BackgroundIn the worldwide, each year registered about 357 million new cases of sexual transmitted diseases.39 % of all infectious diseases were STI diseases in Mongolia in 2013 and which also 56.8 % of totalinfectious diseases Dornod province.ObjectiveTo investigate sexual transmitted diseases among the population of Dornod province and its commonrisk-factors.Materials and MethodsIn the survey were chosen 600 persons which is aged from 15 to 64 by random selection methodand divided into 6 cluster and each cluster had 100 persons. In the survey attended 300 male, 300female.ResultsThe survey respondents were married 59.1%, 50.7% of the employed, and 49.3% of the unemployed.2,1% of the survey population has already been tried drug abuse, but in the group of age 15-24,indicate level of the knowledge about drug abusing is very low which is 29,4%, a little or less knowabout drug abusing 35,6%, not know about drug abusing 35%. In other hand beverage usage levelwas very high which is 67% and 51,3% is using an alcohol in the last year constantly.Examination of specialized doctors 38.3% were suspected of sexual transmitted infections. Theyincluded laboratory testing.The 4.9 percent of total respondents had sexually transmitted diseases. It were syphilis 57.1%,gonorrhea 10.2%, trichomonasis 6.1%.The 83 percent of total respondents had sexual intercourse. The average age of first sexualintercourse was 18 ± 1 (95% CI 16.8 - 19.1), 7.1% had two or more sexual partners. Men had toused alcohol while sexual intercourse was 32.1 percent. Women were 49.2 percent and 38.5 percentof people infected with sexually transmitted diseases not use condoms during sexual intercourse.Conclusion1. One in 20 people surveyed, women aged 15-24 and men aged 35-44 have sexual transmissioninfection.2. Risk factors are had two or more sexual partners, had to used alcohol while sexual intercourseand using condoms during sex with casual partners are not enough.

Hemochromatosis is a common inherited disorder of iron metabolism in which an inappropriate increase in intestinal iron absorption results in deposition of excessive amounts of iron in parenchymal cells with eventual tissue damage and impaired organ function. The human HFE gene was identified as the most common form of hemochromatosis in 1996. A homozygous G A mutation resulting in a cysteine to tyrosine substitution at position 282 (C282Y) is the most common mutation. It is identified in 85–90% of patients with hereditary hemochromatosis in populations of northern European descent. A second relatively common HFE mutation (H63D) results in a substitution of histidine to aspartic acid at codon 63. Homozygosity for H63D is not associated with clinically significant iron overload. Some compound heterozygotes (e.g., one copy each of C282Y and H63D) have moderately increased body iron stores but develop clinical disease only with cofactors such as heavy alcohol intake or hepatic steatosis. Thus, HFE-associated hemochromatosis is inherited as an autosomal recessive trait; heterozygotes have no, or minimal, increase in iron stores. However, this slight increase in hepatic iron can act as a cofactor that modifies the expression of other diseases such as porphyria cutanea tarda (PCT) and nonalcoholic steatohepatitis. Mutations in other genes involved in iron metabolism are responsible for non-HFE-associated hemochromatosis, including juvenile hemochromatosis, which affects persons in the second and third decade of life. Mutations in the genes encoding hepcidin, transferrin receptor 2 (TfR2), and hemojuvelin result in clinicopathologic features indistinguishable from HFE-associated hemochromatosis. However, mutations in ferroportin, responsible for the efflux of iron from enterocytes and most other cell types, result in iron loading of reticuloendothelial cells and macrophages, as well as parenchymal cells.

Autosomal dominant PKD (ADPKD) is the most common monogenic genetic disease, and affects one in 500–1000 humans. Approximately half of all affected patients develop end-stage renal disease in the fifth to sixth decade of life. In a majority of cases (80-85%), the gene involved is PKD1, which is located on chromosome 16 (16q13.3) and encodes polycystin-1, a large receptor-like integral membrane protein that contains several extracellular mo-tifs indicative of cell-cell and cell-matrix interaction. In the remaining (10-15%) cases, the disease is milder and is caused by mutational changes in another gene (PKD2), which is located at chromosome 4 (4q21-23) and encodes polycystin-2, a transmembrane protein, which acts as a nonspecific calcium-permeable channel. ADPKD is gener¬ally a late-onset multisystem disorder characterized by bilateral renal cysts; cysts in other organs including the liver, seminal vesicles, pancreas, and arachnoid membrane; vascular abnormalities including intracranial aneurysms, dilatation of the aortic root, and dissection of the thoracic aorta; mitral valve prolapse; and abdominal wall hernias. Renal manifestations include hypertension, renal pain, and renal insufficiency. PKD1 and PKD2 gene mutations result in similar extra-renal manifestations, including PLD and intracranial aneurysms. Autosomal recessive polycystic kidney disease (ARPKD) is an important cause of childhood renal- and liver-related morbidity and mortality with variable disease expression. While most cases manifest peri-/neonatally with a high mortality rate in the first month of life, others survive to adulthood. ARPKD is caused by mutations in the Polycystic Kidney and Hepatic Disease 1 (PKHD1) gene on chromosome 6p12. PKHD1 is an exceptionally large gene (470 kb) with a longest open reading frame transcript of 67 exons predicted to encode a 4,074-amino acid (aa) (447 kDa) multidomain integral membrane protein (fibrocystin/polyductin) of unknown function.

Introduction: Leading cause of mortality was cardiovascular disease alone last two decade and occurs5500-6000 deaths annually in Mongolia. Familial hypercholesterolemia is the most common inheritedmetabolic disorders and is characterized by severely elevated LDL-cholesterol levels. The prevalenceof the heterozygous state has been estimated at 1 in 200 to 1 in 500 and of the homozygous state from1 in 160,000 to 1 in 1,000, 000.Goal: To identify Heterozygous Familial hypercholesterolemia among the patients with cardiovasculardisease and study clinical features.Materials and Methods: After view medical examination patients with coronary heart disease andcerebral vascular disease, we selected 183 patients among 26 family who possible to have HeterozygousFamilial hypercholesterolemia. We analyzed family history, clinical examination and lipid parameters.And identifi ed Heterozygous Familial hypercholesterolemia by diagnostic criteria of Netherlands.Results: The mean age for males was 42.3±14, for females was 45.8±15 and gender distribution was42.6% (78) male, 57.4% (105) female. Hypertension occurred in 80.9% (148). BMI was increasedwith age in both sexes (P<0.001). The frequency of tendon xanthoma was 26.8% (49) and cornealarcus was 36.6% (67). The level of total cholesterol and LDL-C were signifi cantly elevated in patients.Identity Heterozygous Familial hypercholesterolemia by criteria of Netherlands was certain-36.1%,probable-42.6%, possible-18.6%, unlikely FH-2.7%.Conclusion: Identifi cation of these individuals at an early age and an aggressive treatment of all knownrisk factors are important for reduce mortality of cardiovascular disease. The Netherland’s criteria issuitable for diagnosing Familial hypercholesterolemia in the Mongolian population, although it does notdiagnose the condition at the genetic level.

Background and Purpose Liver disease that caused by iron metabolism failure is called Hemochromatosis (clinically “Bronze diabetes”, “Over spotted liver cirrhosis”). The two types of hemochromatosis are primary and secondary. Primary hemochromatosis is caused by a defect in the genes that control how much iron the human body absorb from food. Secondary hemochromatosis usually is the result of another disease or condition that causes iron overload. According to the study there is a real need to study the clinical reveals of hemachromatosis in Mongolian patients. The purpose of the study to determine the hemachromatosis in patients with liver cirrhosis and cancer.Methods and Materials: The study involved 68 patients with diagnosis Liver cirrhosis and HCC (1st stage) who were hospitalized in Clinic of Gastroenterology of Shastin clinical hospital and “Shagdarsuren” Hepatic hospital from April to July, 2011. All patients were increased blood iron and iron compounded proteins (ferritin, transferrin). DNA analyze have made in Molecular Biological Laboratory of Institute of Biology, Mongolia. Sequencing assay has made in Molecular Biological Laboratory of Humboldt University, Germany.Results. The patient’s age was 25-86, the mid aging – 55.42±1.7. The allele frequencies of the C282Y, H63D, and S65C mutation (which in chromosome 6) were 16/136, 11.7% (heterozygous 7, homozygous 2), 9/136, 6.6% (heterozygous 0, homozygous 9), 3/136, 2.2% (heterozygous 0, homozygous 3), equally 28/136, 20.5% (heterozygous 7, homozygous 14). Conclusions. In conclusion, the occurrence of the C282Y, H63D, and S65C mutation within HFE in this studied cohort of hereditary hemochromatosis. Therefore, these data incline that other factors than the HFE gene may play a role in determining hereditary hemochromatosis in Mongolians.

Background and purpose: Liver disease that caused by iron metabolism failure is called Hemochromatosis (clinically "Bronze diabetes", "Over spotted liver cirrhosis"). The two types of hemochromatosis are primary and secondary. Primary hemochromatosis is caused by a defect in the genes that control how much iron the human body absorb from food. Secondary hemochromatosis usually is the result of another disease or condition that causes iron overload. According to the study there is a real need to study the clinical reveals of hemachromatosis in Mongolian patients. The purpose of the study to determine the hemachromatosis in patients with liver cirrhosis and cancer.Materials and Methods: The study involved 50 patients with diagnosis liver cirrhosis and cancer (1st stage) who were hospitalized in Clinic of gastroenterology of Shastin clinical hospital and "Shagdarsuren" hepatic hospital from April to July, 2011. The special questionnaire was used in the study. The biochemical laboratory examinations were taken and analyzed in lab "MED ANALYTIC". Biochemical tests performed on HumaStar 80 fully automatic analyzer. Determination of Iron level was performed by Photometric colorimetric test for iron with lipid clearing factor (normality 37-148ug/dl), transferring level by Turbidimetric monoreagent for the quantitative determination of transferring (normality 170-340ug/dl), glucose level by (GOD-PAP method) Enzymatic colorimetric test for glucose method without Deproteinisation (normality 75-115ug/dl). The ferritin level performed by ELISA analyzer (normality 15-240ng/ml).Results: The patient's age was 25-86, the mid aging-55.42. From all patients (29 male and 21 female) who were participated in the study, the 25 were with diagnosis liver cirrhosis and 18 of them clinically has the Child Pugh "B" cirrhosis, 7 has Child Pugh "A". The other 25 patients were with diagnosis liver cancer first stage.According to biochemical analyzes iron (n=35;70%); ferritin (n=41;82%); transferring (n=27; 54%); sugar (n=21;42%) levels were elevated.During the liver disease caused by iron overloading the following clinical symptoms were observed:- Skin spotting, n=48 (98%)- Hepatomegaly, n=33 (66%)- Splenomegaly, n=28 (56%)- Diabetes mellitus symptoms, n= 30 (60%)- Cardiovascular disease, n=16 (32%)- Respiratory system disorders, n=11 (22%)- Gonadotrophy, n= 2 (4%)The average serum iron level in case of livercirrhosis was 189.84+18.5mg/dl, in liver cancer 160.4±13.91 mg/ dl, ferritin level in case of liver cirrhosis was 407.69+50.08ng/ml, transferrin 375.68±47.38mg/dl, glucose 121.1±7.15mg/dl, ferritin level in liver cancer was 391.67±47.79ng/ml, transferring 388.76±47.38mg/dl, glucose 114.59±5.78mg/dl.