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Competent Treatment Hyperplazia the Left Adrenal Gland

Dmitrieva Elena Germanovna

Correspondence Address :

Dmitrieva Elena Germanovna
Clinical Pharmacist
Charitable Pharmaceutical Clinic, 153012
Russia
Email: cyrix2003@mail.ru

Received on: June 01, 2018, Accepted on: June 22, 2018, Published on: July 17, 2018

Citation: Dmitrieva Elena Germanovna (2018). Competent Treatment Hyperplazia the Left Adrenal Gland

Copyright: 2018 Dmitrieva Elena Germanovna, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Abstract

Fulltext
The left adrenal gland of the semilunar form. Right - has the cone form.


Small adrenal glands on the size carry out the major functions in a human body; they provide its normal functioning. They completely are responsible for all kinds of exchange processes, support balances, in big to a measure salt. They develop hormones that are responsible for a sexual inclination both female, and a male. These hormones have the prominent features, which considerably differ at different floors. Only adrenal glands are ill, integrity, normal work of all system of an organism fails and then the person in danger.
To begin with it is necessary to consider the reasons of problems with adrenal glands. Allocate dangerous situations when adrenal glands actively develop the hormones necessary to an organism. At such adverse reasons, they are developed in big to a measure that already is a deviation from a normal condition. Because of it variety of illnesses develops.
I will describe only whenever possible one variant connected with hyperplazia of the left adrenal gland at girls and women. This variant often not can define at once since the left adrenal gland it is badly visible on scaniroval, and Computer tomography adrenal glands do occasionally. Thus more often, such women treat for a hypertension and <<heal>> to even big problems. Though, it is necessary to define primacy or secondariness of pathology, to consider weight of nuances.

Often provocations hyperkalemia and hypertension go from medicines for pressure decrease, for example, Indapamid (Arifon). At long application only in the mornings, but at low general peripheral resistance of vessels (GPRV for neurophysiology) and low renin in blood plasma (blood biochemistry) - is formed hyperkaliemia and hyponatriemia, patients lose salt, sodium becomes less, it would be desirable some salt, patients eat with handfuls salt to stabilise a condition.
Biochemical diagnostics: Outsets of biochemical analyses are important. Steroidogenez in a bark of adrenal glands passes through a number of the enzymes which insufficiency needs to be regarded as a primary pathology of adrenal glands. I can describe them later in other articles. But there is also a considerable surplus 18-gidroksikortikosteron (its concentration in whey is increased in 30 times and more). It occurs on normal reaction of an organism to an infection and other kinds of stress. Level adrenocortocotropic gormon (AKTG) in plasma is raised not so strongly, as at other conditions accompanied by deficiency cortizol (it speaks partial preservation of effect of a negative feedback as 18-gidroksikortikosteron possesses some glucocorticoid activity). Production usually LG and FSG because of deficiency of sexual hormones is sharply raised. There is also a secondary pathology hyperplazia adrenal glands

Early Signs in the Childhood
1. Fevers, sometimes shaking - more often in the evening.
2. Head pains in the field of a forehead.
3. at girls - a dystonia of vessels - the lowered or raised pressure and cold finitenesses.
4. у girls during time mensis - acne, nausea and vomiting, pains in a stomach.
At adult women (such signs arise after long application
hypotensive preparations because of not true diagnoses).
1.Increase arterial pressure usually second half of night and at daybreak and in the evening - 16 when kidneys become more active.
2. allocation light or brown urine - the second half-fault of night and at daybreak.
3. hyperemia persons from any stressful situation or pressure (mental or physical).
4.absence pulse on a tonometer or a pulsation faltering.
5.strengthening symptoms in heavy days - strengthening of solar activity, change of atmospheric pressure, weather conditions.
6.pulse in the left ear (tinnitus), abdominal a pulsation.
7.pulsations and 1 and 2 tones of heart at reception of preparations, hypotensive a medicines.
8. vascular hyperkinazes (jumpings up of heart, a diaphragm, feet).
9. Tolerance infringement to glucose - in the morning, as a rule - hypoglicemia, after meal - hypergliсemia.
10. in morning - allocation of is strong-sour gastric juice.
11. Adiposity - weight jumps on 8-10 kg a month.
12. nicturia and polyuria.
13. discomfort and a pain in a waist
14. in morning face edemas and a century
15. Pigmentaion on the person.
16. Decrease libido
17. increase growth of hair (girsutism).
18. Irritation
19. occurrence irregular pulse - jerks with the subsequent supraventricular extrasistolia and persist vibrating aritmia.
20.bradisfigmia.
21.apatia
22.anemia.
23.pastoz shins and face edemas, feet as a result of a liquid delay in an organism.
In Laboratory Indicators
1. Low renin
2. The general peripheral resistance of vessels (GPRV) it is lowered
3. Tonus the main vessels the high
4. Increase men - eritropoetine, at women - can have different values.
5. Disbalanse vitamins - В12 and others (I have author's diagnostics).
6. Surplus kalium - hyperkaliemia at application Diuretics and as consequence - a bradycardia.
7. Increase FSG and LG.
8. Increase - dofamin and dofamin-gidroksilaza.

Occurrence Original Causes Hyperplazia Adrenal Glands

The problem occurrence tumours excites many years, but as in medicine treat only a consequence of the reason or the reasons to cure illness it is not possible. Meanwhile, many destinies break, after all illness does not allow to live qualitatively. At me longterm research is carried out.
At once I will begin with original causes
1. A pathology of character of mothers (isteroid-shizoid) with tendencies epileptoid. They since the early childhood scoff at children, teaching them without a measure, abuse for everything, that do.
2.At mothers it is possible to see pigmentation on the person, especially it are shown after sorts. Occurrence of pathology at children is justified, as in the childhood such mothers have transferred strong chronic stress which was characterised by strong experiences from mothers. In the childhood such mothers too lived without caress though, lived in full families, often cried, shouted, or were silent, worrying insults in it. At many fathers had the burdened psychiatric semiology. But in Russia the psychiatry always was politized, therefore psychiatrists paid attention to children from simple families a little. There it was interesting to pursue by means of psychiatry when the party instructions on objectionable and far-outers were given. But schizoid it was always visible. At people citizens behaved decently, but houses without another's eyes could and tragedies, charges, abuse, insults, unwillingness to give to children that they want were played. It were not necessarily beatings, but the humiliation of own advantage was enough that the chronic stress gave the raised emission of hormones of stress from adrenal glands. The vicious circle of increase of hormones was fixed in a proof hypertensia. In Russia and now doctors are not able to treat it. All is lined under standards essencial hypertensions that is not true. Patients, their families suffer from it and a rating of the medicine.
3. Relations of parents in marriage without love that was often transferred to children. All the rage was focused on them - on the most defenceless.
The Jatropatic (poisonings from preparations) reason - long reception of preparations for pressure decrease - at me is such cases when start tumor formations occurs from statement not the true diagnosis - essencial a hypertension and constant reception antihypertensive preparations. It is shown by pressure jumps, ricochets on medicines for pressure decrease, a burdensome condition, pressure usually rises at daybreak when there is a raised emission of hormones of adrenal glands in blood. Differential diagnostics of tumours of adrenal glands from a primary hypertension And, hyperplazia the left adrenal gland it is shown differently, than right (I will describe later). Treatment Yatropatic (poisonings) the reasons - refusal of reception of causal preparations, differential diagnostics of illnesses of adrenal glands and selection of other therapy. I find some chemical compounds for treatment of tumours of adrenal glands. Still it is necessary to spend inspection completely to introduce new methods for treatment and cured. Early Signs at Children
1. weight reduction or adiposity.
2. head pains in a frontal part.
3. increase pressure or a hypotonia.
4. gyperemia on the person.
5. infringement a chair



Necessary Hormonal Researches For an Estimation of Function of Adrenal Glands are that

1. dezoxicortizol
2. free cortizol
3.18-gidroksikortikosteron
4.tetrahydrocortizol
5.gonadotropines (FSG, LG and etc.)
6.sexual hormones - anfrogenes, an estrogen, a progesterone, its predecessors.
7. 17-gidroksiprogesteron
8. aldosterone
9.dofamin and dofamin-gidroksilaza
10.AKTG and others (it is described in the text)

Features of Diagnostics

At suspicion on congenital hyperplazia barks of adrenal glands at newborns spend special screening-test on definition of hormones in whey of blood and a saliva. Also at presence not a correct structure of genitals to the baby carry out analyses on definition kariotype and sexual chromatine's. To teenagers methods of tool diagnostics are necessarily appointed. For example, at Ph-grafia beam of the carpal joints the advancing of growth of bones in comparison with age comes to light. Indicative method of research both at children, and at adults is ultrasonic diagnostics, computer a tomography of adrenal glands (better with contrast - contrast introduction) which show their increased sizes. Tool methods of diagnostics also are intended for revealing of degree of dysfunction of internal bodies. The differential diagnosis at newborns and chest children spend with different kinds man's hermafroditizm, at children is more senior and at adults of disease of adrenal glands differentiate with tumours of adrenal glands, sexual glands and also with polykistoz's sexual glands at girls.
In Soviet time the blood biochemistry was investigated a little. Looked to clinical signs more.
In prepubertat at girls it was often marked - hardly the accelerated puberty, adiposity, mensis were painful, and in pregnancy - adiposity became considerable. Arterial pressure was hardly raised to 140/100. The item that marked as a dystonia of vessels. After sorts quickly developed vilirizacia. Approximately 60-70 % of patients with a classical variant of illness at young age have a hypertensia. It usually develops in the first years of a life. Pressure increase usually moderated, in third of cases it becomes complicated defeat of kidneys, retinopatia, a hypertrophy left stomach heart and other complications. Increase pressure is frequent remains long years not noticed.
Surplus mineralocorticoid hormones can lead hypokaliemia (to the lowered level kalium's in blood) and metabolic alcaloz which is shown by muscular weakness and chair infringement. The strengthened deducing of sodium from an organism can be rare display of illness, that I observed in clinic. It is shown hyponatriemia, hyperkaliemia and heavy hypovolemia (reduction of volume of blood).
As a result of raised level AKTG there can be the hyperpigmentation (dimness) of a skin similar to those which is observed at illness Addisson's. At boys skin dimness sexual glands is characteristic.
But in Russia levels of all hormones necessary for the exact diagnosis practically it is not investigated. Levels of sexual hormones are not investigated.

Features of Treatment by Hormones

Initial researches

Tests with medicines - Kalium, Furasemid, Aldosteron, Isotonic Solution (NaCl).
Arterial hypertension with low ARP (activity renin plasmas). Approximately at 30 % sick by hypertensive illness ARP it is lowered, and level aldosteron in the normal. Spontaneous hypokaliemia it is observed only at very small number of such patients.
Reception mineralocorticoid overdose Fludrocortizone (it sometimes appoint at ortostatic hypotonias or constant application of the aerosols containing Fluprednizolone (at a chronic rhinitis can cause an arterial hypertension and hypokaliemia. ARP and level aldosterone thus decrease.

Arterial hypertension and illnesses of adrenal glands

Increase the pressurae accompanies many illnesses of a bark of adrenal glands In case of primary hyperaldosteronism (at a tumour of a bark of adrenal glands or bilateral hyperplazia barks of adrenal glands increase the pressure is caused by a sodium delay. Detaining sodium, aldosteron promotes its exchange on kalium in nephritic channels, therefore for primary hyperaldosteronism it is characteristic hypokaliemia and inspection of such patients should be begun with level definition kalium blood. Diagnostics is appreciably based on that fact, that constantly raised general circulation of blood (GCB) and a sodium delay suppress secretion renin.
In normal conditions activity renin plasmas corresponds to level aldosteron in plasma and urine, but at primary hyperaldosteronism because of uncontrollable secretion aldosteron its level is high and stable enough, while activity renin is lowered and only poorly grows at reduction of level of sodium in blood.
Glucocorticoids hyperproduction angiotensinogen's and pressure increase speaks. At congenital hyperplazia barks of adrenal glands the caused insufficiency 11beta-gidroksilaz or insufficiency 17alfa-gidroksilaz a sodium delay are caused by surplus 11-dezoksikortikosteron there is hyporenin an arterial hypertension.
Secretion of adrenaline and noradrenaline a tumour (more often it is in brain substance of adrenal glands) conducts to superfluous stimulation adrenoreceptors, to growth GPRV (the general peripheral resistance of vessels), reduction a myocardium, to change FWR (frequency of warm reductions) and pressure. If supressive therapy by glucocorticoids begin, when the bone age exceeds 10 years there can come true premature sexual development.
Treatment by glucocorticoids causes fast decrease in levels corticosteroids. Insufficiency 11beta-gidroksilaz (the hypertensive form hyperplazias) prevalence. Among the described cases hyperplazia 5-8 % are necessary on an insufficiency share 11beta-gidroksilaz. This defect meets approximately at 1 of 100000 newborn white races. At the same time among sefards (Jews - natives of northern Africa) its frequency above. It is not excluded, as in other populations it is more extended, than was considered earlier.

Treatment

Treatment by glucocorticoids suppresses secretion AKTG, 11-Dezoksikortikosteron and androgens it is recommended to Children of younger age Hydrocortizone in a dose of 10-20 mg/ m2/days; in postpubertat age it is possible to apply more powerful and it is long operating preparations, such, as Prednizone or Dexamethasone. Level decrease 11-dezoksikortikosteron's is accompanied by strengthening excretion sodium with urine, strengthening diurez's, decrease GCB and increase ARP that stimulates production aldosteron. At a proof arterial hypertension, resistant to glucocorticoids, others can be demanded hypotensive means - Ingibitors ATE Angiotensin - transforming enzyme (provided that renin blood high), or antagonists of calcium.
Treatment by glucocorticoids brakes superfluous secretion kortocosteroids (11-dezoksikortizol's, 11-dezoksikortikosterone, androstendione), thereby, interferes further virilizacia and causes remission of an arterial hypertension. As well as at  insufficiency 21-gidroksilaz, correct treatment can provide normal growth, normal sexual development and fertil. The general treatment: 1. At primary adrenal glands replaceable therapy by glucocorticoids and mineralokorticoids is necessary for insufficiency and Replaceable glucokorticoid therapy. Appoint Prednizone inside in fractional doses: 5 mg in the morning and 2,5 mg in the evening. Such treatment covers requirement for glucocorticoids at patients of any growth and weight. It is necessary to consider, however, that secretion level kortizol is directly proportional to the area of a surface of a body and raises at physical activity, and at adiposity the exchange kortizol is accelerated. Therefore at adiposity or the big physical activities the big doses Prednizolone can be demanded. To increase doses it is necessary and when patients simultaneously receive the medical products accelerating an exchange korticosteroids (for example, barbiturats, fenitoin, rifampicin).
On the contrary, at elderly, at heavy diseases of a liver (exchange delay korticosteroids), at a diabetes, the arterial hypertension, a stomach ulcer accept smaller doses Prednizone's. Criteria of a correct choice of doses Prednizone is an increase in weight and hyperpigmentation disappearance.
Replaceable minelarokorticoid therapy also is necessary at primary adrenal glands for insufficiency. Appoint synthetic mineralocorticoid - Fludrokortizone inside in a dose of 1 times of 0,05-0,3 mg a day. After restoration general a blood circulation (GBC) and elimination hyponatriemia it is possible to begin reception Fludrokortizone on 0,1 mg/days at unlimited consumption of salt. If there is a proof arterial hypotonia in a prone position or ортостатическая a hypotonia or proof hyperkaliemia, a dose Fludrokortizone is increased. On the contrary, an arterial hypertension, hypokiliemia and hypostases - indications for dose reduction. A dose Fludrokortizone change gradually (to 0,05 mg/days).

Century with hypogonadizm is required to some patients replaceable therapy by sexual hormones.
Training, First of all, patients warn that at accompanying diseases it is necessary to correct doses of glucocorticoids.
Patients should carry always a counter or a bracelet with an inscription <<adrenal insufficiency>> and with instructions of requirement for glucocorticoids. For long trips recommend to have with itself bottles with kortizone acetate for inside the muscular injections, and also an ampoule with Hydrokortizone (100 mg) for Intravenously introductions (on a case of rendering of the urgent help medical workers).
Accompanying diseases and stress demand correction of doses of glucocorticoids, but not mineralokorticoids. At easy diseases and traumas (for example, at respiratory infections, removal of a teeth) accept the doubled doses of glucocorticoids until the condition is not normalised. At vomiting or a diarrhoeia of the patient hospitalise, as reception of glucocorticoids inside in these cases is inefficient and can quickly develop dehydratation. At heavy stresses the maximum daily requirement for glucocorticoids is equivalent 300 mg Hydrokortizone's.
On the eve of surgical intervention (evening) в/в enter 100 mg Hydrokortizone's, and then on 100 mg everyone 8 ч. This treatment continue in the postoperative period until the condition of the patient is not stabilised. After stabilisation of a condition a dose Hydrokortizone's quickly reduce (for 3-5 days) to initial sizes. To increase doses mineralokorticioids it is not required, as Hydrokortizone possesses sufficient mineralokorticioid activity. At heavy traumas, urgent operations, a sepsis, a myocardium heart attack spend the same treatment, as at hypoadranal a crisis. 2. Secondary adrenal glands insufficiency. At secondary adrenal glands treatment mineralokorticioids is not required to insufficiency. At accompanying deficiency LG and FSG there can be a necessity for replaceable therapy by sexual hormones. Reception of glucocorticoids in a day. At the initial stage of treatment glucocorticoids accept every day. Unitary reception of all daily dose at early morning o'clock is desirable, that most corresponds to a secretion biorhythm endogenic kortizol. To warn complications, use glucocorticoids of short action (Hydrokortizone, Prednizone), instead of it is long operating preparations (Dexamethasone, Beclomatazone). The interval between receptions of short-range preparations is sufficient for partial restoration of function gipotalamus-gipofizar-adrenal systems. Then gradually pass from unitary daily reception of glucocorticoids to unitary reception in day. The first variant of change of a mode of treatment: the patient in one stage translate on reception of glucocorticoids in day; a daily dose of glucocorticoids thus double (for example, Prednizone on 50-100 mg at early morning o'clock in day). The second variant: On 5 mg from a daily dose Prednizone transfer next day. When the dose falling to <<unloading>> day, will decrease to 5 mg, of 1 mg/days continue to reduce it with a speed.

Decrease in a Dose of Glucocorticoids

As soon as the dose Prednizone will decrease to 5 mg/ sut, pass on Hydrokortizone on 20-25 mg every morning. As Hydrokortizone it is quickly deduced from blood, the interval between preparation receptions is sufficient for partial restoration of function gipotalamus-gipofizar-adrenal systems. Monthly define level kortizol in whey at 8:00. Level kortizol <10 mkg of % testifies that function gipotalamus-gipofizar-adrenal systems was not restored yet. When level kortizol will exceed at 8:00 10 mkg of %, Hydrokortizone it is possible to cancel. For a detailed estimation of function gipotalamus-gipofizar-adrenal systems spend test with AKTG. Concentration increase kortizol in whey more than on 6 mkg of % or the maximum concentration kortizol's > 20 mkg of % specify in full restoration of function gipotalamus-gipofizar-adrenal systems. If level kortizol's at 8:00> 10 mkg of %, but reaction on AKTG it is lowered, at heavy accompanying diseases can be demanded again ekzogenic glucocorticoids. This requirement will remain until secretor reaction of adrenal glands on AKTG is not normalised. Important! Enzyme - Hydroxisteroiddehydrogenaza, it is localised near to receptors kortizol's. Nevertheless, surplus kortizol's can give the same effect, as surplus mineralokorticoids. Important! The main regulator of secretion aldosteron - renin-angiotenzin system. The renin, gives a secret cages ukstaglomerular the device of kidneys, katalis transformation of the circulating inactive predecessor of angiotensin II - angiotenzinogen's in angiotensin I. Last turns to angiotensin II under the influence of Ingibitors enzyme angiotensin-transforming (EAT) Production of angiotensin II depends from general blood circulation (GBC) and sodium level. Reduction GBC causes increase ARP and by that increase in production of angiotensin II. Angiotensin II stimulates secretion aldosteron's which causes a sodium and water delay and restoration GBC. On the contrary, increase GBC reduces ARP and suppresses formation of angiotensin II and secretion aldosteron's; as a result excretion sodium and water increases. Secretion aldosteron's depends also from AKTG and level kalium's. Even small increase of level kalium's in blood causes considerable strengthening of secretion aldosteron's, that, in turn, increases excration kalium's. At hypokaliemia secretion aldosteron's is braked, and excretion kalium's decreases. Important! But synthetic hormones are increased by risk of a hypertensia and development of a steroid diabetes, therefore my problem - to develop new methods of treatment. It is necessary to pay attention of levels dofamin and eritropoetin. It is necessary to give to attention to any nuances. I personally define also weak bodies, I count parametres of work of kidneys. All it is very important for competent diagnostics and competent treatment. Additional factors for treatment hyperplazia adrenal glands. Always it is necessary to search for an original cause of illness and to influence it then it is possible to cure practically any disease.
Important! Work of many emzimes demands presence additional to-factors. Their role is carried out by all vitamins, microcells. Means, that vitamins, antioxidants for treatment hyperplazia adrenal glands are necessary. Good functional activity of a liver is important.
It is important to strengthen work Hydroxilases in a human body to clean displays of illnesses of adrenal glands. Hydroxilases - class enzymes oxidoreductazes, kataliz process hydroxilization, one of the major biochemical processes of a metabolism at animals, plants, and also at are localised hydroxilazes mainly in microcatfishes. Microcatfishes of adrenal glands are especially rich with hydromanholes which participate in oxidation of various intermediate products of an exchange of steroid hormones.
The Hydroxilazes divide into three basic groups:
1.In reactions, kataliz Hydroxilazes. The first group, as the donor of hydrogen serves restored NAD and NADF. To this group hydroxilaz carry aril-4-gidroksilaz, kinurenin-3-gidroksilazu, scvalenhydroxilaze's, kinurenat-gidroksilaz's, imidazolatsetat-gidroksilaz's, a steroid - 11-beta-; a steroid - a 17-alpha-; a steroid - 21; cholesterol - 20-beta-; estradiol - 6-6 estriol - 2-gidroksilaz's. Means, that it is possible to use the antioxidants operating on NAD and NADF. It is in detail described in my book but while it is not published. 2.For hydroxilazes the second group the donor of hydrogen is ascorbic acid (dofamin- hydroxilaza the second group the donor of hydrogen is ascorbic acid (dofamin- hydroxilaza, p-oksifenilpiruvatgidroksilaza). Means, that it is possible to use ascorbic acid.
3.As the donor of hydrogen for hydroxilaz's the third group - phenilalanin - 4-gidroksilaza - serves restored pteridin. Figures in the name of enzymes specify that position into which the OHgroup is entered. Means, that it is possible to include in treatment - some aminoacids.
Properties Hydroxilazes are studied it was not possible insufficiently as because of high lability to receive these enzymes in the cleared condition yet. It is established, that into structure of a molecule of the majority enters - atom of copper or iron. Inhibitors hydroxilazes are: EDTA (trilon B), cistein, serotonin, gistamin, triptamin. Means, that it is impossible to include in treatment - komslexons, some aminoacids (cistein, serotonin, triptamin), it is impossible to take the alcohol, some cheeses and other products.
Reactivators in case of inhibition komplexone-formations as connections salts of bivalent iron or copper serve. Genetic Infringement of Synthesis of Some Hydroxilazes is the Reason of Heavy Diseases So, absence phenilalanin-hydroxilaz's, kataliz hydroxiliration L-fenilalanina to L-tirozina causes the hardest disease - phenilketonuria, and congenital infringement of synthesis p-oksifenilpiruvatgidroksilaz is the reason tirosinemia - exchange infringements tirosin's (alkaptonuria). Genetic insufficiency a steroid - 21-gidroksilaz in a combination to deficiency of other enzymes leads to accumulation not metabolic predecessors kortizol's, to superfluous formation androgens and to development of a various pathology: adreno-genital a syndrome raised excretion sodium (<<salt the losing a syndrome>>), etc.
Result of insufficiency of synthesis the steroid - 11-betagidroksilazy is a sodium delay in an organism with development of a hypertension owing to sharply raised formation dofaminhydroxilaz's. Genetically caused insufficiency dofaminhydroxilaz's.
leads to biosynthesis oppression noradrenalin's at a stage hydroxilation diоxfeniletilamin's (dofamin's); because of it at feochromacitima excrecia dofamin's with urine can be raised at the normal maintenance in urine noradrenalin's.
Activity increase dofamin-hydroxilaz's in blood whey mark at hypertensive illness (in difference, from symptomatic hypertensions), at neuroblastomas, a trochee, hepatoma's, leukosis; reduction of activity of this enzyme in blood whey is observed at parkinsonizm's. So, for example, level oxidoreductaz change in the course of inflammation reactions a chronic tonsillitis that is important for preventive maintenance of diseases of adrenal glands. As an example it is possible to bring enzyme alcogol-dehydrogenaz's (alcohol-over-oksidoreduktaza), participating in an ethanol metabolism in fabrics. For this reason alcohol at diseases of adrenal glands is counter-indicative.
Probably, that through oxidoreductazes it is possible to find and other ways of treatment of diseases of adrenal glands. On many enzymes it is possible to influence and clean symptoms of illnesses. I am convinced of it at treatment of the most different illnesses.

Any treatment after diagnostics begin with a diet.

Diet at hyperplazia adrenal glands.

To exclude from a diet it is necessary products of fast preparation, noodles, chips, the sausage, the aerated drinks, soluble juice, alcohol, mayonnaise, table salt. To refuse nuts and chocolate, fried and smoked meat and fish. In any case it is necessary to exclude salty meal. Instead of the products harmful to work of adrenal glands, it is necessary to pay attention to following products:
1.grain cereals, including sprouted, bran;
2.eggs (crude chicken yolks);
3.fish (a sardine, a mackerel, a herring);
4.salo, the bird's fat (chicken, duck);
5.greens of sprouts radishes, a lettuce, oranges, a currant, carrots;
6.vegetative fats (vegetable oils);
7.liver and kidneys;
8.marina crude salt.
Application of these products will give the chance to fill necessary for work of adrenal glands vitamins, minerals, aminoacids. After there will be passed diagnostics and is found authentically out, hyper-or dysfunction of adrenal glands became the reason of the arisen negative condition, it is possible to add medical actions with herbal medicine application. Only the exact existing diagnosis will let know how to treat adrenal glands and for what.

Competent Treatment

I have found new methods of treatment hyperplazia. It is a number of new chemical compounds, for example, a phytoestrogen, phytoprogestines, phytoandrogens, phytoalexine and others.
At not true diagnoses which put in Russia, lining under hypertension standards, suffer set of patients as from application of the preparations reducing pressure, there are ricochets, there are rare forms aritmia, the bradycardia (warm blows in a minute less than 50 blows in a minute even in the afternoon when the person is awake) is formed, tinnitus (a pulsation in ears), that only aggravate illness of adrenal glands. Other measures of treatment and cured are necessary.

Preparations are counter-indicative:

1.antidepressants and tranquilizers.
2.antihypertensive preparations, except some diuretics and vasodilatators.

The Main Conclusions

1. But revision of existing treatment is necessary for carrying out of additional researches, the Grant is necessary to me. Then I can describe all forms of diseases of adrenal glands with accompanying diagnoses precisely to select competent treatment. 2. Application Immunometabolic is necessary for therapy at diseases of adrenal glands, after all in mitochondrii other enzymes which too can cause insufficiency, after all activity of oxidationreduction enzymes of cycle Crebsa's localised in mitochondrii contain, defines a condition of power of a cage. It says only that True Therapy of diseases of adrenal glands is extremely difficult.

The Bibliography

1. Mardashev S.R. Biochemical problems of medicine, with. 52, М, 1975;
2. Shamraj E. F and Pashchenko A. E. Clinical biochemistry, ML, 1970.
3. Ingraham L. L. Enzymatic activation of oxygen, in Book.: Gomprehens. biochem., ed. by M. Florkin a. E. H. Stotz, v. 14, p.
424, Amsterdam a. o., 1966.
4. Savchenko A.A. Vitamins as a basis Immunometanolic therapies - Krasnoyarsk: Publishing house KrasGMU2011. 2011.
5. Savchenko A.A Basis clinical Immunobolomica. Novosibirsk. Science2012.
References
1. Azziz R, Wells G, Acton RT, Zacur HA. Pseudogene/functional gene ratio in late-onset 21-hydroxylase-deficient adrenal hyperplasia. Am J Obstet Gynecol. 1990;162:633.
2. Biglieri EG, Kater CE. 17 alpha-hydroxylation deficiency. In DH Nelson (ed), New aspects of adrenal cortical disease. Endocrinol Metab Clin North Am. 1991;20:257.
3. Bongiovanni AM. Acquired adrenal hyperplasia, with special reference to beta-hydroxysteroid dehydrogenase. Fertil Steril. 1981;35(6):599.
4. Bongiovanni AM. Congenital adrenal hyperplasia due to 3 betahydroxysteroid dehydrogenase deficiency. In MI New, LS Levine (eds), Adrenal Diseases in Childhood. Basel: Karger. 1984;13:72.
5. Bouchard M, et al. Familial observation of congenital hyperplasia of the overrenal cells due to 11 beta hydroxylase deficiency. Failure to prevent sexual ambiguity and antenatal diagnosis. Pediatrie. 1989;44:647.
6. Cravioto MDC, Ulloa-Aguirre A, Bermudez JA, et al. A new inherited variant of 3 beta-hydroxysteroid dehydrogenase-isomerase deficiency syndrome: Evidence for the existence of two isoenzymes. J Clin Endocrinol Metab. 1986;62(3):360-367.
7. Cutler GB, Lane L. Congenital adrenal hyperplasia due to 21-hydroxylase deficiency. N Engl J Med. 1990;323:1806.
8. Degenhart HJ. Prader's syndrome (congenital lipoid adrenal hyperplasia). In MI New, LS Levine (eds), Adrenal Diseases in Childhood. Basel: Karger. 1984;13:125.
9. Dupont B, et al. Close genetic linkage between HLA and congenital adrenal hyperplasia (21-hydroxylase deficiency). Lancet. 1977;2:1309.
10. Eldar-Geva T, Hurwitz A, Vecsei P, Palti Z, Milwidsky A, Rosler A. Secondary biosynthetic defects in women with late-onset congenital adrenal hyperplasia. N Engl J Med. 1990;323(15):855-863.
11. Feuillan P, Pang S, Schurmeyer T, Avgerinos PC, Chrousos GP. The hypothalamic-pituitary-adrenal axis in partial (late-onset) 21-hydroxylase deficiency. J Clin Endocrinol Metab. 1988;67(1):154-160.
12. Gueux B, Fiet J, Couillin P, et al. Prenatal diagnosis of 21 hydroxylase deficiency congenital adrenal hyperplasia by simultaneous radioimmunoassay of 21-deoxycortisol and 17 hydroxyprogesterone in amniotic fluid. J Clin Endocrinol Metab. 1988;66(3):534-537.
13. Keenan BS, Eberle AE, Lin TH, Clayton GW. Inappropriate adrenal androgen secretion with once-a-day corticosteroid therapy for congenital adrenal hyperplasia. J Pediatr. 1990;116(1):133-136.
14. Kohn B, Levine LS, Pollack MS. Late-onset steroid 21-hydroxylase deficiency: A variant of classical congenital adrenal hyperplasia. J Clin Endocrinol Metab. 1982;55(5):817-821.
15. Lachance Y, Luu-The V, Labrie C. Characterization of human 3 betahydroxysteroid dehydrogenase/ DELTA 5- DELTA 4-isomerase gene and its expression in mammalian cells. J Biol Chem. 1990;265(33):20469-20475.
16. Levine LS, Pang S. Prenatal diagnosis and treatment of congenital adrenal hyperplasia. In A Milunsky (ed), Genetic Disorders and the Fetus. Baltimore: Johns Hopkins University Press. 1992:Pp. 425.
17. Levine LS, Zachmann M, New MI. Genetic mapping of the 21-hydroxylase deficiency gene within the HLA linkage group. N Engl J Med. 1978;299(17):911-915.
18. Linder B, Feuillan P, Chrousos GP. Alternate day prednisone therapy in congenital adrenal hyperplasia: Adrenal androgen suppression and normal growth. J Clin Endocrinol Metab.1989;69(1):191-195.
19. Mantero F, Scaroni C. Enzymatic defects of steroidogenesis: 17 alphahydroxylase. In MI New, LS Levine (eds), Adrenal diseases in childhood [Laron Z, ed Pediatric and adolescent endocrinology; vol 13]. Basel: Karger. 1984;13:83.
20. Matteson KJ, Chung BC, Urdea MS, Miller WL. Study of cholesterol side-chain cleavage (20,22 desmolase) deficiency causing congenital lipoid adrenal hyperplasia using bovine sequence P450scc oligodeoxyribonucleotide probes. Endocrinol. 1986;118(4):1296-1305.
21. Mendonca BB, Bloise W, Arnhold IJ, et al. Male pseudohermaphroditism due to nonsalt-losing 3 beta-hydroxysteroid dehydrogenase deficiency: Gender role change and absence of gynecomastia at puberty. J Steroid Biochem. 1987;28(5):669-675.
22. Migeon CJ. Comments about the need for prenatal treatment of congenital adrenal hyperplasia due to 21 hydroxylase deficiency (Editorial). J Clin Endocrinol Metab. 1990;70(4):836-837.
23. Miller WL. Molecular biology of steroid hormone synthesis. Endocr Rev. 1988;9(3):295-318.
24. Miller WL, Levine LS. Molecular and clinical advances in congenital adrenal hyperplasia. J Pediatr. 1987;111(1):1-17.
25. Miller WL, Morel Y. The molecular genetics of 21 hydroxylase deficiency. Annu Rev Genet. 1989;23:371-393.
26. Morel Y, et al. Frequency of the 8 known deleterious point mutations of the CYP21B gene in more than 100 families with 21-hydroxylase deficiency (CAH): Implications for prenatal diagnosis. Program and Abstracts; Annual Meeting of the Endocrine Society. 1991;P. 375.
27. Morel Y, Andre J, Uring-Lambert B. Rearrangements and point mutations of P450c21 genes are distinguished by five restriction endonuclease haplotypes identified by a new probing strategy in 57 families with congenital adrenal hyperplasia. J Clin Invest. 1989;83(2):527-536.
28. Mulaikal RM, Migeon CJ, Rock JA. Fertility rates in female patients with congenital adrenal hyperplasia due to 21-hydroxylase deficiency. N Engl J Med. 1987;316(4):178-182.
29. Oberfield SE, Mayes DM, Levine LS. Adrenal steroidogenic function in a black and Hispanic population with precocious pubarche. J Clin Endocrinol Metab. 1990;70(1):76-82.
30. Pang S, Clark A. Newborn screening, prenatal diagnosis, and prenatal treatment of congenital adrenal hyperplasia due to 21-hydroxylase deficiency. Trends Endocrinol Metab. 1990;1(6):300-307.
31. Pang S, et al. Puberty in congenital adrenal hyperplasia. In MM Grumbach, PC Sizonenko, ML Aubert (eds), Control of the Onset of Puberty. Baltimore: Williams & Wilkins. 1990:Pp. 669.
32. Pang S, Lerner AJ, Stoner E. Late-onset adrenal steroid 3 betahydroxysteroid dehydrogenase deficiency. I. A cause of hirsutism in pubertal and postpubertal women. J Clin Endocrinol Metab. 1985;60(3):428-439.
33. Pang S, Clark AT, Freeman LC, et al. Maternal side-effects of prenatal dexamethasone therapy for fetal congenital adrenal hyperplasia. J Clin Endocrinol Metab. 1992;75(1):249-253.
34. Pang S, Hotchkiss J, Drash AL, Levine LS, New MI. Microfilter paper method for 17 alpha hydroxyprogesterone  radioimmunoassay: Its application for rapid screening for congenital adrenal hyperplasia. J Clin Endocrinol Metab. 1977;45(5):1003-1008.
35. Pang S, Levine LS, Stoner E, et al. Nonsalt-losing congenital adrenal hyperplasia due to 3 beta-hydroxysteroid dehydrogenase deficiency with normal glomerulosa function. J Clin Endocrinol Metab. 1983;56(4):808-818.
36. Pang S, Wallace MA, Hofman L, et al. Worldwide experience in newborn screening for classical congenital adrenal hyperplasia due to 21-hydroxylase deficiency. Pediatrics. 1988;81(6):866-874.
37. Pescovitz OH, Comite F, Cassorla F, et al. True precocious puberty complicating congenital adrenal hyperplasia: Treatment with a luteinizing hormone-releasing hormone analog. J Clin Endocrinol Metab. 1984;58(5):857-861.
38. Rheaume E, Simard J, Morel Y, et al. Congenital adrenal hyperplasia due to point mutations in the type II 3 beta-hydroxysteroid dehydrogenase gene. Nature Genet. 1992;1(4):239-245.
39. Rosler A, Lieberman E. Enzymatic defects of steroidogenesis: 11 betahydroxylase deficiency congenital adrenal hyperplasia. In MI New, LS Levine (eds), Adrenal Diseases in Childhood. Basel: Karger. 1984;13:47.
40. Rosler A, Weshler N, Leiberman E, et al. 11 beta-hydroxylase deficiency congenital adrenal hyperplasia: Update of prenatal diagnosis. J Clin Endocrinol Metab. 1988;66(4):830-838.
41. Speiser PW, New MI. An update of congenital adrenal hyperplasia. In F Lifshitz (ed), Pediatric Endocrinology. New York: Dekker. 1990;1038(1):307.
42. Speiser W, New MI, White PC. Molecular genetic analysis of nonclassic steroid 21-hydroxylase deficiency associated with HLA-B14,DR1. N Engl J Med. 1988;319(1):19-23.
43. Strachan T. Molecular genetics of congenital adrenal hyperplasia. Trends Endocr Metab. 1989;1(2):68-72.
44. Tusie-Luna MT, Traktman P, White PC. Determination of functional effects of mutations in the steroid 21 hydroxylase gene (CYP21) using recombinant vaccinia virus. J Biol Chem. 1990;265(34):20916-20922.
45. Wells G, Azziz R. Late onset adrenal hyperplasia: Mutation at codon 282 of the functional 21-hydroxylase gene is not ubiquitous. Fertil Steril. 1990;54(5):819-823.
46. White PC. Analysis of mutations causing steroid 21 hydroxylase deficiency. Endocr Res. 1989;15(1-2):239-256.
47. White PC, Maria I. New, Bo Dupont. Congenital adrenal hyperplasia. N Engl J Med. 1987;316:1519-1580.
48. White PC, Curnow KM, Pascoe L. Disorders of steroid 11 beta hydroxylase isoenzymes. Trends Endocrinol Metab. 1992;3(6):229-234.
49. White PC, Dupont J, New MI, Leiberman E, Hochberg Z, Rosler A. A mutation of CYP11B1 (Arg-448---His) associated with steroid 11 beta-hydroxylase deficiency in Jews of Moroccan origin. J Clin Invest. 1991;87(5):1664-1667.
50. Yanase T, Simpson ER, Waterman MR. 17 alpha hydroxylase/17,20-lyase deficiency: From clinical investigation to molecular definition. Endocr Rev. 1991;12(1):91-108.
51. Zachmann M, Tassinari D, Prader A. Clinical and biochemical variability of congenital adrenal hyperplasia due to 11 beta-hydroxylase deficiency: A study of patients. J Clin Endocrinol Metab. 1983;56(2):222-229.
Tables & Figures

Table 1: Arterial hypertension: changes ARP (activity renin plasmas) and Aldosteron's
N- norma, б - increase, бб- strong increase, в- fall.
а) At the majority of patients
b) At 30% of patients
c) Depends on weight of disease

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