Angiotensin-converting enzyme – glycoprotein, is present mainly in the lungs and in small amounts in the brushing of the epithelium of the proximal tubules of the kidneys, the endothelium of the blood vessels and the blood plasma. ACE catalyzes the conversion of angiotensin 1 into angiotensin 2 (one of the most potent vasoconstrictors) and hydrolyses the bradykinin vasodilator to an inactive peptide.

Materiali : Serum | Metoda : Fotometri

Prostatic acid phosphatase (PAP)
Acid phosphatase (CF) catalyzes the hydrolysis of esters of phosphoric acid and organic compounds. This lysosomal enzyme is found in virtually all tissues. The highest concentration is observed in the epithelium of the prostate gland (prostatic fraction), then in the liver, spleen, erythrocytes (extraisosomal localization), thrombocytes, bone marrow. High activity of acid phosphatase is noted in macrophages and osteoclasts. The activity of acidic phosphatase of the prostate gland does not appear until the sexual maturity. In men, the total acidic serum phosphatase consists of prostatic CF and, in part, the CP of the liver and CF resulting from the destroyed platelets and erythrocytes. It is the main component of seminal fluid, it is detected in sperm, urine, in insignificant concentrations in the blood. There are no circadian fluctuations in the norm, however, in prostate cancer (PCa) there are diurnal fluctuations, which must be taken into account in the dynamic control of the level of the prostatic CF. The main clinical significance is monitoring the effectiveness of treatment with PCa (hormonal, surgical removal – reduced to undetectable levels after cardinal and effective removal). At the diagnostic stage, it has a low diagnostic sensitivity of 40%, but high specificity is 80%, so it can only be used as an additional marker. Does not correlate with the mass of the tumor. It is effective to use for the control of relapse and metastases (however it is effective only in 50% of patients). which must be taken into account in the dynamic control of the level of prostatic CF. The main clinical significance is monitoring the effectiveness of treatment with PCa (hormonal, surgical removal – reduced to undetectable levels after cardinal and effective removal). At the diagnostic stage, it has a low diagnostic sensitivity of 40%, but high specificity is 80%, so it can only be used as an additional marker. Does not correlate with the mass of the tumor. It is effective to use for the control of relapse and metastases (however it is effective only in 50% of patients). which must be taken into account in the dynamic control of the level of prostatic CF. The main clinical significance is monitoring the effectiveness of treatment with PCa (hormonal, surgical removal – reduced to undetectable levels after cardinal and effective removal). At the diagnostic stage, it has a low diagnostic sensitivity of 40%, but high specificity is 80%, so it can only be used as an additional marker. Does not correlate with the mass of the tumor. It is effective to use for the control of relapse and metastases (however it is effective only in 50% of patients). but high specificity – 80%, therefore can be used only as an additional marker. Does not correlate with the mass of the tumor. It is effective to use for the control of relapse and metastases (however it is effective only in 50% of patients). but high specificity – 80%, therefore can be used only as an additional marker. Does not correlate with the mass of the tumor. It is effective to use for the control of relapse and metastases (however it is effective only in 50% of patients).

Materiali : Serum | Metoda : Fotometri

Uric acid

Uric acid is a product of the exchange of purine nucleosides, which are part of nucleic acids (RNA and DNA). In this case, uric acid can be formed from foods coming from food, and as a result of the breakdown of the body’s own nucleic acids. From the liver uric acid is transported by plasma to the kidneys, where approximately 70% is filtered and released. The remaining amount of uric acid is excreted through the gastrointestinal tract. Food purines under the influence of digestive enzymes break down to uric acid already in? the gastrointestinalpath, and then absorbed into the bloodstream. Formed uric acid is secreted by the kidneys. In blood plasma uric acid is in the form of a salt – sodium urate. This salt has a low solubility, and at a concentration just above the norm, urate crystals form. Overproduction of uric acid occurs in the following situations: excessive catabolism of nucleic acids, massive production and destruction of cells or inability to excrete the final product. Although hyperuricemia and hypo-uricemia are not an independent disease, hyperuricemia is a risk factor for the development of metabolic disorders and may underlie some diseases, and hypo-uricemia may indicate a latent pathological condition. The level of uric acid in the blood is labile and is associated with factors such as age, sex, alcohol consumption

Materiali : Serum | Metoda : Fotometri | Grupi : Paneli biokimik

Valproic acid – 2-propylvaleric acid – antiepileptic broad spectrum. Valproic acid suppresses the enzyme GABA-transferase and, as a result, increases the content of the inhibitory neurotransmitter – gamma-aminobutyric acid (GABA) – in the nervous system. In conditions of accumulation of GABA in the central structures of the brain, the threshold of excitability and the level of convulsive readiness decrease. Valproic acid penetrates well through the blood-brain barrier and through the placenta, in lactating women enters the milk. Valproic acid has a positive effect in various types of seizures. Valproic acid drugs are quickly and almost completely absorbed in the gastrointestinal tract, reaching a maximum concentration in the blood after 1.5-4 hours. And they are characterized by a non-linear (dose-dependent) pharmacokinetics, when the concentration of the drug in the blood increases or decreases more rapidly than the increased or decreased dose. If the upper limit of their average therapeutic level is exceeded, it is necessary to take into account the greater probability of side effects, in some cases – up to intoxication. Valproic acid is mainly metabolized in the liver, and can cause damage to it, especially during the first 6 months after the start of treatment. Therefore, before therapy with valproic acid, each patient must pass a series of tests to investigate liver function The first tests for the content of the drug in the blood should be carried out 2-3 days after the start of treatment. When using the drug, it is necessary to monitor the functions of the liver, pancreas and blood coagulability. When used in pregnant women, neural tube defects should be avoided. Inductors of enzymes (for example, phenobarbital, phenytoin, carbamazepine) increase the metabolism of valproic acid. Mefloquine can reduce plasma concentrations of valproic acid. Indications for the study: administration of valproic acid in a dose of more than 50 mg / kg / day; change in the dose of the drug (and also 2-3 days after its administration); the administration of another antiepileptic drug; appearance of signs of toxicosis; resumption of epileptic seizures. An increase in the level of valproic acid: excess dosage and / or an incorrect regimen of administration of valproic acid preparations; acute poisoning with valproic acid. The reasons for lowering the level of valproic acid: the withdrawal of drugs valproic acid from the body.

Materiali : Serum |

Materiali : Serum | Metoda : CLIA

ACTH – peptide hormone secreted by the anterior pituitary gland under the influence of tropic hormones of the hypothalamus ( corticotropin-releasing hormone), consists of 39 amino acid residues with a molecular weight of 4,500 Da. Half-life in the blood – 3-8 minutes. Its transformation occurs mainly in the liver and in a small number – in the kidneys. To a greater extent, its influence is expressed on the bundle zone of the adrenal cortex, which leads to an increase in the formation of glucocorticoids, in less – to the glomerular and reticular zones, so it does not have a significant effect on the production of mineralocorticoids and sex hormones. Vnenadococcal effects of ACTH are to stimulate lipolysis (mobilizes fats from fat stores and promotes fat oxidation), increased secretion of insulin and growth hormone, accumulation of glycogen in muscle cells, hypoglycemia, which is associated with increased secretion of insulin, increased pigmentation due to the effect on pigment cells of melanophores . The secretion of ACTH increases with stress, as well as under the influence of factors, causing stressful conditions: cold, pain, physical activity, emotions. Hypoglycaemia increases the production of ACTH. Deceleration of ACTH production occurs under the influence of glucocorticoids themselves. Excess ACTH leads to hypercortisy. This disease develops with the adenoma of the pituitary gland and is called the diseaseItenko-Cushing . The main manifestations of the disease – hypertension, obesity, having a local character (face and body), hyperglycemia, decreased immune defenses of the body. Lack of a hormone leads to a decrease in the production of glucocorticoids and the development of hypocorticism, which is manifested by a violation of metabolism and a decrease in the body’s resistance to various environmental influences. Secretion of ACTH in the blood is subject to daily rhythms – the concentration is maximal at 6 am, minimal in the evening and at night (about 22 hours). The normal daily rhythm of hormones testifies to the integrity of the functioning of all links of the system ” hypothalamus-pituitary- adrenal cortex”.

Materiali : Serum | Metoda : CLIA

Interpretation of results: Differential diagnosis is carried out with influenza and other respiratory viral infections, infectious mononucleosis, typhoparathyphoid diseases, HIV infection
Discovered
Confirms the adenoviral nature of the disease

Materiali : Fece | Metoda : Serologji

Grupi : Paneli bakterologjik | Metoda : Serologji

Alpha Fetoproteinduring pregnancy is synthesized by the cells of the yolk sac, then the liver of the fetus. It is excreted into the amniotic fluid with urine, absorbed into the mother’s blood and leads to a rise in the serum level of pregnant women. It is known that in the presence of a neural tube defect in the fetus, anterior abdominal wall, anomalies of the development of the urinary system, a much larger amount of AFP enters the amniotic fluid, which leads to a sharp increase in the level of AFP in the serum of the mother. The level of increase is directly correlated with the degree of defect. This was the basis for the use of this marker in the biochemical prenatal screening to detect, first of all, the presence of neural tube defects (a rise of more than 2 Mo in the second trimester after 14 weeks, an optimal period of 16-18 weeks). When interpreting the elevated level of AFP, that the level of AFP can increase with oncological pathology of the liver of a pregnant woman – hepatocellular carcinoma, metastatic liver damage, etc. Therefore, with an increase in the level of this indicator and normal data of ultrasound of the fetus in regard to neural tube defects, it is necessary to examine pregnant women for liver pathology. In addition, antenatal fetal death also leads to an increase in AFP, therefore, in detecting an increase in AFP, it is necessary to guide pregnant women to perform ultrasound in the shortest possible time, especially when combined with low B-hCG and estriol. A decrease in the level of AFP is observed if the fetus has a chromosomal pathology (Down’s syndrome). Therefore, with an increase in the level of this indicator and normal data of ultrasound of the fetus with regard to defects in the development of the neural tube, it is necessary to examine pregnant women for liver pathology. In addition, antenatal fetal death also leads to an increase in AFP, therefore, in detecting an increase in AFP, it is necessary to guide pregnant women to perform ultrasound in the shortest possible time, especially when combined with low B-hCG and estriol. A decrease in the level of AFP is observed if the fetus has a chromosomal pathology (Down’s syndrome). Therefore, with an increase in the level of this indicator and normal data of ultrasound of the fetus with regard to defects in the development of the neural tube, it is necessary to examine pregnant women for liver pathology. In addition, antenatal fetal death also leads to an increase in AFP, therefore, in detecting an increase in AFP, it is necessary to guide pregnant women to perform ultrasound in the shortest possible time, especially when combined with low B-hCG and estriol. A decrease in the level of AFP is observed if the fetus has a chromosomal pathology (Down’s syndrome). therefore, in detecting an increase in AFP, pregnant women should be referred for ultrasound in the shortest possible time, especially when combined with low B-hCG and estriol. A decrease in the level of AFP is observed if the fetus has a chromosomal pathology (Down’s syndrome). therefore, in detecting an increase in AFP, pregnant women should be referred for ultrasound in the shortest possible time, especially when combined with low B-hCG and estriol. A decrease in the level of AFP is observed if the fetus has a chromosomal pathology (Down’s syndrome).

Grupi : Paneli hormonal | Materiali : Serum | Metoda : CLIA

Albumin is a non-glycosylated protein synthesized by parenchymal cells of the liver in an amount of 12-15 g / day. Its content is about 60% of the total protein. In plasma, albumin is responsible, mainly, for maintaining the oncotic pressure, and also participates in the transport of various compounds (free fatty acids, bilirubin, hormones, metal ions and medicines). In this regard, a decrease in the concentration of albumin in the blood has a significant effect on the pharmacokinetics of drugs. Also albumin serves as a protein reserve organism. Serum albumin has a half-life of 18-20 days. This period is reduced in conditions of increased catabolism: in severe infections, bleeding, surgical interventions, loss of protein in cases of impaired renal function, gastrointestinaltract and skin. Thus, albumin is considered a “negative” activator of the acute phase (the reaction to acute infectious and inflammatory processes decreases). Albumin is also an indicator of the overall nutritional status of the body, especially in the elderly with various chronic diseases. The determination of the level of albumin allows monitoring the patient’s nutrition and is a remarkable test for assessing liver function. Albumin levels below 2.0-2.5 g / dL, associated with nephrotic syndrome, liver cirrhosis or enteropathy with protein loss, can lead to swelling.

Grupi : Paneli biokimik | Materiali : Serum | Metoda : Fotometri

Aldosterone is a steroid hormone, it is synthesized from cholesterol in the cells of the glomerular layer of the adrenal cortex. This is the main and most potent mineralocorticoid. Metabolized in the liver and kidneys, causes an increase in the reabsorption of sodium and chlorine in the renal tubules. As a result, sodium and chlorine retention in the body is observed, a decrease in the release of fluid in the urine, in parallel, there is an increase in the excretion of potassium. Aldosterone is involved in the regulation of electrolyte balance, maintenance of blood volume and blood pressure. Normal secretion of aldosterone depends on many factors – the activity of the renin-angiotensin system, potassium content (hyperkalaemia stimulates, and hypokalemia suppresses aldosterone production), ACTH (a short-term increase in aldosterone secretion under physiological conditions is not the main factor in the regulation of secretion), magnesium and sodium in the blood. Excess aldosterone causes hypokalemia, metabolic alkalosis, a noticeable sodium retention and increased urinary potassium excretion, which is clinically manifested by hypertension, muscle weakness, seizures and paresthesia, and arrhythmias. With primary hyperaldosteronism (Connes syndrome), an autonomous increase in the secretion of aldosterone is observed, the cause of which is most often adenoma of the glomerular zone of the adrenal cortex (up to 62% of all observations). Secondary hyperaldosteronism is associated with congestive heart failure, cirrhosis with the formation of ascites, certain kidney diseases, excess potassium, low-sodium diet, toxicosis of pregnant women, stenosis of the renal arteries (2-3% of all cases of hypertension). Primary hyperaldosteronism is characterized by an increase in the level of aldosterone, combined with a low activity of plasma renin, for secondary hyperaldosteronism – an increase in aldosterone concentration is combined with a high plasma renin activity. Hypoaldosteronism is usually accompanied by hyponatremia, hyperkalemia, a decrease in the excretion of potassium in the urine and an increase in the excretion of sodium, metabolic acidosis and hypotension. The most common cause of this condition is decreased production of renin due to kidney damage (giporeninemic hypoaldosteronism), especially in diabetics. Chronic insufficiency of the adrenal cortex (Addison’s disease) due to its primary damage in tuberculosis, autoimmune pathology of the adrenal gland, amyloidosis is accompanied by a decrease in the level of aldosterone and an increase in plasma renin level. Before determining aldosterone, the patient should be transferred to medications with minimal effect on the level of the hormone.

Grupi : Paneli hormonal | Materiali : Serum | Metoda : CLIA

Aldosterone is a steroid hormone, it is synthesized from cholesterol in the cells of the glomerular layer of the adrenal cortex. This is the main and most potent mineralocorticoid. Metabolized in the liver and kidneys, causes an increase in the reabsorption of sodium and chlorine in the renal tubules. As a result, sodium and chlorine retention in the body is observed, a decrease in the release of fluid in the urine, in parallel, there is an increase in the excretion of potassium. Aldosterone is involved in the regulation of electrolyte balance, maintenance of blood volume and blood pressure. Normal secretion of aldosterone depends on many factors – the activity of the renin-angiotensin system, potassium content (hyperkalaemia stimulates, and hypokalemia suppresses aldosterone production), ACTH (a short-term increase in aldosterone secretion under physiological conditions is not the main factor in the regulation of secretion), magnesium and sodium in the blood. Excess aldosterone causes hypokalemia, metabolic alkalosis, a noticeable sodium retention and increased urinary potassium excretion, which is clinically manifested by hypertension, muscle weakness, seizures and paresthesia, and arrhythmias. With primary hyperaldosteronism (Connes syndrome), an autonomous increase in the secretion of aldosterone is observed, the cause of which is most often adenoma of the glomerular zone of the adrenal cortex (up to 62% of all observations). Secondary hyperaldosteronism is associated with congestive heart failure, cirrhosis with the formation of ascites, certain kidney diseases, excess potassium, low-sodium diet, toxicosis of pregnant women, stenosis of the renal arteries (2-3% of all cases of hypertension). Primary hyperaldosteronism is characterized by an increase in the level of aldosterone, combined with a low activity of plasma renin, for secondary hyperaldosteronism – an increase in aldosterone concentration is combined with a high plasma renin activity. Hypoaldosteronism is usually accompanied by hyponatremia, hyperkalemia, a decrease in the excretion of potassium in the urine and an increase in the excretion of sodium, metabolic acidosis and hypotension. The most common cause of this condition is decreased production of renin due to kidney damage (giporeninemic hypoaldosteronism), especially in diabetics. Chronic insufficiency of the adrenal cortex (Addison’s disease) due to its primary damage in tuberculosis, autoimmune pathology of the adrenal gland, amyloidosis is accompanied by a decrease in the level of aldosterone and an increase in plasma renin level. Before determining aldosterone, the patient should be transferred to medications with minimal effect on the level of the hormone.

Grupi : Paneli biokimik | Materiali : Serum | Metoda : Fotometri

AMA M2 – 3E – antibodies to the main epitope of antimitochondrial antibodies of type 2. They are found together with AMA-M2 in patients with primary biliary cirrhosis, their detection increases the sensitivity of the examination. AMA is a heterogeneous group of autoantibodies against various proteins located on the inner and outer membranes of mitochondria. Antigen by structure is a lipoprotein, which participates in the transport functions of the membrane. It is possible to determine both total and individual antibody subtypes. At present, 4 subtypes of AMA are isolated. For primary biliary cirrhosis (PBC), antibodies to the mitochondrial antigen M-2 , which is the E2 subunit of the pyruvate dehydrogenase complex ( E2-PDH, are considered specific). Diagnostic sensitivity is 98%, specificity is 96%. PBC is a chronic liver disease that occurs with a nasal, destructive inflammation and obstruction of the intrahepatic bile ducts and the development of hepatic insufficiency. In a third of patients, other autoantibodies (ANA, SMA) are detected. AMA can be detected in patients with PBC for many years before the manifestation of the disease. The presence of AMA is considered as a sign of “preclinical” PBC (10-15% of patients). Up to 80% of cases of PBC are associated with other AIZ: more often with Sjogren’s syndrome and hypothyroidism, which appears before PBC. Approximately 10-20% of patients with PBC develop secondary AIG (CC). The frequency of detection of AMA-2 in AIG is 17-34%. The detection of AMA in AIG-1 can identify a subpopulation of patients at risk of developing cholestasis syndrome. AMA is used to differentiate 2 homogeneous groups of patients with the variant CC-AIG + PBC: AMA-negative patients have a lower level of transferases, higher levels of alkaline phosphatase and GGTP, all have ANA or SMA, they are characterized by more severe bile duct damage, including destructive cholangitis , ductopenia, duct hyperplasia and fibrosis.

 Materiali : Serum | Metoda : Smc Alegria

AMA M2 – 3E – antibodies to the main epitope of antimitochondrial antibodies of type 2. They are found together with AMA-M2 in patients with primary biliary cirrhosis, their detection increases the sensitivity of the examination. AMA is a heterogeneous group of autoantibodies against various proteins located on the inner and outer membranes of mitochondria. Antigen by structure is a lipoprotein, which participates in the transport functions of the membrane. It is possible to determine both total and individual antibody subtypes. At present, 4 subtypes of AMA are isolated. For primary biliary cirrhosis (PBC), antibodies to the mitochondrial antigen M-2 , which is the E2 subunit of the pyruvAMG is a hormone that is produced by Sertoli cells in men (in utero and after birth) and granulosa cells in women (only after birth). One of the main functions of AMG is to ensure the sex differentiation in the embryo, namely, the inhibition of the development of female reproductive organs from the rudiment, called the Mullerian duct (hence the very name of the hormone). It is known that up to 5-6 weeks of development the fetus has rudiments of both female (Mullerian duct) and male (Wolff’s duct) reproductive organs. Synthesis by Sertoli AMG cells, which starts at 6-7 weeks, provides an inhibition of the development of female reproductive organs and the development of masculine. If the fetus has a mutation of the AMG gene or its receptor, then there is no inhibition, and the fetus simultaneously develops the reproductive organs of both sexes, at birth the child has primary sexual characteristics according to the male type and it is impossible to suspect this pathology. However, in the future this is one of the causes of male infertility. In female fetuses, the synthesis of AMG does not occur, which determines the sex differences in the level of AMH at birth – in boys this is a high level, in girls – almost undetectable. This allows you to use AMG to establish the sex of the child in doubtful cases and to identify the cause of impaired development of the genitals. In addition, in boys AMG provides a physiological process of lowering the testicles into the scrotum, thus, insufficient synthesis of it can lead to the development of cryptorchidism. To determine the tactics of conducting a boy – the advisability of surgical treatment – it is necessary to conduct differential diagnosis between cryptorchidism and anarchy. The optimal test in this case is to determine the level of AMH, which will be determined only in the case of cryptorchidism. In childhood, the dynamics of AMH levels in boys and girls has diametrically opposite direction – in boys gradual decline to the pubertal period, in girls, on the contrary, – increase. This allows you to use AMG to diagnose the pathology of puberty (premature or delayed). In adulthood, AMG provides for men the synthesis of androgens and spermatogenesis. A low level of AMH is observed with non-obstructive azoospermia. This allows us to use it for differential diagnosis between obstructive and non-obstructive azoospermia, to identify the causes of male infertility. In childhood, the dynamics of AMH levels in boys and girls has diametrically opposite direction – in boys gradual decline to the pubertal period, in girls, on the contrary, – increase. This allows you to use AMG to diagnose the pathology of puberty (premature or delayed). In adulthood, AMG provides for men the synthesis of androgens and spermatogenesis. A low level of AMH is observed with non-obstructive azoospermia. This allows us to use it for differential diagnosis between obstructive and non-obstructive azoospermia, to identify the causes of male infertility. In childhood, the dynamics of AMH levels in boys and girls has diametrically opposite direction – in boys gradual decline to the pubertal period, in girls, on the contrary, – increase. This allows you to use AMG to diagnose the pathology of puberty (premature or delayed). In adulthood, AMG provides for men the synthesis of androgens and spermatogenesis. A low level of AMH is observed with non-obstructive azoospermia. This allows us to use it for differential diagnosis between obstructive and non-obstructive azoospermia, to identify the causes of male infertility. This allows you to use AMG to diagnose the pathology of puberty (premature or delayed). In adulthood, AMG provides for men the synthesis of androgens and spermatogenesis. A low level of AMH is observed with non-obstructive azoospermia. This allows us to use it for differential diagnosis between obstructive and non-obstructive azoospermia, to identify the causes of male infertility. This allows you to use AMG to diagnose the pathology of puberty (premature or delayed). In adulthood, AMG provides for men the synthesis of androgens and spermatogenesis. A low level of AMH is observed with non-obstructive azoospermia. This allows us to use it for differential diagnosis between obstructive and non-obstructive azoospermia, to identify the causes of male infertility. In women, beginning with the pubertal period, the synthesis of AMH occurs constantly in the granulosa cells of primordial follicles, regardless of the day of the menstrual cycle. The intensity of AMG synthesis most accurately reflects the woman’s ovarian reserve and reproductive capacity. With age, the follicle pool decreases, and the level of AMH decreases to an undetectable level during the menopause. To date, the determination of the level of AMG is recognized as the most optimal test for assessing the ovarian reserve and the predictor of menopause. Physiological significance of AMH in women consists in regulating the maturation of folli

Grupi : Paneli hormonal |  Materiali : Serum | Metoda : CLIA

Amylase – a hydrolytic enzyme, decomposes starch and glycogen to maltose. Amylase is formed predominantly in the salivary glands and pancreas, then enters respectively into the oral cavity or the lumen of the duodenum and participates in the digestion of carbohydrates. In the serum, pancreatic and salivary isozymes of amylase are isolated. Significantly lower amylase activity is also experienced by organs such as the ovaries, fallopian tubes, the small and large intestine, and the liver. Therefore, the level of amylase can be increased in a number of diseases that have a similar pattern with acute pancreatitis (acute appendicitis, peritonitis, perforated gastric ulcer, intestinal obstruction, cholecystitis, mesenteric thrombosis, pheochromocytoma, diabetic acidosis, after operations for heart defects, drugsetc.). The increase in amylase activity is, in most cases, reactive. In acute pancreatitis, the activity of blood and urine amylase increases 10-30 times in 4-6 hours after the onset of the disease, reaches a maximum after 12-24 hours, then decreases rapidly and comes to normal on the 2-6th day. The level of increase in serum amylase does not correlate with the severity of pancreatitis. Amylase can form large complexes with immunoglobulins and other plasma proteins (macroamylase), so it does not pass through the renal glomeruli. At the same time, its content in the serum increases, in the urine normal activity of amylase is observed. In pancreatic cancer, the activity of amylase is increased slightly or remains normal, therefore, for the diagnosis of pancreatic cancer the test is poorly informative.

 Materiali : Serum | Metoda : Fotometri

Amphetamines are a group of psychoactive synthetic substances, derivatives of phenylalkylamine, a pharmacological analogue of adrenaline and noradrenaline hormones, which are strong stimulants of the central nervous system. The mechanism of action of amphetamines is associated with activation of adrenergic transmission, an increase in the release of norepinephrine and dopamine in synapses and inhibition of their re-uptake, stimulation of peripheral adrenergic receptors. Amphetamines are able to easily penetrate the blood-brain barrier and have a powerful effect on the central nervous system: they cause vasoconstriction, increased blood pressure, increased heartbeats, dilated pupils, and excessive sweating. The nature of their effects, duration and severity of symptoms depends on the effectiveness of the drug and on the dose. Psychological dependence arises very quickly. Abstinence syndrome occurs 9 hours to 4 days after drug withdrawal and can persist for up to 1-10 weeks. The half-life period from the blood of amphetamines and their metabolites, on average, is 8-12 hours (depending on the dose, nutrition and substance – from 6 to 34 hours). The detection of amphetamines in the test sample confirms the use of amphetamines in the previous 8-12 hours in the study of blood.

Materiali : Urinë | Metoda : Imunoturbinimetri

Antinuclear antibodies are a group of autoantibodies that react with various components of the nucleus. Determination of antibodies to nuclear antigens in serum is a test for systemic connective tissue diseases. The main goal of the study is to exclude SLE, since in this disease, ANA is detected in 95% of patients within 3 months after its onset. Definition of ANA is of great importance for the diagnosis of AIH connective tissue, the presence of these antibodies can be associated with SLE, RA, NWST, scleroderma, polymyositis, discoid lupus erythematosus, CREST syndrome, nodular periarteritis, dermatomyositis. With SLE, the antinuclear factor test has a high sensitivity (89%), but moderate specificity (78%), compared to the test for antibodies to native DNA (sensitivity – 38%, specificity 98%). Correlation between the height of the titer and the clinical condition of the patient is not present. Antinuclear antibodies are part of 11 criteria for diagnosing SLE of the American College of Rheumatism. The cell nucleus contains more than 100 different antigens (nucleic acids, histones, nuclear membrane proteins, spliceosome components, ribonucleoproteins, nucleolus proteins and centromeres, etc.). Ana can be divided into three groups: true ANA – to dsDNA, ssDNA, histones, nuclear RNA, AT to the extracted nuclear AG – to Sm, n-RNP , Scl 70, cytoplasmic AH – to SS-A (Ro) *, SS-B (La) * and Jo-1 . * SS-A (Ro) and SS-B (La) can be localized both in the cytoplasm and in the nuclei. A positive test result indicates that the patient has one or a combination of several varieties of ANA. A negative result of such a test in more than 95% of cases allows excluding SLE, lupus erythematosus (LBV), NOS, SZST, systemic sclerosis, DM and PM.

Materiali : Serum | Metoda : Smc Alegria

Etiology. Hepatitis D virus or delta virus (Hepatitis D Virus, HDV) – RNA containing a virus, the smallest of known viruses that cause human diseases. The hepatitis D virus does not have its own skin and uses the envelope of the hepatitis B virus, is a defective virus, has the ability to suppress HBsAg production. Epidemiology.The source of infection for a person is only a patient or a carrier of the virus. The main ways of transmission of the virus: parenteral, sexual. It is possible to transfer from mother to fetus together with hepatitis B virus. Infection occurs only when hepatitis B virus is infected: simultaneously with hepatitis B virus infection (coinfection) or as superinfection with chronic viral hepatitis B (HBV), in carriers of HBsAg. When co-infected with hepatitis D virus, the course of acute hepatitis B is more severe than with monoinfection (infection with HBV alone), with a higher frequency of occurrence of fulminant forms (the frequency is increased by 100 times according to some data), therefore, in cases of severe acute hepatitis B, infection should always be excluded HDV. In addition, co-infection with HDV leads to more frequent cases of chronic disease. Clinical manifestations. The disease occurs 1-6 months after infection with the virus and is accompanied by a clinic characteristic of hepatitis, often with severe course, complications, pronounced changes in transaminases. The period of the onset of convalescence is prolonged, in 4-7% of cases the chronic course develops. Diagnostics. Laboratory diagnostics is based on the detection of serological markers (immunoglobulins IgM and total antibodies) and molecular methods (detection by PCR of a virus in a qualitative format of the output of the result). Evaluation of serological markers refers to indirect methods of diagnosing infections – it allows you to assess the presence of an immune response of the body to the introduction of an agent into the body. As a screening, the determination of total antibodies is used, in the case of a positive result, the detection of antibodies of IgM class, which can be determined not only in acute hepatitis, but also in chronic. These studies are recommended for patients with viral hepatitis B and carriers of HBsAg to exclude the infection of HDV as a cause of a more severe course of hepatitis. To confirm active replication of the virus, PCR methods are used – detection of the RNA of the virus.

Materiali : Serum | Metoda : Elisa

Antibodies to Scl-70 (anti-sclerodermal antibodies with a molecular mass of 70 kD, antibodies to topoisomerase I) often appear in diffuse (40%), less often – with limited (20%) form of systemic scleroderma, CREST-syndrome . They are highly specific for scleroderma (sensitivity – 20-40%, specificity – 90-100%) and are a poor prognostic sign for the development of pulmonary fibrosis. The presence of these antibodies in systemic scleroderma in combination with HLA-DR3 / DRW52 carries a 17-fold increase in the risk of pulmonary fibrosis. The detection of Scl-70 antibodies in the blood in patients with an isolated Raynaud phenomenon indicates a high probability of systemic sclerodemia.

Materiali : Serum | Metoda : Smc Alegria

Annexin V, also known as placental anticoagulant protein (PAP I), not only belongs to the family of calcium-dependent proteins that bind phospholipids, but is also a possible vascular anticoagulant protein. The cause of miscarriage in the middle and late stages with the progression of antiphospholipid syndrome (AFS) is the development of thrombotic vasculopathy of the spiral arteries of the placenta. The role of annexin V in the. the genesis of fetal loss syndrome in patients with APS, whose reduction on the surface of villi leads to the development of thrombosis and infarction of the placenta. Annexin V is present in many tissues, mainly on endothelial cells and the placenta. At low concentrations annexin V is present in platelets, in higher concentrations in erythrocytes and leukocytes. It has pronounced anticoagulant properties, which is due to its high affinity for anionic phospholipids and the ability to prevent activated blood clotting factors from binding to phospholipids of cell membranes. The affinity of annexin V to phosphatidylserine (a type of negatively charged phospholipid) is 1000 times higher than that of prothrombin. The plasma membrane of a cell is characterized by an asymmetric structure, and its disappearance is the first sign of apoptosis. Under normal conditions, phosphatidylserine is localized on the cytoplasmic side of the cell membrane, while in apoptosis it is located on the outer surface of the membrane, where it binds highly specifically to annexin V. Annexin V covers phosphatidylserine as a carpet, with a local anticoagulant effect. Therefore, during physiological pregnancy, despite the long-term location of phosphatidylserine on the surface of the trophoblast, there is no permanent thrombus formation. In patients with APS, including against the background of an infectious process, the production of autoantibodies to this protein is possible. These antibodies displace annexin V from the surface of endotheliocytes and trophoblast cells, leading to hypercoagulation and pregnancy loss. As pregnancy progresses, the processes of thrombus formation in the vessels of the placenta become more important. The presence of antibodies to annexin V can be associated with arterial and venous thrombosis, the development of rheumatoid arthritis, systemic lupus erythematosus and persistent miscarriage. Antibodies to annexin V are not included in the laboratory criteria of APS, but are one of the auxiliary (“non-criteria”) APS markers and are found in 15-20% of cases.

Materiali : Serum | Metoda : Smc Alegria

The detection of specific IgM and IgA antibodies is used in the diagnosis of acute infection. IgA antibodies in combination with the corresponding symptoms indicate an active infection. The detection of IgM antibodies is particularly useful for diagnosis in young children, in whom the IgA response is often reduced or absent. According to WHO definitions, the increase in levels and IgG and / or IgA antibodies to one or more Bordetella pertussis antigens in unvaccinated children confirms the presence of whooping cough. For optimal laboratory diagnosis of whooping cough in children, two methods of investigation should be used simultaneously: sowing of material from the nasopharynx and determining the level of specific antibodies of class G, A and M to two toxins (CT and PHA) by means of an enzyme immunoassay (ELISA). In the presence of typical clinical manifestations, ELISA confirms the diagnosis, and with erased and atypical forms of infection, this method may be crucial.
Antibodies IgA – detection indicates an acute phase of the disease.

Materiali : Serum | Metoda : Smc Alegria

The detection of specific IgM and IgA antibodies is used in the diagnosis of acute infection. IgA antibodies in combination with the corresponding symptoms indicate an active infection. The detection of IgM antibodies is particularly useful for diagnosis in young children, in whom the IgA response is often reduced or absent. According to WHO definitions, the increase in levels and IgG and / or IgA antibodies to one or more Bordetella pertussis antigens in unvaccinated children confirms the presence of whooping cough. For optimal laboratory diagnosis of whooping cough in children, two methods of investigation should be used simultaneously: sowing of material from the nasopharynx and determining the level of specific antibodies of class G, A and M to two toxins (CT and PHA) by means of an enzyme immunoassay (ELISA). In the presence of typical clinical manifestations, ELISA confirms the diagnosis, and with erased and atypical forms of infection, this method may be crucial.
IgG antibodies are evidence of an acute infection or vaccination, appear 2-3 weeks after infection, are strictly specific for the pathogen, persist for life, the level does not reflect the activity of the process

Materiali : Serum | Metoda : Smc Alegria

Antibodies of class IgG to C1q are responsible for the formation of immune complexes. C1q is a glycoprotein consisting of 18 polypeptide chains and three unidentified subunits, in combination with two C1r and two C1s molecules forms the first complement component (C1). Activation of complement by the classical pathway is triggered when C1q is bound to immune complexes or to various other activating substances. After C1q binding, the conformational rearrangement of C1r and C1s occurs to proteolytic enzymes, which correspond to 4J for the continuation of activation along the classical pathway. In 1984, autoimmune antibodies to C1q in the serum of patients with systemic lupus erythematosus (SLE) were detected. These antibodies are found in large numbers in autoimmune diseases and kidney diseases. It was found, that the presence of autoimmune antibodies to C1q is directly associated with disease of immune complexes, especially with hypocomplexary urticarial vasculitis (the presence of antibodies to C1q is the main criterion) and diffuse proliferative lupus nephritis. Although it has not been proven that the availability of these antibodies to C1q is a diagnostic criterion for any of these diseases, determining the content of antibodies to C1q can be a valuable tool in the clinical examination of patients with SLE. Antibodies to C1q were observed in 15-60% of patients with SLE and in 95% of patients with lupus nephritis. A negative result of the determination of antibodies to C1q excludes the risk of kidney inflammation in the following months with a sensitivity of 95% (negative predictive value). In addition, the determination of autoimmune antibodies to C1q is important in monitoring patients, suffering from lupus. Successful treatment of active lupus nephritis with immunosuppressive drugs usually leads to a decrease in the content of these antibodies. The content of autoantibodies to C1q only slightly correlates with the content of antibodies to double-stranded DNA, but directly correlate with the content of C1q antigen.

Materiali : Serum | Metoda : Smc Alegria

Citrulline is a ubiquitous amino acid that is not part of proteins, which is an intermediate product of urea metabolism. In many proteins of the synovial fluid, arginine residues are found. The enzyme peptidyl arginine deziminaza (PAD), which is found in large amounts in the synovial fluid in inflammation (as isoforms PAD2 and PAD4), catalyzes the conversion process of arginine to citrulline. Isoferments PAD2 and PAD4 citrulline many synovial proteins, including vimentin. CCPs activate T-lymphocytes and bind to HLA-DR4 on the surface of antigen-presentingcells. ACCPs are detected in 76% of RA patients. The diagnostic sensitivity of these antibodies for RA is 78%, specificity is 96%. The study of these antibodies should be used for early diagnosis, as the frequency of their detection is higher in patients with a short history of the disease compared with other antibodies. The presence of ATSPP can serve as a prognostic indicator of the development of erosive rheumatoid arthritis.

Materiali : Serum | Metoda : Smc Alegria

Chlamydia are a group of obligate intracellular parasites that are close to Gram-negative bacteria, which have lost the ability to synthesize ATP, GTP, and a number of other enzyme systems. This determines their intracellular growth. All chlamydiae are similar in morphological features, have a common group antigen and multiply in the cytoplasm of the host organism, passing through certain stages of development. The infectious principle is an elementary body, 0.3 ?m in diameter, which penetrates into the host cell by phagocytosis, and a vacuole is formed from the surface membranes of the cell around the elementary body. The elementary body is divided into a reticular body with a diameter of about 0.5-1.0 ?m. Inside the formed vacuole, the coarse particle grows and is divided many times by the formation of a transverse septum, and eventually the entire vacuole is filled with elementary particles (up to 200-1000 infectious units) and turns into inclusion in the cytoplasm of the host cell. Newly formed elementary corpuscles leave the cell and can infect new cells. The entire cycle takes 48-72 hours. Relate to the family Chlamydiaceae, and, according to the new classification, are divided into two genuses: Chlamydia and Chlamydophila : The genus Chlamydia includes species of Chl. trachomatis , Chl.muridarum and Chl.suis , of which Chl. trachomatis is exclusively a human parasite, and the other two species cause diseases of rodents and ruminants. Different strains of Chl. trachomatis can cause trachoma, urogenital tract diseases, some forms of arthritis, conjunctivitis and pneumonia in newborns. The genus Chlamydophila is composed of Chl. psittaci , Chl. pneumoniae and Chl. pecorum , Chlamydophila abortus , Chlamydophila caviae and Chlamydophila felis .

Materiali : Serum | Metoda : Smc Alegria

Chlamydia are a group of obligate intracellular parasites that are close to Gram-negative bacteria, which have lost the ability to synthesize ATP, GTP, and a number of other enzyme systems. This determines their intracellular growth. All chlamydiae are similar in morphological features, have a common group antigen and multiply in the cytoplasm of the host organism, passing through certain stages of development. The infectious principle is an elementary body, 0.3 ?m in diameter, which penetrates into the host cell by phagocytosis, and a vacuole is formed from the surface membranes of the cell around the elementary body. The elementary body is divided into a reticular body with a diameter of about 0.5-1.0 ?m. Inside the formed vacuole, the coarse particle grows and is divided many times by the formation of a transverse septum, and eventually the entire vacuole is filled with elementary particles (up to 200-1000 infectious units) and turns into inclusion in the cytoplasm of the host cell. Newly formed elementary corpuscles leave the cell and can infect new cells. The entire cycle takes 48-72 hours. Relate to the family Chlamydiaceae, and, according to the new classification, are divided into two genuses: Chlamydia and Chlamydophila : The genus Chlamydia includes species of Chl. trachomatis , Chl.muridarum and Chl.suis , of which Chl. trachomatis is exclusively a human parasite, and the other two species cause diseases of rodents and ruminants. Different strains of Chl. trachomatis can cause trachoma, urogenital tract diseases, some forms of arthritis, conjunctivitis and pneumonia in newborns. The genus Chlamydophila is composed of Chl. psittaci , Chl. pneumoniae and Chl. pecorum , Chlamydophila abortus , Chlamydophila caviae and Chlamydophila felis .

Materiali : Serum | Metoda : Smc Alegria

Chlamydia are a group of obligate intracellular parasites that are close to Gram-negative bacteria, which have lost the ability to synthesize ATP, GTP, and a number of other enzyme systems. This determines their intracellular growth. All chlamydiae are similar in morphological features, have a common group antigen and multiply in the cytoplasm of the host organism, passing through certain stages of development. The infectious principle is an elementary body, 0.3 ?m in diameter, which penetrates into the host cell by phagocytosis, and a vacuole is formed from the surface membranes of the cell around the elementary body. The elementary body is divided into a reticular body with a diameter of about 0.5-1.0 ?m. Inside the formed vacuole, the coarse particle grows and is divided many times by the formation of a transverse septum, and eventually the entire vacuole is filled with elementary particles (up to 200-1000 infectious units) and turns into inclusion in the cytoplasm of the host cell. Newly formed elementary corpuscles leave the cell and can infect new cells. The entire cycle takes 48-72 hours. Relate to the family Chlamydiaceae, and, according to the new classification, are divided into two genuses: Chlamydia and Chlamydophila : The genus Chlamydia includes species of Chl. trachomatis , Chl.muridarum and Chl.suis , of which Chl. trachomatis is exclusively a human parasite, and the other two species cause diseases of rodents and ruminants. Different strains of Chl. trachomatis can cause trachoma, urogenital tract diseases, some forms of arthritis, conjunctivitis and pneumonia in newborns. The genus Chlamydophila is composed of Chl. psittaci , Chl. pneumoniae and Chl. pecorum , Chlamydophila abortus , Chlamydophila caviae and Chlamydophila felis . Diseases caused by Clamydia trachomatis (Chl. Trachomatis) Chlamydia trachomatis is the most common bacterial pathogen of STIs in the world, especially among young people. There are three serovars and 15 biovars Chl. trachomatis , in particular trachomal biovar, urogenital biovar and biovar causing venereal lymphogranuloma. Most often, chlamydia is transmitted through direct sexual contact, children can become infected while passing through the birth canal. The level of infection with direct sexual contact exceeds 75%, thus, partner notification and timely treatment are extremely important. In women Chl. trachomatis causes cervicitis, urethritis, postcoital bleeding, pelvic inflammatory disease (PID), proctitis. Considering the high percentage of asymptomatic forms (up to 90%), timely diagnosis and treatment often do not take place, the process acquires a chronic course and complications develop (salpingitis, endometritis, adhesion in tubes, ectopic pregnancy), which lead to infertility Infertility in 80% of cases is caused by Chl. trachomatis ). This determines the need to exclude infection not only in cases of vivid clinical manifestations, but also in all cases of infertility. In men Chl. trachomatis causes non-gonococcal urethritis, epididymitis, proctitis. May lead to the development of Reiter’s syndrome. The asymptomatic forms are less common than in women, but still make up about 50% of all cases, which determines the need to exclude this infection not only with a pronounced lesion clinic, but also in all cases of infertility. In newborn infants, infection during passage through the birth can lead to the development of a clinic of conjunctivitis or pneumonia in the first weeks of life. In addition, the clinical manifestations of chlamydial infection caused by Chl. trachomatis , ophthalmologic diseases (trachoma, conjunctivitis), venereal lymphogranuloma (a clinic of urethritis with purulent inguinal lymphadenitis), Reiter’s syndrome (triad: urethritis, conjunctivitis, arthritis), proctitis, proctocoliths, more rare lesions of the conjunctiva, upper respiratory tract, endocarditis, perihepatitis.

Materiali : Serum | Metoda : Smc Alegria

Etiology. Human herpesvirus type 4 ( HHV-IV ) , or the Epstein-Barr virus , is a lymphotropic virus whose etiological role is known in infectious mononucleosis, Burkitt’s lymphoma, nasopharyngeal carcinoma, lymphoproliferative syndrome associated with the X chromosome , and chronic fatigue syndrome. This DNA genomic virus of the genus Lymphocryptovirus of the subfamily Gammaherpesvirinae of the Herpesviridae family has 4 main antigens: early antigen (EA), capsid antigen (viral capcide antigen – VCA), membrane antigen (MA);nuclear antigen ( Epstain-Barr Nuclea antigen – EBNA). Each of them is formed in a certain sequence and induces the synthesis of the corresponding antibodies. Epidemiology. The source of infection is an infected person (with a manifest or erased form of the disease, as well as a virus carrier). Primary infection often occurs in childhood or young age. Ways of transmission of the virus: airborne , contact-household , transfusion, sexual, transplacental. After infection, replication of the virus in the human body and the formation of an immune response can occur asymptomatically, or manifest as minor signs of acute respiratory viral infection. In some cases, more often when there is a significant weakening of the immune system at this time, the patient may develop a picture of infectious mononucleosis. About 90% of the world’s adult population is infected with the Epstein-Barr virus and after the primary infection remain lifelong carriers of the virus. Pathogenesis. The entrance gates for infectious mononucleosis is the mucous membrane of the mouth and upper respiratory tract. The Epstein-Barr virus penetrates through intact epithelial layers by transcytosis into the underlying lymphoid tissue of the tonsils, in particular B-lymphocytes . After infection, the number of affected cells is increased by means of virus-dependent cell proliferation. Infected B-lymphocytescan be a significant time in tonsillar crypts, which allows the virus to be released into the external environment with saliva. With infected cells, the virus spreads through other lymphoid tissues and peripheral blood. In virus-infected cells, two kinds of reproduction are possible: lytic, that is, leading to death, lysis of the host cell , and latent, when the number of viral copies is small and the cell does not collapse. With acute or active infection, lytic replication of the virus predominates. The virus can be in the B-lymphocytes and epitheliocytes of the nasopharyngeal region and salivary glands for a long time . In addition, it is capable of infecting other cells: T-lymphocytes , NK cells , macrophages, neutrophils, and vascular epitheliocytes. In the corethe host cell of the virus DNA can be inserted into the genome, causing chromosomal abnormalities. Active virus multiplication can occur as a result of weakening of immunological control, as well as stimulation of multiplication of cells infected by the virus under the influence of a number of factors: acute bacterial or viral infection, vaccination, stress , etc. Clinical manifestations. Infectious mononucleosis is an acute anthroponous viral infectious disease characterized by fever, infection of the oropharynx, lymph nodes, liver and spleen, and specific changes in the hemogram. The incubation period of the disease is 4-6 weeks. In the prodromal period, the infection manifests itself in muscle pain, fatigue, and general malaise. Then they are joined by fever, sore throat, enlarged lymph nodes, spleen and sometimes liver. In some cases, there is a rash on the arms and trunk. Symptoms persist for 2-4 weeks. In children, the infection is often asymptomatic. Perhaps several options for the outcome of an acute infectious process: 1. Recovery. 2. Asymptomatic virus or latent infection. 3. Chronic recurrent infection: a) chronic active infection (persistence of symptoms of infectious mononucleosis more than 6 months); b) generalized form (possible damage to the nervous system (encephalitis, polyneuropathy, meningitis), other internal organs (myocarditis, glomerulonephritis, lymphocytic interstitial pneumonia, hepatitis), c) hemophagocytic syndrome associated with EBV infection; d) erased or atypical forms (prolonged subfebrile condition of unknown origin, clinic of secondary immunodeficiency – recurrent bacterial, fungal, often – mixed infections of the respiratory and gastrointestinal tract, furunculosis , etc. ); e) development of the oncological (lymphoproliferative) process (multiple polyclonal lymphomas, nasopharyngeal carcinoma, leukoplakia of the tongue and oral mucosa, stomach and intestinal cancer, etc.); e) development of autoimmune processes (SLE, rheumatoid arthritis, Sjogren’s syndrome, etc.); g) the Epstein-Barr virus can play an important role in the onset of chronic fatigue syndrome. The prognosis for a patient with an acute infection caused by the Epstein-Barr virus depends on the presence and severity of immune dysfunction,

Materiali : Serum | Metoda : Smc Alegria

Etiology. Human herpesvirus type 4 ( HHV-IV ) , or the Epstein-Barr virus , is a lymphotropic virus whose etiological role is known in infectious mononucleosis, Burkitt’s lymphoma, nasopharyngeal carcinoma, lymphoproliferative syndrome associated with the X chromosome , and chronic fatigue syndrome. This DNA genomic virus of the genus Lymphocryptovirus of the subfamily Gammaherpesvirinae of the Herpesviridae family has 4 main antigens: early antigen (EA), capsid antigen (viral capcide antigen – VCA), membrane antigen (MA);nuclear antigen ( Epstain-Barr Nuclea antigen – EBNA). Each of them is formed in a certain sequence and induces the synthesis of the corresponding antibodies. Epidemiology. The source of infection is an infected person (with a manifest or erased form of the disease, as well as a virus carrier). Primary infection often occurs in childhood or young age. Ways of transmission of the virus: airborne , contact-household , transfusion, sexual, transplacental. After infection, replication of the virus in the human body and the formation of an immune response can occur asymptomatically, or manifest as minor signs of acute respiratory viral infection. In some cases, more often when there is a significant weakening of the immune system at this time, the patient may develop a picture of infectious mononucleosis. About 90% of the world’s adult population is infected with the Epstein-Barr virus and after the primary infection remain lifelong carriers of the virus. Pathogenesis. The entrance gates for infectious mononucleosis is the mucous membrane of the mouth and upper respiratory tract. The Epstein-Barr virus penetrates through intact epithelial layers by transcytosis into the underlying lymphoid tissue of the tonsils, in particular B-lymphocytes . After infection, the number of affected cells is increased by means of virus-dependent cell proliferation. Infected B-lymphocytescan be a significant time in tonsillar crypts, which allows the virus to be released into the external environment with saliva. With infected cells, the virus spreads through other lymphoid tissues and peripheral blood. In virus-infected cells, two kinds of reproduction are possible: lytic, that is, leading to death, lysis of the host cell , and latent, when the number of viral copies is small and the cell does not collapse. With acute or active infection, lytic replication of the virus predominates. The virus can be in the B-lymphocytes and epitheliocytes of the nasopharyngeal region and salivary glands for a long time . In addition, it is capable of infecting other cells: T-lymphocytes , NK cells , macrophages, neutrophils, and vascular epitheliocytes. In the corethe host cell of the virus DNA can be inserted into the genome, causing chromosomal abnormalities. Active virus multiplication can occur as a result of weakening of immunological control, as well as stimulation of multiplication of cells infected by the virus under the influence of a number of factors: acute bacterial or viral infection, vaccination, stress , etc. Clinical manifestations. Infectious mononucleosis is an acute anthroponous viral infectious disease characterized by fever, infection of the oropharynx, lymph nodes, liver and spleen, and specific changes in the hemogram. The incubation period of the disease is 4-6 weeks. In the prodromal period, the infection manifests itself in muscle pain, fatigue, and general malaise. Then they are joined by fever, sore throat, enlarged lymph nodes, spleen and sometimes liver. In some cases, there is a rash on the arms and trunk. Symptoms persist for 2-4 weeks. In children, the infection is often asymptomatic. Perhaps several options for the outcome of an acute infectious process: 1. Recovery. 2. Asymptomatic virus or latent infection. 3. Chronic recurrent infection: a) chronic active infection (persistence of symptoms of infectious mononucleosis more than 6 months); b) generalized form (possible damage to the nervous system (encephalitis, polyneuropathy, meningitis), other internal organs (myocarditis, glomerulonephritis, lymphocytic interstitial pneumonia, hepatitis), c) hemophagocytic syndrome associated with EBV infection; d) erased or atypical forms (prolonged subfebrile condition of unknown origin, clinic of secondary immunodeficiency – recurrent bacterial, fungal, often – mixed infections of the respiratory and gastrointestinal tract, furunculosis , etc. ); e) development of the oncological (lymphoproliferative) process (multiple polyclonal lymphomas, nasopharyngeal carcinoma, leukoplakia of the tongue and oral mucosa, stomach and intestinal cancer, etc.); e) development of autoimmune processes (SLE, rheumatoid arthritis, Sjogren’s syndrome, etc.); g) the Epstein-Barr virus can play an important role in the onset of chronic fatigue syndrome. The prognosis for a patient with an acute infection caused by the Epstein-Barr virus depends on the presence and severity of immune dysfunction,

Materiali : Serum | Metoda : CLIA

Etiology. Human herpesvirus type 4 ( HHV-IV ) , or the Epstein-Barr virus , is a lymphotropic virus whose etiological role is known in infectious mononucleosis, Burkitt’s lymphoma, nasopharyngeal carcinoma, lymphoproliferative syndrome associated with the X chromosome , and chronic fatigue syndrome. This DNA genomic virus of the genus Lymphocryptovirus of the subfamily Gammaherpesvirinae of the Herpesviridae family has 4 main antigens: early antigen (EA), capsid antigen (viral capcide antigen – VCA), membrane antigen (MA);nuclear antigen ( Epstain-Barr Nuclea antigen – EBNA). Each of them is formed in a certain sequence and induces the synthesis of the corresponding antibodies. Epidemiology. The source of infection is an infected person (with a manifest or erased form of the disease, as well as a virus carrier). Primary infection often occurs in childhood or young age. Ways of transmission of the virus: airborne , contact-household , transfusion, sexual, transplacental. After infection, replication of the virus in the human body and the formation of an immune response can occur asymptomatically, or manifest as minor signs of acute respiratory viral infection. In some cases, more often when there is a significant weakening of the immune system at this time, the patient may develop a picture of infectious mononucleosis. About 90% of the world’s adult population is infected with the Epstein-Barr virus and after the primary infection remain lifelong carriers of the virus. Pathogenesis. The entrance gates for infectious mononucleosis is the mucous membrane of the mouth and upper respiratory tract. The Epstein-Barr virus penetrates through intact epithelial layers by transcytosis into the underlying lymphoid tissue of the tonsils, in particular B-lymphocytes . After infection, the number of affected cells is increased by means of virus-dependent cell proliferation. Infected B-lymphocytescan be a significant time in tonsillar crypts, which allows the virus to be released into the external environment with saliva. With infected cells, the virus spreads through other lymphoid tissues and peripheral blood. In virus-infected cells, two kinds of reproduction are possible: lytic, that is, leading to death, lysis of the host cell , and latent, when the number of viral copies is small and the cell does not collapse. With acute or active infection, lytic replication of the virus predominates. The virus can be in the B-lymphocytes and epitheliocytes of the nasopharyngeal region and salivary glands for a long time . In addition, it is capable of infecting other cells: T-lymphocytes , NK cells , macrophages, neutrophils, and vascular epitheliocytes. In the corethe host cell of the virus DNA can be inserted into the genome, causing chromosomal abnormalities. Active virus multiplication can occur as a result of weakening of immunological control, as well as stimulation of multiplication of cells infected by the virus under the influence of a number of factors: acute bacterial or viral infection, vaccination, stress , etc. Clinical manifestations. Infectious mononucleosis is an acute anthroponous viral infectious disease characterized by fever, infection of the oropharynx, lymph nodes, liver and spleen, and specific changes in the hemogram. The incubation period of the disease is 4-6 weeks. In the prodromal period, the infection manifests itself in muscle pain, fatigue, and general malaise. Then they are joined by fever, sore throat, enlarged lymph nodes, spleen and sometimes liver. In some cases, there is a rash on the arms and trunk. Symptoms persist for 2-4 weeks. In children, the infection is often asymptomatic. Perhaps several options for the outcome of an acute infectious process: 1. Recovery. 2. Asymptomatic virus or latent infection. 3. Chronic recurrent infection: a) chronic active infection (persistence of symptoms of infectious mononucleosis more than 6 months); b) generalized form (possible damage to the nervous system (encephalitis, polyneuropathy, meningitis), other internal organs (myocarditis, glomerulonephritis, lymphocytic interstitial pneumonia, hepatitis), c) hemophagocytic syndrome associated with EBV infection; d) erased or atypical forms (prolonged subfebrile condition of unknown origin, clinic of secondary immunodeficiency – recurrent bacterial, fungal, often – mixed infections of the respiratory and gastrointestinal tract, furunculosis , etc. ); e) development of the oncological (lymphoproliferative) process (multiple polyclonal lymphomas, nasopharyngeal carcinoma, leukoplakia of the tongue and oral mucosa, stomach and intestinal cancer, etc.); e) development of autoimmune processes (SLE, rheumatoid arthritis, Sjogren’s syndrome, etc.); g) the Epstein-Barr virus can play an important role in the onset of chronic fatigue syndrome. The prognosis for a patient with an acute infection caused by the Epstein-Barr virus depends on the presence and severity of immune dysfunction,

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : CLIA

Materiali : Serum | Metoda : CLIA

Materiali : Serum | Metoda : Electroliz

Materiali : Serum | Metoda : CLIA

Materiali : Serum | Metoda : CLIA

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Antitrupat e Tiroperokidazes (TPO)

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Tiroide Peroksidaza (TPO) – nje enzime e perfshire ne sintezen e hormoneve tiroid triiodotironine (T3) dhe tiroksine (T4). Katalizon dy reaksione: oksidimin e jodit inorganik (I-) dhe lidhjen e tirozinave te jodit. Proteina transmembranore e glikolizuar- TPO ?e cila eshte lokalizuar ne pjesen apikale te qelizave folikulare, shprehet vetem ne tirocite. Eshte nje nga antigjenet me te rendesishme te tiroides tek te cilat gjithashtu lidhet tiroglobulin dhe receptori i TSH (i vendosur ne membranen bazale te qelizave folikulare te tiroides).

Tiroidja eshte nje organ target ne shume semundje autoimune te tilla si semundja Graves, Thirotoksikosis dhe Tiroiditi i Hashimotos, qe ?on ne hipotiroidizem. Nje karakteristike e ketyre semundjeve eshte humbja e tolerances imunologjike ndaj peroksidazes tiroide, dhe markeret specifik per keto semundje jane antitrupat ndaj peroksidazes tiroide.

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Percaktimi i nivelit te ATPO-se perben testin me te ndjeshem per zbulimin e semundjes autoimune te tiroides. ATPO-ja identifikoi ne 90-95% te pacienteve me tiroiditin e Hashimotos dhe 80% te pacienteve me semundjen e Graves, si dhe 15-20% te pacienteve me semundje tiroide jo-autoimune.

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Pacientet me hipotiroidizem subklinik dhe prania e ATPO-se rrezikon zbulimin e hipotiroidizmit.

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Gjate shtatezanise, perkufizimi i nivelit te antitrupave ndaj peroksidazes tiroide mund te ndihmoje ne identifikimin e grave me risk te larte te tiroiditis postpartum, qe ndodh ne 5-10% te te gjitha grave pas lindjes dhe vazhdon me faza te alternuara te tirotoksikozes destruktive dhe hipotiroidizmit te perkohshem. Per mbartesit e ATPO-se ky rrezik eshte rreth 50%.

Per te percaktuar nivelet dhe ?per te percaktuar ATPO ATTG, se bashku me vleresimin e funksionit tiroid, eshte e pershtatshme per pacientin para se te perdore amiodarone, medicament te tipit interferon etj, qe te behet nje vleresim i riskut te semundjes se gjendres tiroide.

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Materiali : Serum | Metoda : CLIA

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Smc Alegria

Materiali : Serum | Metoda : Serologji

Materiali : Serum

Materiali : Serum | Metoda : Fotometri

Metoda : Smc Alegria

Materiali : Serum

Materiali : Plazem | Metoda : Koagulim