Although stomach cancer immunohistochemistry is similar tothe immunohistochemistry of other organ, it has great impact on diagnosis and treatment, such as its ability to reveal whether the cancer is primary or metastatic and which treatment model would be more effective in individual case. Lately, CK7, CK20 and CDX-2 immunohistochemical markers are commonly used in stomach cancers. Stomach cancer prognosis is different in each patient, depending on several factors, patients’ health status, cancer cell differentiation, and cancer cell growth. To evaluate these factors,immunohistochemic al analysis is more effective and for this purpose they use Ki-67, CD 34, BCL-2, p53, Cyclin D1, andHer- 2 markers.The evaluation of HER-2 expression should be carefully carried out, as following: 1. HER-2 expression should be evaluated on minimum 5 positive stained cells. The evaluation criteria aremicroscopic magnification and cytoplasmic membrane-stained pattern. 2. Other than the membrane-stained pattern must be excluded. HER2 gene evaluation (FISH) can confirm the HER2 IHCexpression. 3. Usage of FDA approved antibody (4B5) has the advantageof increased sensitivity. 4. The algorithm for the evaluation of HER-2 expression used for breast cancer has 50% possibility of false negativity if it is used for stomach cancer. Therefore, it is needed to beevaluated with another specific algorithm. Because HER-2 2+ and 3+ cases can improve outcome with usingTrastizumab treatment.

Appendiceal mucocele is an obstructivedilatation of the appendix caused byintraluminal accumulation of mucoid material.It is a rare disease. The incidence is 0.2%to 0.3% of all appendectomied specimens.The brush size to 3 cm are considered to besmall, up to 6 cm - average and more than9 cm - giantCases: the patient 50 years old, man,place of residence: the city of UB songinokhairkhan duureg. Specialists of the driver,in the year immediately 2015,02,02 wasoperated with the diagnosis of acuteappendicitis. Complaints on admission:pain on the right side of the abdomen, anagging pain when moving and walking,stomach rumbling. History of the disease:the pain started with 2015,01,31 at 8 pmfrom the bottom of the abdomen. tookhome chloramphenicol but not helpedso 2015,02,02 year at 9 o’clock enteredvia ambulance. Medical examination: thesatisfactory condition of the active position,the skin clean, moist, blood pressure160/110, pulse 98 beats per minute Spo298%. 10*7,7*5,5 см size /Fig.1-2/ , white /Fig. 3-4/ , smooth surface /Fig.1-4/, insideslimy gray mucinous /Fig. 5-6/ bag /Fig. 5/above listed items on a standard attached,aims to study the histology. The result ofthe following: Mucocele of the appendixwith hyalinized wall and with the additionof acute inflammation with microabscesses.

Introduction.M.Colombo, W.Lange studies showed that 30-40% of people became chronic after suffering fromHepatitis B and C virus, about 50% of chronic cases transformed into primary liver cancer. There arefew studies in our country were conducted on hepatitis among healthcare professionals, particularnursing personnel.Goal.To identify antigens and antibodies of hepatitis B and C virus among nursesMaterials and Method.We carried out cross-sectional study among selected nurses, to determine surface antigen of hepatitisB virus and antibodies to hepatitis C virus. For identification of these antibodies and antigen, andvalidation of results Serodia tests from Fujinebo Company (Japan) and Beringnost (Germany) wereused respectively.Results.There were 598 nurses from the State Central Clinical Hospital, Shastin’s State Hospital, Hospitalof Military of Justice and Internal Affairs, and the National Center of Maternal and Child Health, whoparticipated in the study. From 5 hospitals a 598 nurses surveyed and revealed the hepatitis B virussurface antigen positive 18.9%, hepatitis C virus antibodies in 23.2%, B and C viruses detected by1.2% combined.Conclusion.The study identified that 43.2 percent of nurses surveyed on hepatitis B and C viruses were detected;it shows a high prevalence among the nurses. There is an urgent need to provide knowledge tomedical personnel regarding standards during procedures, concerning hepatitis infections, monitoringand improve technology used during procedures.

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.

Goal: The aim of the study was to identify economic burden from hypertention in Ulaanbaatar and develop some recommenadations. Material and Method: The top down approach was used to calculate direct costs of hypertension in five hospitals of the secondary and tertiary levels. To calculate cost of hypertension financial reports and cost centres data were used. A self-administered questionnaire was used to calculate indirect costs from the disease. Patients, admitted to six UB district and three tertiary level hospitals due to hypertension filled in the questionnaire. Data was analysed using SPSS 15 programme.Results: Some 114 patients were surveyed. The average cost of hypertension was 143914 ± 38189.5 (average bed days 8.7) and 264756 ± 40760.4¥ (average bed days 9.5) in the selected district and tertiary level hospitals respectively. The average cost for per out-patient visit was 4237 ± 2123.5¥ in the selected district hospitals and 3,162 ± 308.3¥ in the selected tertiary level hospitals. The indirect costs included transport cost to and from hospital, food, transport cost of relatives to visit them, cost of medications, and some other expenses related to their admission. Average indirect cost of an admission of patients with the hypertension was 253,395 and 212,717.44¥ in district and tertiary level hospitals respectively. Economic burden from temporary loss of working ablility due to hypertension was 177.1 millions tugrigs. National average wage was 300500¥ in 2009. Some 65.8% of respondents used antihypertension drugs at least once a day and average cost was 653.4¥ per patient per day. Annual and 10 years drug use estimates were 238491 and 2.3 million tugrigs per patient respectively (Inflation and price changes were not counted).Conclusion: Indirect and direct costs for admission were 1.1 billion (49.6%) and 939 million (42.5%) tugrigs respectively. Cost of hypertension in Ulaanbaatar was 2.2 billion tugrigs in 2009 and it is 1.1% of total health sector financing.

BACKGROUND:Acute inflamed process in gallbladder stand no more in the list of contraindication for its laparoscopicremoval, although specifity of operational technics need to be elaborated in details.PURPOSE:The purpose of the study to determine feasibility and specifity of laparoscopic cholecystectomy.METHODS AND MATERIALS:Based on standard instructions three holes were punched on the front wall of the abdominal cavity forinsertion of fibroscopic instrument, Olympus-2008, Model-Uni 3, input-120/240V, 50/60Hz, 150VA. Patientselection included 108 individuals hospitalized during 2009-2013 in the department of urgent surgery, IIIShastin Clinical Hospital.RESULTS:Average ages of the patients were 38. Clinical diagnosis based on signs and symptoms revealed at thephysical examination confirmed by echosonographic investigation for final diagnosis. Specificity of surgicaltechnics were incision and infusion of large amount of antibiotic solution into the inflamed gallbladder at theinoculation; use blunt edge for inoculation of the duct and artery of gallbladder; switching to open surgeryin case of revealed massive enzymatic infiltration and adhesive scars.CONCLUSION: Laparoscopic cholecystoectomy is feasibility operative procedure having advantages anddisadvantages, requiring necessary preventive measures of the complications.

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.