sensitivity towards it Primary hyperparathyreosis

28. Z.Kheladze,Zv.Kheladze Rare Critical Conditions- Hyperparathyroid storm Critical Care Medicine Institute,Tbilisi,Georgia

Classification of diseases conditioned from disorder of parathyroid secretion sensitivity towards it Primary hyperparathyreosis, secondary hyperparathyreosis and and other forms. Clinical image of hyperparathyreosis is defined by hypercalcaemia resulted in parathyroid hormone’s hypersecretion. Primary hyperparathyreosis is divided into following formsL bone, kidney, stomach-gastric(gastric ulcer, pancreatitism cholecystitis) and cardiac-blood vessel forms. In clinical image: general weakness, loss of appetite, vomitting, nausea, weight loss, osallgies, myalgies, periodical polydypsia-polyurea, partial tetany. Muscular weakness and myalgies are conditioned by progressive atrophy of muscles. Objective changes are expressed by exhaustion, ground-like color of skin, deformation of spine vertebras and limbs, reduce in height, palpation of parathyroid glands’ adenomas is practically imposible if there is no gigantic adenoma. In 90% adenoma is localized in upper parathyroid glands and has solid elastic consistency, by roentgen there are revealed osteophorosis of various localization: cysts are expressed in roots of tooth, then in tubular bones.

Key Words:Rare Critical Conditions,Hyperparathyroid storm Critical Care Medicine

It is a small review of rare critical conditions and they are integrated by two factors: they are represented as critical conditions and at the same time they appear on the “stage” of critical care medicine. Professional activity of some doctors may occur without meeting with them. Despite all doctors of critical care medicine is obliged to have complete information. Because of the limited time a doctor is not able to have direct information about a condition. Moreover, if an information is little and insignificant. Georgian Institute of Critical Care Medicine does it’s best to improve this condition. This time from these cycles of works we would like to represent a little information about Hyperparathyroid storm . Classification of diseases conditioned from disorder of parathyroid secretion and sensitivity towards it Primary hyperparathyreosis Pathogenetic forms • adenoma ( adenomes) • hyperplasia of parathyroid hormones • multiple endocrinic neoplasia with I type hyperparathyreosis- Wermer • multiple endocrinic neoplasia with II type hyperparathyreosis • clinical forms • form of bone • osteophorotic • phibrotic- cystic osteytis • “ Peggetic’ • visceropathic with most damage of kidneys • gastro-intestinal tracts predominant damage • nervous-psychic sphere’s dominant damage • blended form secondary hyperparathyreosis • kidney pathology : chronic kidney failure, tibulypathy, kidney racitis

• intestinal pathology: syndrome of malabsorption • bone pathology: sinyl osteomalation,puerperral, idiopathic, Paggette disease. • Deficiency of D-vitamin: diseases of kidneys, liver, congenital fermentopathies Malignant diseases: myeloma illnesses Tertiary hyoerparathyreosis pseudohypoparathyreosis hormonally inactive cystic and cancerous creatures of parathyroid glands hypoparathyreosis • congenital undeveloped parathyroid glands or aplasia • idiophatic [ autoimmune] • post-surgery • irradiation injuries • injure of parathyroid glands’ after hemorrhage pr infarct • infective disease pseudo-hypoparathyreosis • I type-lack of sensitivity of parathyroid hormones towards target organs_ adenylyl cyclase dependent • II type-adenylyl cyclase- independent-with autoimmune genesis pseudo-pseudohypoparathyreosis Is a complication of chronic hyperparathyreosis and is conditioned by parathyroid hormone’s hypersecretion with acute hypercalcaemia that poisons an organism. Hypercalcaemia is a general symptom os hyperparathyreosis and occurs during other diseases as well: -hypercalcaemia associated with parathyroid hormone’s hyperproduction: priimary, secondary, triarty hyperparathyreosis, multiple endocrinic adenomatosis of I and II type, hypercalcaemia during ectopic secretion of parathyroid hormones.

-endocrinophatic hypercalcaemiasL thyreotoxicosis, adrenal gland chronic failure, pheochtomocytoma, acromegally. -hypercalcaemias assoociated with neoplastic processes: osteolitic metastases of malignant cancers in bones, diseases of blood system. -medicinal hypercalcaemias: alkaline-lactatic syndrome during treatment with diuretics, exceed of A and D vitamins, treating with lithium drug. -hypercalcaemias conditioned by immobilization (bone ruptures). Hyperparathyreosis is a chronic disease that is conditioned by parathyroid hormone’s hyperproduction. Primary hyperparathyreosis is a disease of parathyroid glands that is revealed by hyperproduction of parathyroid hormone and development of hypercalcaemia syndrome. Is frequent – 25 cases at 100 000 population. 35% of hypercalcaemic syndrome is related to the disease. It is the number two disease after thyreotoxicosis and diabetes insipidus. The peak of illness is 40-50 ages and women become ill 2 times more. In post-menopausal period primary hyperparathyreosis occurs in 3% of females. The primary hyperparathyreosis is an independent disease. Secondary hyperparathyreosis is represented as compensative hyperfunction and hyperplasia of parathyroid glandsl is developed when there is long-term hypocalcaemia of various genesis and hyperphosphatemia. When there is tertiary hyperparathyreosis we have a deal with autoimmune hyperproduction of paratyroid hormone near hyperplasic thyroid glands or formation of parathyroid glands’ adenomas during long-term existence of secondary hyperparathyreosis. Pathogenesis: most common reason in solitary adenoma-parathyroma of parathyroid glands-80-90%, rarely multiple adenomas-5%. 2-6% primary hyperplasia of parathyroid glands, 0,5-3% parathyroid glands’ tumor. Primary hyperplasia of all parathyroid glands occurs in 15%. The mass of ademonas is between 25-90mg. Hyperparathyroid storm occurs in 5% OF patients with hyperparathyreosis and is developed when in plasma calcium in more than 4mmol/l and is provoked by

longterm laying regimen, usage of tyasid diuretics, consumption of calcium and Dvitamin. Hyperproduction of parathyroid hormone conditiones in strengthened excretion of phosphate by kidneys which plasma level decrese stimulates synthesis of calcitriole and it conditiones in over-absorption of Ca-2++ in intestines. Hypercalcaemia is also elevated when osteoclastes are stimulated by parathyroid hormone. The overplus of parathyroid hormone causes metabolism in bone tissue, fastening of bone’s resorbtional and bone-creating processes, in addition to this, bone-creating proocesses stay back than reasorbtional ones that causes generalized osteophorosis and osteodystrophya, washing out of calcium from bone depos. Hypercalcaemia, hypercalciuria causes damage of kidney tube epithelium and create nephrodense calcium. Nephrodense calcium causes progressive worsening of kidney function. The basis of genesis of stomach and duoden intestine ulcery diseases is hypercallcaemia of arteriosclerosis and bloodvessel classification. Hypercalcaemia along with arterial hypertonia causes hypertrophy of left ventricle which causes dense calcium of valvular, coronary and miocardial. Hypercalcaemic storm is developed when calcium level in blood sharply elevates. This can be provoked by over-supply of exogenous calcium in orgaanism, also by strengthened wash out of calcium from bones. In bone tissue calcium with phosphorus is represented as compounds which create hydroxylapatitis crystals. In norm, calcium volume in blood plasma is 2,42,0mmol/l(9,5-11,5g%), as a biological activity only ionized calcium can be distinguished that is 1, 2mmol/l in plasma (5mg%), protein calcium in plasma 1mmol/l(4mg%),non-ionized is 0,5mmol/l (2mg%). Protein-related calcium fraction level elevated in parallel with pH alkaliness deviation. The general stock of calcium in an organism is located in bone tissue (95-99%). Daily require on calcium in aduls is 0,5-1,0g. During hyperparathyreosis hypercalcaemic storm (coma) is manly provoked by over-incretion of parathyroid hormone by parathyroid adenoma or hyperplasic epithelial bodies. In norm parathyroid hormone along with thyreocalcitonine promotes permanency of calcium level in plasma. By the influence of parathyroid hormone calcium level in plasma is increased, it controls level of ionized calcium and phospphorus in blood (non-organic phosphorus). In norm phosphorus volume in plasmma is 3,2-4,8mmol/l (10-15%) from which non-organic

phosphorus-0,97-1,6mmol.l (3-5%). Lipid phosphorus 2,6mmol/l (8mg%), in bone tissue phosphorus amount implies 66% of total organism phosphorus. In regulation of phosphorus and calcium metabolis also ACTH, glucocorticoids, somatotropine, thyroxine, androgens, estrogens, and vitamin D participate in. Mentioned hormones in difference with parathyroid hormone has hypocalcaemic effect. D vitamin mostly strengthenes calcium and phosphorus absorption in guts, also stimulates reabsorption of themm by kidneys. From bone depos phosphorus and calcium mobilization effect of D vitamin is insignificant. When hyperparathyreosis by hyperproduction of parathyroid hormone by direct influence of it on bone tissue osteoclasts are activated by excretion of citrate that results in mobilization of calcium and phosphorus from bone tissue in conditions of acydosis. After demineralization of bones cysts are generated in them, osteomalatic and phibrotic processes and finally pathologiocal ruptures. .Clinical image of hyperparathyreosis is defined by hypercalcaemia resulted in parathyroid hormone’s hypersecretion. Primary hyperparathyreosis is divided into following formsL bone, kidney, stomach-gastric(gastric ulcer, pancreatitism cholecystitis) and cardiac-blood vessel forms. In clinical image: general weakness, loss of appetite, vomitting, nausea, weight loss, osallgies, myalgies, periodical polydypsia-polyurea, partial tetany. Muscular weakness and myalgies are conditioned by progressive atrophy of muscles. Objective changes are expressed by exhaustion, ground-like color of skin, deformation of spine vertebras and limbs, reduce in height, palpation of parathyroid glands’ adenomas is practically imposible if there is no gigantic adenoma. In 90% adenoma is localized in upper parathyroid glands and has solid elastic consistency, by roentgen there are revealed osteophorosis of various localization: cysts are expressed in roots of tooth, then in tubular bones. There are characteristic changes like erosion of outer cortiocid surface, generalized demineralization, local destructive processes, cystic changes and pathological ruptures that are slowly healed. According of internal organs there is revealed injury of cardiac-blood vessel system-arterial hypertonia, calcinosis of coronary arteries with high risk of stenocardia. hypercalcaemia stimulates secretion of gastrin and salt acid that

elevates the propability of diseases of stomach and duodenal intestine (12-20%) that is severe during hyperparathyreosis and tends to complication of perforation. In 7-12% chronic pancreatitis, hepatitis, cholecistitis are developed, gallstone disease developmennt with mechanical yellowness. Urinary tract is injured in 60% and in rare cases it can be the first revelation of hyperparathyreosis. Urinary-stone illness is freqquent: 15%-arterial stones, 25-30% multiple stones, 30-32% doublesides injury. The content of stones is represented by oxylates and phosphates that conditiones in frequent recurrence, creation of multiple coral-like concrements. Clinically urolithiasis is revealed by dysurrea,pain in waist, underhip and spacing. Parathyreoid nephropathy is accompanied by arterial hypertonia and nephrotic syndrome (ptoteinurea, hematuria, cylindruria with probable uremia. Accompaniment with inflammatory processes fastens development of kidney failure. Hypercalcaemia of various etiology conditions in accumulation of calcium in eye conreal cover and linear keratopathy. Neurologic symptomatics are revealed as pain in waist and limbs, radiculitis and disorder of pelvic floor organs’ function, because of suppression on intervertebral disks. Disorder of psychic is revealed by increased sleepiness, lack of memory, phobias and depression. For hyperparathyroid storm it is characteristic to be developed suddenly. The storm is before handed by symptomatic of hyperparathyreosis: weakness, adynamy, dyspeptic disorders-nausea, vomiting, constipation, lack of appetite. When storm is more developed a general weakness is increased, low muscle tone, hypoflexia, osalgias, and myalgias. Dyspeptic and neural-psychic disorders are frequent. Stomach-intestinal tract dysfunction is revealed by profussive vomiting that causes dehydration of an organism and imbalance of water and electrolytes. There are developed spastic pains in abdomen mostly in epigastrium area. Sometimes such pain simulates appendicitis that can become a reason of probable surgery. When the storm is stomach-intestinal form then perforation of peptic ulcer can be developed, gastro-duodenal bleeding, acute pancreatitis. Hypercalcemic storm causes insipid syndrome; polyuria -polydipsia, tachycardia is revealed, hyperpyrexia

(body temperature more than 40oC). Some kind of form of hypercalcaemic storm is an acute metastatic calcification of lungs that complicates diagnosis of the storm between pulmonary congestion and acute pneumonia. In some cases is developed in brain, myocardium and other organs with massive calcification and necrosis that can become a reason of critical care condition by its own. When there is a kidney form there are images of acute kidney failure or uremic coma. When there is hypercalcaemic storm elevation of urea and creatinine, phosphate in blood indicates to the development of acute kidney failure on the background of hypercalcaemia and progressing uremia. Neural-psychic disorders are revealed by increased sleepiness, asthenia, depression. Time by time delaying processes or on the contrary, psycho-motoric irritation, visionary hallucinations, clinical signs of epilepsy, reactive psychosis that ends as development of deep coma. Hypercalcaemia is expressed by 5mmol/l cardiac-blood vessel dysfunction, acute respiratory failure with pulmonary congestion and oligo-anuria, high lethality. The direct reason of lethal outcome can be acute thrombosis of magisterial blood vessels and iatrogenic blood vessels’, with formation of infarct of various organs that is the result of poisoning of organism with calcium. Diagnosis: the diagnosis of hyperparathyreosis is bases on clinical, laboratorial, anamnesis and diagnostic analyses. Hyperparathyreosis is marked by: hypercalcaemia> 3,0mmol/l; hypercalciurea > 200mg/daynight or >6-11mmol/l; hypophosphatemia 16-25mmol/l; increase in alkaline phosphatase activity >5un; reduce in phosphorus tubular reabsorption 5075%(norm 85-95,3%); TSH level elevation in serum >65pg/ml(65ng/l Ci-units) and in urine. In general image of blood anemia, eosinophilia, neutropenia occur. After urine analysis- isohypostenuria, proteinuria, cylindruria, micro hematuria. When there is an acute or chronic failure of kidneys-appropriate indexes of nitrogen metabolism. Roentgen reveals diffusive osteoporosis, supperyostal resorption, cysts, multiple ruptures and scar changes. Roentgen and ultra sound analyses reveal nephrocalcinosis and nephrolithiasis. For determination of parathyroid gland’s sizes there are utilized roentgen of neck with contrastive analysis(angiography, CT, thermography, ultrasound sonography and etc). TSH evaluation happens by means of immuneferment methods. To diagnose hidden hyperparathyreosis there are used

diagnostic attempts with thiazide diuretics, glucocorticoids and parathyreodine. When there is hyperparathyroid storm diagnostic means lose their value because of limited time. The classic signs of ECG hypercalcaemia are: Q-T interval shortening, ST depression, atrioventricular blockage. Echoscope reveals hypertrophy of left ventricle, dense calcium in myocardium. For topical diagnostics there are used nonselective arteriography with contrast and catheterization of vein with selective determination of parathyroid hormone. Differential diagnosis includes differentiation of conditions that are marked by hypercalcaemia, also metabolic osteopathies, malignant cancers, pseudohyperparathyreosis, secondary and tertiary hyperparathyreosis. The differentiation of hyperparathyreoid coma from metabolic and dyselectrolytemic comas. For effective treatment of hyperparathyroid storm a constant monitoring of plasma electrolytes, acid-alkaline balance, ECG, diuresis is important. Also defining of parathyroid hormone’s concentration, knowing reasons of it’s hyperproduction. In case of existence of adenomas and hormone-producing cancers in parallel with treating of storm preparing for surgery is also begun. The beginner stage of the treatment is rehydration of an organism in aids of 2-4l sodium chloride (average infusion speed in 1l/hr) that is followed by biphosphonates’ intravenous injection (pamidronate or etidronate) during 4-24 hours. Before nowadays it was recommended to use so-called “loop-like diuretics and now it is not advised because utilization of them complicates dehydration more. Furosemide is injected not earlier than 30 min after rehydration with constant control of electrolytes. Reinforcement of diuresis is directed to decrease of hypercalcaemia and is conducted in such way: on the background of infusion of 3l physiological solution during 2-3 hours Furosemide (Lazix) of 40-60-100mg is injected. Then the speed of infusion is reduced (8-10l/day). Considering kidney function and blood vessel systemFurosemide injection is continued with dosage of 40-80mg at 3-4 hours of intervals according to an effect. Calcitonine is especially safe drug. When there is a storm it is recommended to inject 4-8ME once in 6-12 hours. When non-organic phosphorus has low level (1mmol/l) then drugs that replace phosphorus salts are injected. For blockage of plasma calcium when kidney function is normal 2,5% 250ml sodium

citrate can be used. According to some authors it is recommended to infuse sodiumpotassium-phosphate buffer solution during 8-12 hours with the following content: HPO4-81mmol(11,583gr); KH2PO4-19mmol (2,662gr); 5% glucose solution 1000ml; solutions pH 7,4. 1l of solution contains 100mmol phosphorus. When the solution is infused calcium level decrease is possible with 0,5-1,75mmol/l. At the time of treating the storm ethylendiamintetra lactic acid’s salt (NA2ЭДТА)is used as usual. If hypercalcaemic storm is developed on the background of malignant cancers’ osteolytic metastases the cytostatic Mitramicine is used that is antagonist of parathyreoine-10-25mg/kg. in addition to that when liver and kidneys are damaged Mitramicine injection is not recommended. The toxic effect of the medicinal is revealed by thrombocytopenia, reduce of prothrombine, development of glomerulosclerosis. When the storm is conditioned by exceeding of D vitamin glucocorticoids are used, they reduce calcium absorption in guts, block action of D vitamin and strengthen excretion of calcium by urine, reduce collapse events. Mostly there are used water soluble Hydrocortisone hemisuccinate or Prednyzolone 30mg 2-3 times a day. When hypercalcaemia is accompanied by acute or chronic failure of kidneys the most effective method is hemodialysis with calcium-less buffer. Also peritoneal dialysis is possible but it is less effective. In parallel with pathogenetic therapy symptomatic therapy is also conducted according to indication, with usage of artificial pulmonary ventilation. For relief of storm hyperparathyreosis is traditionally treated. During Parathyroid gland’s hyperplasia the total parathyreoidectomy is recommended with partial implantation of extracted gland’s tissue in front arm area.

References: Z.kheladze,Zv.Kheladze „Critical Care Medicine“,Tbilisi,Georgia,2015,first book,

z.xelaZe,zv.xelaZe iSviaTi kritikuli mdgomareobebi – hiperparaTireoiduli krizi კრიტიკული მედიცინის ინსტიტუტი , თბილისი.saqarTvelo

ganpirobebulia paraThormonis hipersekreciis Sedegad mwvave hiperkalcemiiT da organizmis mowamvliT.hiperkalcemia hiperparaTireozis ZiriTadi simptomia, Tumca igi gvxvdeba sxva daavadebebis drosac:paraThormonis hiperproduqciasTan asocirebuli hiperkalcemia: pirveladi, meoradi, mesameuli hiperparaTireozi, I da II tipis mravlobiTi endokrinuli adenomatozi, hiperkalcemia paraThormonis eqtopiuri sekrecisas (fsevdohiperparaTireozi);endokrinopaTiuli hiperkalcemiebi: Tireotoqsikozi, Tirkmelzeda jirkvlis qronikuli ukmarisoba, feoqromocitoma, akromegalia;neoplastiur procesebTan asocirebuli hiperkalcemiebi: avTvisebiani simsivneebis osteolizuri metastazebi ZvlebSi, sisxlis sistemis daavadebebi (leikozi, limfoma, mielomuri daavadeba, limfogranulematozi);medikamenturi hiperkalcemiebi: tutovan-laqtaturi sindromi Tiaziduri diuretikebiT mkurnalobisas, А d a D vi dozis gadameteba, liTiumis preparataminebis tebiT mkurnaloba;imobilizaciiT ganpirobebuli hiperkalcemiebi (Zvlebis motexilobebi); paTogenezi. qronikuli daavadebaa. ganpirobebulia paraThormonis hiperproduqciiT. pirveladi hiperparaTireozi paraTireoiduli jirkvlebis daavadebaa. vlindeba paraThormonis hiperproduqciiTa da hiperkalcemiis sindromis ganviTarebiT. xSiria_25 SemTxveva 100 000 mosaxleze weliwadSi. masTanaa dakavSirebuli hiperkalcemiuri sindromis 35%. Tireotoqsikozisa da Saqriani diabetis Semdeg sixSiriT mesame endokrinuli daavadebaa. avadobis piki 40-50 wlis asakSi uwevs, 2-jer xSirad avaddebian qalebi. postmenopauzur

periodSi pirveladi hiperparaTireozi aReniSneba qalTa 3%..meoradi hiperparaTireozi warmoadgens paraTireoiduli jirkvlebis hiperfunqciisa da hiperplaziis Sedegs. viTardeba sxvadasxva genezis xangrZlivi hipokalcemiisa da hiperfosfatemiis Sedegad. mesameuli hiperparaTireozisas adgili aqvs hiperplazirebuli farisebraxlo jirkvlebis mier paraThormonis avtonomiur hiperproduqcias, an paraTireoiduli jirkvlebis adenomis formirebas xangrZlivad arsebuli meoradi hiperparaTireozisas. xSiri mizezia paraTireoiduli jirkvlebis solitaruli adenoma_paraTiroma_ 80-90%, SedarebiT iSviaTia mravlobiTi adenomebi_5%. paraTireoiduli jirkvlebis pirveladi hiperplazia_2-6%, paraTireoiduli jirkvlebis kibo_0,5-3%..hiperparaTireoiduli krizi gvxvdeba hiperparaTireoziT daavadebulebis 5%. viTardeba plazmaSi kalciumis 4mmol/l metad momatebisas.provocirdeba xangrZlivi woliTi reJimiT, Tiaziduri diuretikebis gamoyenebiT, kalciumisa da vitaminis miRebiT. paraThormonis hiperproduqcia ganapirobebs Tirkmlebis mier fosfatis gaZlierebul eqskrecias, romlis plazmuri donis Semcireba astimulirebs kalcitriolis [1,25-( ОH)2sinTezs, es ki -D3] ganapirobebs nawlavebSi Warbi Ca-2++ Sewovas. hipercalcemia matulobs paraThormonis mier osteoklastebis stimulaciis Sedegadac. paraThormonis siWarbe ganapirobebs nivTierebaTa cvlis gaZlierebas Zvlovan qsovilSi, Zvlis rezorbciuli da Zvalwarmomqmneli procesebis daCqarebas, amasTan Zvalwarmomqneli procesebis siCqare CamorCeba rezorbciul procesebs, ris gamoc viTardeba generalizebuli osteoporozi da osteodistrofia, Zvlovani depoebidan kalciumis gamorecxva. hiperkalcemia, hiperkalciuria ganapirobebs Tirkmlis milakebis epiTeliumis dazianebas da nefrokalcinatebis warmoqmnas. nefrokalcinozi iwvevs Tirkmlebis funqciis progresul gauaresebas. kuWisa da Tormetgoja nawlavis wylulovani daavadebis genezis safuZvelia hiperkalcemia arterioloskleroziTa da sisxlZarRvTa kalcifikaciiT. hiperkalcemia arteriul hipertoniasTan erTad iwvevs mar-

cxena parkuWis hipertrofias, romlis funqciis gauaresebas ganapirobebs hiperparaTireozisaTvis damaxasiaTebeli sarqvlovani, koronaruli da miokardialuri kalcinatebi. hiperkalcemiuri krizi viTardeba sisxlSi kalciumis donis mkveTri matebisas.es SesaZloa ganpirobebuli iyos organizmSi egzogenuri kalciumis Warbi miwodebiT, agreTve Zvlebidan kalciumis gaZlierebuli gamorecxviT. Zvlovan qsovilSi kalciumi fosforTan naerTebis saxiTaa warmodgenili, romlebic warmoqmnian hidroqsilapatitis kristalebs. normaSi sisxlis plazmaSi kalciumis Semcveloba 2,4-2,9 mmol/l (9,5-11,5mg%) biologiuri aqtivobiT xasiaTdeba mxolod ionizirebuli kalciumi, romelic plazmaSi 1, 2 mmol/l-ia (5mg%) cilaSekavSirebuli kalciumi plazmaSi 1 mmol/l (4mg%) araionizirebuli Seadgens 0,5mmol/l (2mg%). cilaSekavSirebuli kalciumis fraqciis done matulobs pН tutianobisaken gadaxris paralelurad. kalciumis ZiriTadi maragi organizmSi lokalizdeba Zvlovan qsovilSi (95-99%). sadReRamiso moTxovnileba kalciumze moZrdilebSi Seadgens 0,5-1,0 g.fosforisa da kalciumis cvlis regulaciaSi monawileobs aseve a.k.t.h, glukokortikoidebi, somatotropini, Tiroqsini, androgenebi, estrogenebi da vitamini D. aRniSnul hormonebs paraThormonisagan gansxvavebiT hipokalcemiuri efeqti aqvT. D vitamini ZiriTadad aZlierebs kalciumisa da fosforis Sewovas nawlavebSi, aseve aZlierebs maT reabsorbcias Tirkmlebis mier.Zvlovani depoebidan fosforisa da kalciumis mobilizebis efeqti D vitaminis umniSvneloa. hiperparaTireozisas paraThormonis hiperproduqciis Sedegad misi uSualo zemoqmedebiT Zvlovan qsovilze aqtiurdeba osteoklastebi citratis gamoyofiT, Sedegad adgilobrivi acidozis pirobebSi viTardeba Zvlovani qsovilidan kalciumisa da fosforis mobilizacia, Zvlebis demineralizaciis Sedegad maTSi viTardeba kistebi, osteomalaciuri da fibrozuli procesebi, Sedegad ki xdeba paTologiuri motexilobebi klinika. ganarCeven Zvlovan, Tirkmlis, kuW-nawlavis (kuWis wyluli, pankreatiti, qolecistiti) da gul-sisxlRarRvovan (ar-

teriuli hipertonia) formebs.klinikur suraTSi dominirebs sisuste, umadoba, gulisreva, Rebineba, yabzoba, wonaSi kleba, osalgiebi, mialgiebi, periodulad polidifsia-poliuria, depresia, parciuli tetania. kunTovani sisuste da mialgiebi ganpirobebulia kunTebis progresuli atrofiiT. obieqturi cvlilebebi gamoixateba gamofitviT, kanis miwisferi elferiT, xerxemlis malebis, kidurebis deformaciiT, simaRlis SemcirebiT. paraTireoiduli jirkvlebis adenomis palpacia SeuZlebelia, Tu ar aris giganturi adenoma. 90% adenoma lokalizdeba zeda paraTireoidul jirkvlebSi da aqvs mkvrivi elastiuri konsistencia. rentgenologiurad sxvadasxva lokalizaciis sistemuri osteoporozia: kistebi vlindeba jer kbilis fesvebSi, Semdgom lulovan ZvlebSi. damaxasiaTebeli cvlilebebia gareTa kortikuli zedapiris erozia, generalizebuli demineralizacia, lokaluri destruqciuli procesebi, xSirad viTardeba kisturi cvlilebebi da paTologiuri motexilobebi, romelTa SexorcebiTi procesi mkveTrad Senelebulia. Sinagani organoebis mxriv vlindeba gulsisxlZarRvTa sistemis dazianeba _ arteriuli hipertonia, koronaruli arteriebis kalcinozi,-stenokardiis maRali riskiT.hiperkalcemia astimulirebs gastrinis da marilmJavas sekrecias rac zrdis kuWisa da Tormetgoja nawlavis wylulovani daavadebis albaTobas (12-20%), romelic hiperparaTireozisas mZimed mimdinareobs da midrekilia xSiri gamwvavebebisa da perforirebisaken. 7-12% viTardeba qronikuli pankreatiti, hepatiti, qolecistiti, SesaZlebelia naRvl-kenWovani daavadebis Camoyalibeba meqanikuri siyviTliT. saSarde sistemis dazianeba gvxvdeba 60% da iSviaT SemTxvevaSi SesaZloa iyos pirveladi hiperparaTireozis erTaderTi gamovlineba. xSirad vlindeba Sard-kenWovani daavadeba: 13-15%_arteriuli kenWebi, 25-_30% mravlobiTi kenWebi, 30-32% ormxrivi dazianeba. kenWebis Semadgenloba warmodgenilia oqsalatebiTa da fosfatebiT, rac ganapirobebs xSir recidivs, mravlobiTi marjniseburi konkrementebis warmoqmnas. klinikurad uroliTiazi vlindeba dizuriiT, tkiviliT welis, ferdqveSa da Sorisis areSi. paraTireoidul nefropaTias

Tan axlavs arteriuli hipertonia da nefrozuli sindromi (proteinuria, hematuria, cilindruria SesaZlo uremiiT.). anTebiTi procesis TandarTva aCqarebs Tirkmlis ukmarisobis ganviTarebas.sxvadasxva eTiologiis hiperkalcemia ganapirobebs kalciumis Calagebas Tvalis rqovana garsSi da xazovani keratopaTiis ganviTarebas.nevrologiuri simptomebi vlindeba tkivilebiT welsa da kidurebSi, radikulitiTa da menjis organoebis funqciis moSliT, malTaSua diskebze zewolis gamo. fsiqikis darRveva vlindeba momatebuli ZilianobiT, mexsierebis daqveiTebiT, fobiebiTa da depresiiT.hiperparaTireoiduli krizisTvis damaxasiaTebelia uecari ganviTareba. krizis ganviTarebisas matulobs sisuste, qveiTdeba kunTebis tonusi, vlindeba hiporefleqsia, osalgiebi da mialgiebi. damaxasiaTebelia dispefsiuri da nervul-fsiqiuri moSlilobani. kuW-nawlavis traqtis disfunqcia vlindeba profuzuli RebinebiT, romelic ar aris dakavSirebuli sakvebis miRebasTan da ganapirobebs organizmis dehidrataciasa da eleqtrolituri disbalansis ganviTarebas. viTardeba spastiuri tkivilebi mucelSi, upiratesi lokalizaciiT epigastiumis areSi. zogjer amgvari tkivili mwvave apendicitis simulacias iZleva.krizis kuW-nawlavuri formisas SesaZloa ganviTardes peptiuri wylulis perforacia, gastro-duodenuri sisxldena, mwvave pankreatiti. hiperkalcemiuri krizisas xSiria insipidaruli sindromi; poliuria-polidifsia. vlindeba taqikardia, hiperpireqsia (temperaturis mateba 40° metad.). hiperkalcemiuri krizis Taviseburi formaa filtvebis mwvave metastazuri kalcifikacia. Tavis tvinSi, miokardiumSi da sxva organoebSi viTardeba masiuri kalcifikacia da nekrozebi, rac Tavad SesaZloa gaxdes kritikuli mdgomareobis mizezi. Tirkmlis formisas vlindeba Tirkmlebis mwvave ukmarisobis an uremiuli komis suraTi. hiperkalcemiuri krizisas Tirkmlebis mwvave ukmarisobis ganviTarebis maniSnebelia sisxlSi Sardovanasa da kreatininis, fosfatis donis momateba hiperkalcemiisa da progresirebadi uremiis fonze. nervul-fsiqiuri moSlilobani vlindeba momatebuli ZilianobiT, asTeniiT, depresiiT. viTardeba SekavebiTi

procesebi an fsiqo-motoruli aRgzneba, mxedvelobiTi halucinaciebi, epilefsiis klinikuri gamovlinebani, reaqtiuli fsiqozebi, rac mTavrdeba komis CamoyalibebiT. hiperkalcemiisas (5mmol/l da meti) aRiniSneba gulsisxlZarRvTa funqciis daTrgunva, sunTqvis mwvave ukmaroba filtvebis SeSupebiT da oligo-anuria, maRali letalobiT. diagnozi: hiperparaTireozisaTvis damaxasiaTebelia: hiperkalcemi > 3,05mmol/l; hiperkalciuria > 200mg/dR/RameSi an > 6-11 mmol/l; hipofosfatemia < 0,969 mmol/l; hiperfosfaturia > 16-25 mmol/l; tute fosfatazis aqtivobis momateba > 5 erT; fosforis milakovani reabsorbciis daqveiTeba 50-75% (norma 85-95,3%); TSH donis momateba SratSi .> 65 pg/ml (65ng/l -erTeulebSi) Сi da SardSi. sisxlis suraTSi damaxasiaTebelia anemia, eozinofilia, neitropenia.Sardis gamokvlevisas aris izohipostenuria, proteinuria, cilindruria, mikrohematuria. Tirkmlis mwvave an qronikuli ukmarisobisas maCveneblebi. rentgenologiurad vlindeba difuzuri osteoporozi, subperiostaluri rezorbcia, kistebi, mravlobiTi motexilobebi da nawiburovani cvlilebebi. rentgenologiuri da ultrabgeriTi gamokvlevebisas vlindeba nefrokalcinozi da nefroliTiazi. paraTireoiduli jirkvlebis zomebis dasadgenad gamoiyeneba kisris rentgenografia kontrastuli gamokvleviT (angiografia, kompiuteruli tomografia, Termografia, ultrabgeriTi sonografia da sxva). ТSH gan sazRvra xdeba imunofermentuli meTodebiT. faruli hiperparaTireozis diagnozisaTvis gamoiyeneba diagnostikuri cdebi Tiaziduri diuretikebiT, glukokortikoidebiTa da paraTireoidiniT. hiperparaTireoiduli krizisas sadiagnozo cdebi kargavs Tavis aqtualobas procesis droSi limitirebis gamo. hiperkalcemiis klasikuri e.k.g. niSnebia: Q-T intervalis damokleba, S-T depresia, atrioventrikuluri blokada. eqokardiografiulad vlindeba marcxena parkuWis hipertrofia, kalcinatebi miokardSi. topikuri diagnostirebisaTvis gamoiyeneba araseleqtiuri arteriogra-

fia kontrastirebiT da venebis kaTeterizacia paraThormonis seleqtiuri gansazRvriT. mkurnaloba. krizis mkurnalobis paralelurad iwyeben preooperaciul momzadebas. mkurnalobis sawyisi etapia organizmis rehidratacia 2-4 l natriumis qloridis infuziiT (infuziis saSualo siCqarea 1l/sT), ris Semdegac iwyeba intravenurad bifosfonatebis Seyvana ( pamidronati an etidronati) 4-24 sT ganmavlobaSi. adre rekomendebuli e.w ,,maryuJovani” diuretikebis gamoyeneba sadReisod sawyis etapze ar aris rekomendebuli, vinaidan maTi gamoyeneba kidev ufro amZimebs dehidratacias. furosemidi SehyavT arauadres 30 wT regidrataciis Semdeg eleqtrolitebis mkacri kontroliT. diurezis forsireba mimarTulia hiperkalcemiis Semcirebisaken. forsireba tardeba Semdegi sqemiT: fiziologiuri xsnaris 2-3 sT infuziis (3l) fonze SehyavT 40-60100 mg furosemidi (laziqsi). Semdgom infuziis siCqare mcirdeba (8-10l/dR). Tirkmlis funqciisa da gulsisxlZarRvTa sistemis funqciuri mdgomareobis gaTvaliswinebiT. furosemidis Seyvana grZeldeba 40-80 mg doziT 3-4 sT intervalebiT, efeqtis mixedviT. krizisas rekomendebulia kalcitoninis Seyvana 4-8 ME 6-12 sT erTxel. araorganuli fosforis dabali donisas (1 mmol/l) SehyavT fosforis marilebis Semcveli preparatebi. plazmis kalciumis SeboWvisaTvis Tirkmlebis normaluri funqciisas SesaZloa 2,5% 250 ml natriumis citratis wveTovani Seyvana. rekomendebulia natri- kali- fosfaturi buferuli xsnaris infuzia 8-12 sT ganmavlobaSi buferuli xsnaris Semdegi SemadgenlobiT: HPO4_81 mmoli (11,583gr); KH2PO4_19 mmoli (2,662 gr); 5% glukozis xsnari 1000 ml; xsnaris pH 7,4. xsnaris 1 l Seicavs 100 mmol (3,18gr) fosfors. xsnaris infuziisas kalciumis donis Semcireba SesaZloa 0,5-1,75 mmol/l. krizis mkurnalobisas gamoiyeneba eTilendiamintetraZmarmJavas marili (NA2ЭДTA). Tu hiperkalcemiuri krizi viTardeba avTvisebiani simsivneebis osteolituri metastazebis fonze gamoiyeneba citostatiki mitramicini, romelic paraTireoidinis antagonistia,Seiyvaneba wveTovnad 10-25 mg/kg do-

ziT. amasTan RviZlisa da Tirkmlebis dazianebisas mitramicinis Seyvana ar aris rekomendebuli. preparatis toqsiuri efeqti vlindeba TrombocitopeniiT, proTrombinis daqveiTebiT, glomerulosklerozis ganviTarebiT. D vitaminis dozis gadaWarbebiT ganpirobebuli krizisas gamoiyeneba glukokortikoidebi. isini amcireben kalciumis Sewovas nawlavebSi, axdenen D vitaminis moqmedebis bloks da aZliereben kalciumis SardiT eqskrecias, amcireben kolafsis movlenebs. upiratesad gamoiyeneba wyalSi xsnadi hidrokortizonis hemisuqcinati an prednizoloni 30 mg doziT 2-3 jeradad dReSi. Tirkmlis mwvave an qronikuli ukmarisobiT mimdinare hiperkalcemiuri krizisas mkurnalobis yvelaze efeqturi meTodia hemodializi ukalciumo buferiT. SesaZlebelia peritonuli dializis gamoyenebac, Tumca is gacilebiT nakleb efeqturia. paTogenezuri Terapiis paralelurad tardeba simptomuri Terapia Cvenebis mixedviT, saWiroebisas filtvebis xelovnuri ventilaciis gamoyenebiT.krizis kupirebis Semdeg grZeldeba hiperparaTireozis tradiciuli mkurnaloba. paraTireoiduli jirkvlebis hiperplaziisas rekomendebulia totaluri paraTireoideqtomia, amokveTili jirkvlis qsovilis nawilobrivi implantaciiT winamxris midamoSi.