected, the doctor will definitely refer the pregnant woman for such an analysis as a coagulogram. It is this research method that will help to study the state of the blood coagulation system in more detail and predetermine further tactics of diagnosis and therapy.

Coagulogram indicators determine the following blood parameters:

• fibrinogen - the norm is 2-4 g / l, with an increase in the duration of pregnancy, the indicator increases to 6 g / l;
• thrombin time - the norm is 11-18 s;
• APTT - the norm is 24-35 s, with an increase in fibrinogen due to an increase in the gestational age, this indicator accelerates to 17-20 s;
• prothrombin - the norm is 78-142%;
• lupus anticoagulant - normally absent.

With increased blood density, the coagulogram parameters change as follows:

• fibrinogen - increases;
• thrombin time - accelerates;
• APTT - accelerates;
• prothrombin - increases;
• lupus anticoagulant present.

Remember that only a specialist can decipher the results of a coagulogram and assess the degree of blood density! It is he who will be able to decide on the advisability of prescribing medical treatment.

Is thick blood dangerous during pregnancy for a woman and a fetus?

Having identified a change in blood density in a pregnant woman, the doctor assesses the degree of these disorders and determines the tactics of managing the patient.

It is according to the results of the coagulogram that the specialist will be able to determine the degree of danger of blood clotting during pregnancy. In some cases, with minor changes in indicators, the doctor does not attach serious importance to the density of the blood and gives the woman general recommendations regarding diet and fluid intake aimed at eliminating this symptom. In such situations, you should not worry, because such a thickening of the blood does not pose a threat to either the expectant mother or the fetus, and after childbirth, the coagulation parameters stabilize on their own.

Sometimes the cause of blood clots during pregnancy is the intake of iron-containing drugs, which are prescribed with a decrease in hemoglobin levels. Such a symptom should also not cause excitement in a woman, because after the elimination of anemia and the abolition of these drugs, the blood condition stabilizes.

With more serious changes in the indicators of the coagulogram, the doctor may recommend that the pregnant woman undergo a course of therapy to thin the blood. In such situations, a woman should also not worry, but simply follow all the doctor's prescriptions. The danger of such a thickening of the blood lies in the increased risk of blood clots and obstructed blood flow through the vessels, but this situation can be corrected.

The slow flow of viscous blood through the vessels and a more intense load on the heart causes an insufficient supply of oxygen and nutrients to all tissues and organs. This leads to the appearance of such symptoms in a pregnant woman:

• constant lethargy;
• memory impairment;
• drowsiness;
• dry mouth;
• heaviness in the legs;
• cold extremities.

With a sedentary lifestyle and no treatment, an increased tendency to thrombosis can lead to the development of such complications in a future mother:

• thrombosis;
• thrombophlebitis;
• TELA;
• varicose disease;
• diseases of the cardiovascular system (heart attack, hypertension, stroke, atherosclerosis).

Significantly increased blood density negatively affects the condition of the unborn baby. As a result of increased thrombus formation and slow blood flow from the fetus, the following disorders can be observed:

• miscarriage or premature birth;
• frozen pregnancy;
• hypoxia;
• developmental delay.

It is in connection with the above possible complications of thick blood that women planning a pregnancy should refrain from conception until the completion of the course of therapy for this condition. In some cases, this violation in the blood coagulation system can be life-threatening for the expectant mother and baby, and while carrying a child, a woman can not take all medications. Therefore, it is better to get rid of this symptom before pregnancy.

When planning a conception, the doctor will definitely prescribe a coagulogram to exclude violations in the blood coagulation system. It is especially important to conduct such a study in certain risk groups:

• in the anamnesis of the woman there were cases of miscarriages or missed pregnancies;
• a woman or her relatives have varicose veins;
• close relatives of the woman had thrombosis, heart attacks or strokes;
• a woman professionally goes in for sports, which is associated with intense physical activity.

What to do with thick blood during pregnancy?

When identifying the first symptoms of thick blood, a woman needs to tell the doctor about them. If signs of blood clotting were detected during the tests, then the doctor will definitely prescribe a number of additional studies to the pregnant woman to determine the severity of such a violation of the coagulation system and find out the reasons for its occurrence. A variety of diseases and pathologies can provoke blood clots: antiphospholipid syndrome, liver diseases, blood pathologies, glomerulonephritis, rheumatism, systemic lupus erythematosus, etc. That is why the tactics of further examination will depend on each specific case.

In the absence of significant violations in the coagulogram and diseases, the doctor may recommend to the woman some changes in lifestyle and nutrition. These include:

• sufficient daily fluid intake in small portions (about 1.5 liters, but the daily rate may change in the presence of edema and other diseases);
• sufficient physical activity, which contributes to better blood circulation;
• regular walks in the fresh air, which prevent oxygen starvation;
• the introduction into the daily diet of foods that contribute to blood thinning, and the restriction of those foods that cause it to thicken;
• salt restriction.

For such patients, the doctor will definitely prescribe repeated coagulogram tests, one of which will be carried out after an individually defined period of time (to monitor the effectiveness of preventive measures), and the second - a few weeks before childbirth.

With a more pronounced thickening of the blood of a pregnant woman, it is not enough to adhere to the above recommendations. In such cases, in addition to the course of treatment of the underlying disease that caused the blood density, the doctor will prescribe drug therapy to the woman.

The following drugs may be prescribed to thin the blood:

The duration of treatment, the selection of the dose and the drug can only be performed by a doctor who takes into account the general condition of the woman and is guided by the indicators of the coagulogram (primary and repeated). At the 36th week of pregnancy or 14 days before the expected delivery, all drugs are canceled, because they can cause various complications during childbirth.

Despite the fact that thick blood is found in many pregnant women, all women are advised not only to remain calm, but also to strictly follow the doctor's recommendations. Such a violation of the blood coagulation system does not always indicate a significant risk for the future mother and fetus, but in certain cases it can lead to the development of severe consequences. By fulfilling all the doctor's prescriptions, a woman will be able to prevent formidable complications and preserve the health and life of herself and her unborn baby. Remember this! Do not self-medicate and be healthy!

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Diagnosis of vegetative-vascular dystonia

• 1 When should I see a doctor?
• 2 Methods for diagnosing VVD
  • 2.1 First reception
  • 2.2 Taking anamnesis and examining the patient
  • 2.3 Laboratory tests
  • 2.4 Diagnostic procedures
    • 2.4.1 Performing an ECG
    • 2.4.2 Echocardiography (EchoCG)
    • 2.4.3 Rheoencephalography (REG) of head vessels
    • 2.4.4 Heart rate measurement
    • 2.4.5 Magnetic resonance imaging (MRI)
    • 2.4.6 Other examination methods
  • 2.5 Differential analysis
• 3 Treatment of VVD

Accurate diagnosis of VVD is based on a comprehensive study of the body. To diagnose vegetative dystonia means to exclude the presence of diseases that have similar symptoms. Laboratory blood tests, the help of additional diagnostic devices (ultrasound, ECG, MRI), a thorough analysis of existing chronic diseases will help the attending physician in the diagnosis.

When do you need to see a doctor?

Vegetovascular dystonia reflects problems in the work of the central nervous system. The vegetative system in such conditions does not help the body adapt to changing factors, but, on the contrary, it makes the body function in a feverish mode. Panic attacks occur, the heart beats intermittently, dizziness occurs, heart pains appear, spasms of cerebral vessels, migraines occur, pressure jumps up or down, and blood circulation in the organs is disturbed. All of the above is more than a good reason to see a doctor. If the results of the diagnosis of each organ do not confirm its disease, this is the reason to diagnose VVD.

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Methods for diagnosing VVD

Diagnosis of VVD, which allows you to find out about the presence of pathology, is carried out using devices that allow you to study the electrophysiological work of the heart muscle (on an ECG), identify functional changes in the heart and its valvular apparatus (EchoCG), evaluate the anatomical and functional features of blood flow (MRI), and obtain an objective assessment tone, elasticity of the walls of cerebral vessels, the value of pulse blood filling (REG). Laboratory blood tests include:

• general and biochemical blood test (erythrocyte sedimentation rate, leukocytes, hemoglobin);
• blood sugar content;
• the level of thyroid stimulating hormones,

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First reception

If you consult a doctor in time, you can avoid negative consequences.

Before the first appointment with a doctor, it is necessary to exclude the intake of alcohol, coffee, and refrain from dieting the day before. A complete rest is needed. During the first appointment, the doctor, based on the patient's objective complaints, prescribes further studies that will confirm or refute the diagnosis of VVD. Pay attention to the type of addition, since an asthenic (fragile) physique or, conversely, excessive obesity, are possible with VVD. Are there symptoms of nervous tension, stress. The more detailed and honest the patient's answers are, the more likely it will be possible to make a correct diagnosis.

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Taking anamnesis and examining the patient

During the examination of the patient, the type of addition, the condition of the skin are noted, body temperature is measured, and how cold the limbs are. Is there "marble" skin, areas with impaired blood supply. Since the causes of the development of vegetovascular dystonia include the influence of external factors, the doctor during the initial examination fixes:

• the presence of stressful situations, whether there was emotional stress;
• how the patient leads a correct lifestyle (smoking, alcohol abuse);
• What kind of physical activity does he get?
• what head injuries were in the past;
• how full is the rest period, is it sufficient;
• what hereditary diseases are present in the anamnesis.

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Laboratory tests

For a complete picture of the disease, the doctor will prescribe a set of tests.

As a rule, they begin with general blood and urine tests, which are able to confirm or deny the presence of a certain disease. An increased rate of ESR, leukocytes indicates the development of pathologies in the body, infectious, viral diseases. The content of high levels of thyroid-stimulating hormones in the blood is a sign of thyroid diseases - thyrotoxicosis. A biochemical blood test for potassium content allows you to confirm or refute the disease of the adrenal glands - hyperaldosteronism. Another serious disease - pheochromocytoma - is determined by the level of adrenocorticotropic hormones.

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Diagnostic procedures

With vegetative-vascular dystonia, the nature of the symptoms is similar to other diseases. To make a diagnosis, it is necessary to consult not only a therapist, but also a cardiologist, neuropathologist, gastroenterologist, ophthalmologist, gynecologist. Each doctor gives a referral to examine the work of a particular organ with the help of diagnostic devices.

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Conducting an ECG

Electrocardiography is an inexpensive but valuable examination method. An electrocardiogram allows you to assess the physical condition of the heart, shows acute or chronic damage to the myocardium, determines the frequency and regularity of heart contractions. The cardiologist should decipher the ECG.

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Echocardiography (EchoCG)

Echocardiography is one of the diagnostic methods.

Echocardiography as an ultrasound method allows you to display an image of the heart muscle on the screen. This makes it possible to establish the condition of the soft tissues and the thickness of the walls of the heart, to study the peculiarity of the movement of blood in the atria and ventricles of the heart. The indications are:

• suspicion of coronary artery disease;
• hypertension;
• signs of heart failure.

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Rheoencephalography (REG) of head vessels

The advantage of this research method is the possibility of obtaining information about the state of the arterial and venous systems of the brain. Rheoencephalography helps to diagnose atherosclerosis of cerebral vessels, signs of impaired patency of the main vessels, disorders of cerebral circulation. This procedure is completely painless, but effective.

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Heart rate measurement

Excitability of the ANS leads to cardiac arrhythmias. The pulse rate goes beyond 100 beats per minute, causing tachycardia, or falls below 60 beats/minute, indicating bradycardia. Cardiovascular disorders cause respiratory arrhythmia - on inspiration, the pulse rate increases, on exhalation it decreases. It is necessary to measure the pulse on each hand for 1 minute, paying attention to the rhythm of the beats, their strength.

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Magnetic resonance imaging (MRI)

MRI allows using the technique of magnetic resonance angiography to obtain an image of the lumen of the vessels. This gives an idea of ​​the anatomical, functional features of blood flow. The MR-perfusion method gives an idea of ​​the permeability of the walls of blood vessels, the activity of the venous flow, which makes it possible to determine healthy and pathological altered brain tissues.

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Other examination methods

Ultrasound diagnostics allows you to check all internal organs.

Ultrasound examination of the organs of the gastrointestinal tract, heart, genitourinary system allows you to diagnose diseases of the stomach, heart, pancreas, kidneys. To assess the activity of the vegetative system, such methodological techniques are used as the determination of the Kerdo index. This requires data - pulse rate per minute and diastolic blood pressure. A significant excess of lower blood pressure over the pulse rate indicates the predominance of the sympathetic system in the work of the ANS. The reverse picture indicates the predominance of the parasympathetic department. Normally, lower blood pressure and heart rate should not differ much from each other.