INTRODUCTION Laboratory diagnosis of medical biochemistry activity plays a significant role in the Primary Health Care Center (PHCC), dominated by Family medicine and diagnostic services. Medical biochemical diagnosis has a visible place at all levels of health care, which shows the number of requests for laboratory diagnosis, number and type of required laboratory tests. MATERIALS AND METHODS The study included 1000 requests for laboratory tests at the PHCC in Gracanica in primary health care units. We made an analysis of the most common laboratory tests in the requests by doctors from primary health care based on requests for laboratory diagnosis. RESULTS The requests of primary health care units in PHCC laboratory tests are required at all levels of service: urine, WBC, SE, glucose, total bilirubin, ALT, AST, AF, CK, cholesterol, HDL cholesterol, triglycerides, creatinine, urea, uric acid, CRP, fibrinogen, calcium and phosphorus. The following requirements are the most common laboratory tests with 94% representation: urine, WBC, glucose, cholesterol, triglycerides, aminotransferases, creatinine, and urea. In 1000 requires was required total of 5333 laboratory tests. Test requirements of a general practice make 44, 1%; FM doctors account for 40% and the requirements of other specialists (pediatricians, gynecologists and specialists of occupational medicine) are 15, 3%. The doctors in family practice most often required: glucose, urine, WBC, SE, TGL., Chol., ALT, AST, creatinine and urea. General practitioners are demanding more cholesterol and triglycerides, a family medicine doctors are demanding lower cholesterol and triglycerides and higher CRP, fibrinogen, total bilirubin, ALT, AST, and other specialists the most demanded urine and WBC. DISCUSSION Laboratory diagnosis is a common diagnosis, which shows the representation of required number and type of laboratory tests. In requirements of PHC units in PHCC laboratory tests are required at all levels of service: urine, WBC, SE, glucose, bilirubin, ALT, AST, AF, CK, cholesterol, HDLchol., triglycerides, creatinine, urea, uric acid, CRP, fibrinogen, calcium and phosphorus. The following requirements are the most common laboratory tests at the primary level: urine, WBC, glucose, cholesterol, urea, and found the secondary level of triglycerides, index levels and did not clear the number of searches required by the standards and norms of PHC.
This is the first study performed in population from Bosnia & Herzegovina (BH), in which we analysed a significance of genetic variations in drug-metabolising enzyme, cytochrome P450 (CYP), in pathogenesis of Type 2 diabetes. We have determined allele frequencies for CYP2C9*2, CYP2C19*2, and CYP2D6*4 in diabetic patients and nondiabetic controls. Genomic DNA was extracted from blood samples collected from 37 diabetic and 44 nondiabetic subjects. A real-time polymerase chain reaction was used for the detection of specific CYP polymorphisms, with the application of the specific TaqMan® SNP genotyping tests (Applied Biosystems). Interestingly, results from this study have demonstrated that frequencies of CYP2C19*2 and CYP2D6*4 variants were in line, while frequency of CYP2C9*2 polymorphism seemed to be lower in this sample of BH population as compared to the Caucasians genotype data. Furthermore, no significant difference in allele frequencies for CYP2C9*2, CYP2C19*2, and CYP2D6*4 was demonstrated between diabetic and nondiabetic subjects. Thus, results form this study seem to indicate no relationship between CYP2C9, CYP2C19, and CYP2D6 genotype and diabetes susceptibility in Bosnian population. This in part may reflect a limited study population included in our study and would require larger cohorts to reveal potential relationships between analysed CYP genetic variants and diabetes risk. In addition, it would be pertinent to further explore possible effects of CYP genetic variations on therapeutic and adverse outcomes of oral antidiabetics, which might be the key in optimising therapy for individual patient with Type 2 diabetes.
Background: Mutations in the LPL gene cause familial lipoprotein lipase deficiency. Symptoms of familial LPL deficiency usually begin in childhood and include abdominal pain, acute and recurrent inflammation of the pancreas, skin lesions called eruptive cutaneous xanthoma and an enlargement of the liver and spleen. The risk for two carrier parents to both pass the defective gene and, therefore, have an affected child is 25% with each pregnancy. Aims: Early diagnosis, routine surveillance and treatment of familial LPL deficiency may help to manage some of the symptoms and sometimes prevent related problems. Methods: Clinical genetic testing for familial lipoprotein lipase deficiency may be available through an in person genetic consultation for children who are considered at risk. Triglycerides and total cholesterol were measured using commercially available kits (Boehringer Mannheim). Results: Episodes of abdominal pain are common. Intensity, duration, and localization of episodes are variable. Enlargement of the liver and spleen occurs particularly among affected infants and children. The enlargement of these organs may vary, often in parallel with the fat content of the diet. The risk is the same for boys and girls. Conclusions: Familial lipoprotein lipase deficiency is an inherited condition that disrupts the normal breakdown of fats in the body. It is characterized by absence of lipoprotein lipase activity and a massive accumulation of chylomicrons in plasma and a corresponding increase of plasma triglyceride concentration. Higher levels of plasma LPL activity are associated with decreased TG and increased HDL cholesterol levels in children.
Recent studies have introduced serum uric acid (UA) as a potential risk factor for developing diabetes, hypertension, stroke, and cardiovascular diseases. The value of elevated levels of UA in serum as a risk factor for diabetes development is still under scrutiny. Recent data suggest that clearance of UA is being reduced with increase in insulin resistance and UA as a marker of prediabetes period. However, conflicting data related to UA in serum of patients with Type 2 diabetes prompted us to study the urine/serum ratio of UA levels (USRUA) in these patients and healthy controls. All subjects included in the study were free of evidence of hepatitis B or C viral infection or active liver and kidney damage. Patients receiving drugs known to influence UA levels were also excluded from this study. Analysis of glucose and uric acid were performed on Dade Behring analyzer using standard IFCC protocols. Interestingly, our data demonstrated about 2.5 fold higher USRUA values in diabetic patients as compared to control subjects. Furthermore, there was a trend of correlation of USRUA value with the blood glucose levels in diabetic patients, which was more prominent in diabetic men than in women. With aging, levels of uric acid increased in serum of diabetic patients, and this effect was also more profound in male than in female diabetics. In conclusion, this study showed significantly elevated USRUA levels in patients with Type 2 diabetes, a negative USRUA correlation with the blood glucose levels in diabetic patients, and an effect of sex and age on the uric acid levels. Since literature data suggest a strong genetic effect on UA levels, it would be pertinent to perform further, possibly genetic studies, in order to clarify gender and ethnic differences in UA concentrations.
Th is is the fi rst study performed in population from Bosnia & Herzegovina (BH), in which we analysed a signifi cance of genetic variations in drug-metabolising enzyme, cytochrome P (CYP), in pathogenesis of Type diabetes. We have determined allele frequencies for CYPC*, CYPC*, and CYPD* in diabetic patients and nondiabetic controls. Genomic DNA was extracted from blood samples collected from diabetic and nondiabetic subjects. A real-time polymerase chain reaction was used for the detection of specifi c CYP polymorphisms, with the application of the specifi c TaqMan® SNP genotyping tests (Applied Biosystems). Interestingly, results from this study have demonstrated that frequencies of CYPC* and CYPD* variants were in line, while frequency of CYPC* polymorphism seemed to be lower in this sample of BH population as compared to the Caucasians genotype data. Furthermore, no signifi cant diff erence in allele frequencies for CYPC*, CYPC*, and CYPD* was demonstrated between diabetic and nondiabetic subjects. Th us, results form this study seem to indicate no relationship between CYPC, CYPC, and CYPD genotype and diabetes susceptibility in Bosnian population. Th is in part may refl ect a limited study population included in our study and would require larger cohorts to reveal potential relationships between analysed CYP genetic variants and diabetes risk. In addition, it would be pertinent to further explore possible eff ects of CYP genetic variations on therapeutic and adverse outcomes of oral antidiabetics, which might be the key in optimising therapy for individual patient with Type diabetes. © Association of Basic Medical Sciences of FBIH. All rights reserved
Numerous studies conducted on acetylsalicylic acid (ASA, aspirin) confirmed that ASA inhibits proliferation and induces apoptosis in various types of human cells. Therefore, it was of interest to examine possible effects of different concentrations of ASA on viability and proliferation of lymphocytes in the cell culture. After separation from blood, lymphocytes were suspended in RPMI 1640 medium and cultured at 37 degrees C. Solution of ASA was added to cultures after 24 h, in final concentrations of 1, 3 and 5 mmol/l. After 48 h, proliferative response was evaluated by WST-1 assay. Significant difference in viability between controls and cell cultures treated with ASA in three different concentrations was observed (p<0.01). Percents of viable cells in cultures after application of 1, 3 and 5 mmol/l ASA were 9.9%, 2.5% and 16.9% (compared to controls), respectively. To determine whether this cytotoxic effect was result of induction of apoptosis, DNA from cell cultures was isolated and subjected to agarose gel electrophoresis. Fragmentation of DNA was not detected, excluding apoptosis as possible cause of cytotoxic effects. Addition of ASA caused change of initial extracellular pH value for each treated culture. After addition of 1 mmol/l ASA, pH of culture was 7.19, after 3 mmol/L, 6.99 and after addition of 5 mmol/l solution, pH was 6.75. Decreased lymphocyte viability could be attributed to either the effects of the added substance or possible further acidification of cell cultures during three days of incubation.
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