7 research outputs found

    Autoimune antibodies in thyroid diseases

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    Background: Irrespective of the recommendations to use the measurement of serum TSH as cornerstone of thyroid function testing, the laboratory diagnosis and monitoring of thyroid diseases are based on the thyroid panel including TSH, FT4, TT4, TT3, FT3, anti–TPO and anti-TG. Autoimmune thyroid diseases include Graves' disease, Hashimoto thyroiditis and these types of disorders are caused by immune system malfunction. In other words, instead of protecting the body's healthy tissues, malfunctioning immune cells actually attack them. Methods: Morning serum concentrations of anti-TPO and anti-TG were assessed in a prospective study in 50 subjects with Graves' disease, 50 subjects with Hashimoto thyroiditis and 40 healthy subjects as control 52 BALKAN JOURNAL OF CLINICAL LABORATORY - XXVI, 18, 1 th 26 BCLF 2018 Skopje l October 3 - 5, 2018 group. Serum concentration of anti–TPO and anti-TG were determined by chemiluminescence immunoassay using Immulite 2000 analyzer. Results: The following results were obtained: serum concentration of anti-TPO in the control group was 3.7 IU/mL Β± 0.46, in Graves' disease 195 IU/mL Β± 0.70 and in Hashimoto thyroiditis 238.5 IU/mLΒ± 0.95. Serum concentration of anti-TG in Hashimoto thyroiditis was highest (333.3 IU/mL Β± 0.55). Patients with Graves' disease and Hashimoto thyroiditis showed significantly higher concentrations of anti-TPO and anti-TG compared to healthy individuals (P<0.001). Conclusion: Serum concentrations of anti-TPO and anti-TG organ specific autoantibodies respectively are very precious parameters - markers for reliable diagnosis of autoimune thyroid diseases

    CLINICAL RELEVANCE OF PRECORE MUTATIONS OF HEPATITIS B VIRUS IN CHRONIC LIVER DISEASE

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    Introduction: Hepatitis B is one of the most frequent etiological factors for chronic liver diseases worldwide. Recent studies have suggested the important role of the genetic diversity of the virus on natural course of hepatitis B. Hepatitis B e-antigen negative type of chronic hepatitis is associated with mutations in the precore region and basic core promoter of hepatitis B viral genome. Aim of study was to identify precore mutations in viral genome of patients with chronic hepatitis B and to evaluate clinical patterns of liver disease related to this type of hepatitis B. Methods: Sixty seven patients with hepatitis B were included in the study. In order to evaluate the clinical patterns of chronic liver disease related to hepatitis B viral infection, biochemical and virological investigations were done, as well as a quantification of serum viral load. All patients under went liver biopsy and semiquantification of necroinflammation and/or fibrosis according to Knodell scoring was done. In the group of e anti en-negative patients, molecular analysis was performed in order to identify presence of mutations in precore region of the virus. Results: Study group was divided in 25 HBe Ag-positive and 42 HBe Ag-negative subjects. Alanin-aminotransferase activity and level of viral load were higher in HBe Ag-positive (p < 0.05), but average age and histology activity index were significantly higher in the HBeAg-negative patients (p < 0.01). Precore mutants were found in 38 of 42 patients with HBe Ag-negative hepatitis (90%). Fibrosis was found in 30/38 cases with mutations. Discussion: Mutations in precore region of HBV in HBe Ag-negative patients were more prevalent in older age and were associated with higher rate of fibrosis in liver tissue, meaning more advanced stage of the disease. This could be a consequence of longer duration of HBV infection or more severe clinical course of the disease. Conclusion: Our results suggest that precore mutations are highly responsible for the development of hepatitis B e antigen-negative chronic liver disease in our patients. These mutations are associated with more progressive liver disease and with older age of the patients

    Possible input of diabetes and smoking cigarettes in confirmation of AMI diagnosis

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    OBJECTIVES:Influence of diabetes on development of ACS is well known, as well the active smoking that can pose a particular risk in increasing heart muscle ischemia. Several proposed models by international associations, indicate an increased risk and confirmation of the definition of myocardial infarction (MI) with presence of diabetes and cigarettes smoking habit in patients. MATERIALS and METHODS:Our study included 200 patients admitted to the emergency department with symptoms of AMI. Patients samples were submitted for CK, CKMB, TnT, TnI, Myoglobin determination and estimation for presence of diabetes and smoking habit. The obtained data were compared and statistically processed versus group of patients without any of risk factors. RESULTS:We found that 34% of patients has stable/unstable angina, and 49% was diagnosed as MI. Higher percentage of diabetic patients 28.8% has MI compared to 13.4% in patients with angina pectoris. In terms of smoking as a risk factor, 54.6% of patients with MI were active smokers compared to 34.3% in patients with angina pectoris. At diabetic patients MI was confirm with significant upper CK activity (65%), CKMB (56.8%) and TnT concentration (142%). Regarding the smokers, the most significant change was found in higher CK activity (60%) and myoglobin concentration (127.3%) in patients with AMI. CONCLUSIONS:Result shows that those two risk factors can afford valuable data in primary diagnosis along with some sensitive but not most specific parameters such CK and Myoglobin. This attitude is based concerning their effects on metabolic oxygen supply of heart muscle. Keywords: risk factors,myocardial infarction, cardiac marke

    Role of standard markers and hsp 70 in diagnostic and prognostic managing of acs

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    Atherosclerotic changes followed in plaque formation, instability and rupture lead to serious ischemic events that can be measuredand treated. Chosen panels that can facilitate diagnosis and in that manner protocol in treatment and prognosis are based on standard parameters involve in heart muscle metabolism and activity. Our study is aimed in enlarging the field of option to diagnose, follow up and prognoses further event induced by hypoxia and in same time providing more benefit to the patients, physicians and laboratory workers. With that purpose we try to find out is specific markers for oxidative stress such as Heat shock proteins can fulfill the expectations. METHODS In this study we include measuring of CK, CKMB, (activity or mass concentration) Myoglobin and Troponins. Additionally, measuring of HSP 70 was due to fact that those molecular chaperons are involve in engaging processes for cell and tissue protection Inflammation response was measured by CRP level and leukocytes count.. Spectrophotometry and immunoassay based on electro-chemi-lumiscence were used in measuring enzyme activity and level of CRP, myoglobin, troponin and mass concentration. Presence and concentration of HSP70 antibody was estimated with ELISA technique. RESULTS Statistical analysis shows elevation in activity of CK and CKMB, but most remarkable and significant increase was estimated for CKMB mass concentration and Troponin T at the patient diagnosed with AMI. Since our interest was pointed in level of HSP 70, CRP and leukocytes count, our results show significant differences( p<0,05) between patients values vs control. Namely, concentration of HSP 70 antibody at the patients with AMI was estimated as 26.3 -fold higher values vs control group (p<0,05). As for CRP level increase was pointed at 8,6-fold vs control group while moderate elevation of leukocytes count was found at the patients diagnosed as AMI (2,0-fold increase vs control group). CONCLUSIONS Our result confirm activation of HSP70 in condition of oxidative stress and induction of several mechanisms in protection of tissue stability as well as preventing proteins disintegration in such condition. From here, our standings is that measuring of this protein in follow up period can provide useful information in predicting event and patients outcome

    Identification of pre-core and basal core promoter mutants in patients with chronic hepatitis b in the Republic of Macedonia

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    Background: Recent development of molecular techniques has improved our understanding of the role of various mutations of the HBV genome. Most common are mutations in the precore (PC) and basal core promoter (BCP) region, responsible for more serious course of chronic hepatitis. Aim of the study: was to evaluate the prevalence of PC and BCP mutants in patients with chronic hepatitis B in the Republic of Macedonia. METODI Material and methods: Serum samples from 69 patients with chronic hepatitis B (47 males and 22 females, average age 49Β±20y.) were collected in the period from 2002-2012. All serum samples were tested for HBV, HCV and HDV infection and immediately frozen at -70#C. According to the HBeAg status, these patients were divided in two groups: HBeAg positive (15/69 pts or 21, 74%), and HBeAg-negative (54/69 pts or 78,26%). Molecular examination including extraction and amplification of HBV DNA was performed. To establish if HBeAgnegative status is related to sero-conversion, or as a consequence of viral mutations, we have used INNO-Lipa hybridization assay from Innogenetics to identify the presence of mutations in precore and BCP region of HBV DNA. Molecular analysis was done in 38/54 HBeAg-negative patients (28 males and 10 females). RISULTATI Results: The prevalence of PC mutants in 84,21% (p=0,0000) and BCP mutants in 68,42% (P=0,0033) were extremely high in 38 examined HBeAg-negative patients. Combination of PC and BCP mutants was detected in HBV DNA of 25/38 HBeAg-negative patients (65,78%). CONCLUSIONI As a conclusion, HBeAg-negative stage was predominant in our patients with chronic hepatitis B and was related to mutations in PC and BCP region

    Dyslipidemic profile relations to insulin resistance

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    INTRODUCTION: Insulin resistance and atherogenic dyslipidemic profile are the main characteristics of the metabolic syndrome. The aim of this study was to discover the positive relation between atherogenic dyslipidemic profile and increased insulin resistance determined through homeostatic model assessment (HOMA) in obese women subjects. MATERIALS AND METHODS: HOMA (H) was determined as a ratio of the multiplied fasting glucose (G0) and insulin levels (I0) divided with 22.5 (G0xI0/22.5). According to H the patients were divided in 3 groups: 1 st gr. H<4 and BMI 28Β±8kg/m2 , 2nd gr. H=4-8 and BMI 40Β±73.8kg/m2 and the 3rd gr. H>8 and BMI 41Β±68kg/m2 . The examinees were 90 women divided in 3 equal groups not different according to their age. Triglycerides (TG), total cholesterol (TC), high density lipoprotein (HDL-C), low density lipoprotein LDL-C, expressed in mmol/l and indexes of the atherogenic risk C/HDL-C and LDL/HDL-C were determined. RESULTS: First group had TG values 1.05Β±0.48, TC 4.8Β±0.79, HDL-C 1.19Β±0.47, LDL-C 3.27Β±0.76, C/HDL-C 3.05Β±1.18, LDL/HDL-C 4.45Β±1.48. In the 2nd group the patients had higher correspondent values: 1.39Β±1.01, 4.97Β±0.88, 1.04Β±0.33, 3.33Β±0.48, 3.62Β±1.42 and 5.33Β±1.72. DISCUSSION: Patients in the 3rd gr. had significantly higher TG levels 1.8Β±0.8 (p<0.001), significantly lower HDL-C levels 0.88Β±0.19 (p<0.011), significantly higher C/HDL-C ratio 4.2Β±1.32 (p<0.015) and LDL/HDL-C had significantly higher level 5.26Β±1.69 (p<0.003). HOMA index correlated significantly with TG (p<0.001), LDL-C (p<0.011), C/HDL-C (p<0.001), LDL/HDL-C (p<0.001) and significantly negatively with HDL-C (p<0.001). CONCLUSION: HOMA correlated significantly to dyslipidemic profile and was confirmed as a good indicator of insulin resistance. It was confirmed that insulin resistance determined with HOMA index was associated with dyslipidemic profile

    ΠšΠΎΠΌΠΏΠ°Ρ€Π°Ρ†ΠΈΡ˜Π° Π½Π° Ρ„ΠΈΠ·ΠΈΡ‡ΠΊΠΈΡ‚Π΅ ΠΈ хСмискитС карактСристики Π½Π° ΠΌΠ°Ρ‚Π΅Ρ€ΠΈΡ˜Π°Π»ΠΈ Π·Π° Π΄ΠΈΡ€Π΅ΠΊΡ‚Π½ΠΎ ΠΏΡ€Π΅ΠΊΡ€ΠΈΠ²Π°ΡšΠ΅ Π½Π° ΠΏΡƒΠ»ΠΏΠ°Ρ‚Π°

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    Π¦Π΅Π» Π½Π° ΠΎΠ²Π°Π° ΡΡ‚ΡƒΠ΄ΠΈΡ˜Π° бСшС Π΄Π° сС ΠΎΡ†Π΅Π½Π°Ρ‚ Π±ΠΈΠΎΠ»ΠΎΡˆΠΊΠΈΡ‚Π΅ ΠΈ Ρ„ΠΈΠ·ΠΈΡ‡ΠΊΠΈΡ‚Π΅ ΡΠ²ΠΎΡ˜ΡΡ‚Π²Π° Π½Π° TheraCal, Biodentine I Calcimol. По ΠΏΠΎΠ΄Π³ΠΎΡ‚ΠΎΠ²ΠΊΠ° Π½Π° TheraCal, Biodentine I Calcimol Π³ΠΎ Π°Π½Π°Π»ΠΈΠ·ΠΈΡ€Π°Π²ΠΌΠ΅ ΠΎΡΠ»ΠΎΠ±ΠΎΠ΄ΡƒΠ²Π°ΡšΠ΅Ρ‚ΠΎ Π½Π° ΠΊΠ°Π»Ρ†ΠΈΡƒΠΌΠΎΠ²ΠΈ ΠΈ хидроксилни јони Π·Π° ΠΏΠ΅Ρ€ΠΈΠΎΠ΄ ΠΎΠ΄ 24 цаса, 7 ΠΈ 14 Π΄Π΅Π½Π°. Π‘ΠΈΡ‚Π΅ испитувани ΠΌΠ°Ρ‚Π΅Ρ€ΠΈΡ˜Π°Π»ΠΈ ослободуваат ΠΊΠ°Π»Ρ†ΠΈΡƒΠΌΠΎΠ²ΠΈ ΠΈ хидроксилни јони Π·Π° Π²Ρ€Π΅ΠΌΠ΅ Π½Π° испитуваниот ΠΏΠ΅Ρ€ΠΈΠΎΠ΄. Бпособноста Π½Π° Theracal i Biodentine I Calcimol Π΄Π° ослободуваат ΠΊΠ°Π»Ρ†ΠΈΡƒΠΌΠΎΠ²ΠΈ јони Π·Π° ΠΎΠ΄Ρ€Π΅Π΄Π΅Π½ ΠΏΠ΅Ρ€ΠΈΠΎΠ΄ ΠΌΠΎΠΆΠ΅ Π΄Π° Π³ΠΎ стимулираат ΡΠΎΠ·Π΄Π°Π²Π°ΡšΠ΅Ρ‚ΠΎ Π½Π° Π°ΠΏΠ°ΠΈΡ‚Π½ΠΈ кристали ΠΊΠ°ΠΊΠΎ ΠΈ Ρ„ΠΎΡ€ΠΌΠΈΡ€Π°ΡšΠ΅ Π½Π° Π½ΠΎΠ² Π΄Π΅Π½Ρ‚ΠΈΠ½
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