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1.
Vnitr Lek ; 59(7): 572-7, 2013 Jul.
Article in Czech | MEDLINE | ID: mdl-23909261

ABSTRACT

Number of newly diagnosed cystic pancreatic tumors is permanently increasing. This fact is primarily related to the development of new diagnostic methods. The main representative ones are: serous cystadenoma, mucinous cystic neoplasm, intraductal papillary mucinous neoplasm and solid pseudopapillar tumor. Because of the malignant potential of these lesions, proper indication of surgical treatment is extremely important. The article highlights and describes our experience in diagnostics and therapy of cystic pancreatic tumors diagnosed in the General Teaching Hospital Prague in the period: 1/ 2008- 12/ 2012. All patients were investigated by computerised tomography and endoscopic ultrasound with fine -  needle aspiration biopsy. Thirty seven patients in total were diagnosed with cystic pancreatic tumors: 19 with serous cystadenoma, 5 with mucinous cystic neoplasm, 5 with mucinous cystadenocarcinoma, 5 with intraductal papillary mucinous neoplasm and 3 with solid pseudopapillar tumor. In 14 cases patients were indicated for surgery, in 1 case signs of malignant transformation were found. Determination of the optimal strategy for diagnostic and therapeutic procedures in patients with cystic pancreatic tumors requires the dia-gnosis, treatment and followup observation in adequately equiped specialized centers.


Subject(s)
Carcinoma, Pancreatic Ductal/diagnosis , Cystadenocarcinoma, Mucinous/diagnosis , Cystadenoma, Serous/diagnosis , Neoplasms, Cystic, Mucinous, and Serous/diagnosis , Pancreatic Neoplasms/diagnosis , Carcinoma, Pancreatic Ductal/therapy , Cystadenocarcinoma, Mucinous/therapy , Cystadenoma, Serous/therapy , Endoscopic Ultrasound-Guided Fine Needle Aspiration , Endosonography , Humans , Neoplasms, Cystic, Mucinous, and Serous/therapy , Pancreatic Neoplasms/therapy , Tomography, X-Ray Computed
2.
Prague Med Rep ; 110(3): 181-90, 2009.
Article in English | MEDLINE | ID: mdl-19655694

ABSTRACT

Chronic intake of large quantities of alcohol causes damage to many organs, the liver being the most often affected one. In advanced countries, mortality due to liver diseases is directly proportional to alcohol consumption. 30 g of pure alcohol per day is regarded as a "safe" dose. Alcoholic liver disease may take the form of chronic illness (steatosis, steato-hepatitis, fibrosis and cirrhosis) or acute involvement (alcoholic hepatitis). Whereas steatosis is a relatively benign illness, the presence of cirrhosis of the liver means major life expectancy shortening. The actual stage of cirrhosis depends on the presence of complications--portal hypertension with bleeding oesophageal varices, ascites or hepatic encephalopathy. The median survival time of patients with advanced cirrhosis is 1-2 years. Serious alcoholic hepatitis has a mortality record of up to 50%. Absolute abstinence is a sine qua non condition for any treatment of alcoholic liver disease, the other therapeutic procedure are of a supportive nature and questionable significance. Corticoids can be used in the management of serious alcoholic hepatitis. Treatment in the stage of liver cirrhosis is similar to that in cirrhosis of any other aetiology. Cirrhotic patients who demonstrably abstain can be considered for transplantation leading to a markedly prolonged life expectancy.


Subject(s)
Liver Diseases, Alcoholic , Humans , Liver Diseases, Alcoholic/diagnosis , Liver Diseases, Alcoholic/physiopathology , Liver Diseases, Alcoholic/therapy
3.
Neoplasma ; 56(1): 26-32, 2009.
Article in English | MEDLINE | ID: mdl-19152242

ABSTRACT

Pancreatic cancer (PC) is one of the most frequent gastrointestinal malignancies with extremely poor prognosis. In spite of a relative low incidence of PC, in comparison with other cancers, PC is the fourth leading cause of cancer death in USA in both sexes. The available data clearly suggest that diabetes mellitus (DM) can be both a long-standing cause of PC and an early manifestation of the disease. Besides of DM, insulin resistance and high insulin levels are linked as well with increased cancer risk, including PC. The variable number of tandem repeats (VNTR) locus upstream of the insulin gene (INS) regulates insulin expression and has been associated with susceptibility to many diseases including DM. It is known that there is nearly complete linkage disequilibrium of the insulin variable tandem of repeats (INS-VNTR) alleles I/III with neighboring -23 HphI A/T single nucleotide polymorphism (SNP) in Caucasians. Therefore, we have studied the association between SNP of -23HphI in promoter of INS with PC, DM Type 2 (2TDM) and healthy controls. In this study we investigated 153 subjects (86 M/67 F); 51 patients with newly-diagnosed PC (31 M/20 F), 45 patients with 2TDM (29 M/16 F) and 57 healthy control subjects (26 M/31 F). The polymorphism of -23HphI (A/T) in the promoter of INS was determined by the combination of polymerase chain reaction (PCR) with the restriction fragment length polymorphism (RFLP) methods. The results obtained by the PCR-RFLP analyses of SNP -23HphI were confirmed by a direct studied locus sequencing of the genomic DNA. The frequency of abnormal glucose metabolism (both DM and impaired fasting glucose) was 88 % (45/51) in PC group. The AA genotype in SNP -23HphI was more prevalent (67 % vs. 47 %; P<0.05) among PC patients compared to controls. Additionally, statistically significant differences were found in frequencies (%) of genotypes AA/AT/TT in groups with PC (67/27/6), 2TDM (53/40/7) compared to healthy controls (37/46/17) (P<0.05). Moreover, a statistically significant effect of -23HphI A/T polymorphism on tumor staging was found (P< 0.05). Polymorphism of -23HphI (A/T) in the promoter of INS may play a role in the pathogenesis of PC and could contribute to tumor staging. Key words: pancreatic cancer; insulin gene regulation; polymorphism of -23HphI; diabetes mellitus; disorders of glucoregulation.


Subject(s)
Genetic Predisposition to Disease , Insulin/genetics , Pancreatic Neoplasms/genetics , Pancreatic Neoplasms/pathology , Polymorphism, Single Nucleotide/genetics , Promoter Regions, Genetic/genetics , Aged , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/genetics , Female , Humans , Male , Middle Aged , Minisatellite Repeats/genetics , Neoplasm Staging , Pancreatic Neoplasms/complications , Pilot Projects , Polymerase Chain Reaction , Polymorphism, Restriction Fragment Length
4.
Cas Lek Cesk ; 146(1): 74-6, 2007.
Article in Czech | MEDLINE | ID: mdl-17310589

ABSTRACT

BACKGROUND: Hiatal hernia represents penetration of the oral part of stomach together with the distal part of oesophagus via oesophageal hiatus into the thoracic cavity. On the basis of endoscopic examination hiatal hernia is defined as circular pull out of the gastric mucosa longer then 2 cm from the diaphragm to Z line, measured at the end of examination during removing the endoscope. Hiatal hernia is usually an acquired state which can worsen oesophagitis by holding refluxate and thus by prolonging the duration of purgation. METHODS AND RESULTS: Endoscopic and radiological studies show that 50 to 94 % of patients with gastroesophageal reflux disease have an axial hiatal hernia while in control persons the incidence fluctuates between 13 % and 59 %. Hiatal hernia is a frequent finding during upper gastrointestinal endoscopy. Hernia can contribute to the development of reflux into the proximal oesophagus. A cohort of one thousand patients (18 to 94 years) who underwent upper gastrointestinal endoscopy was analysed retrospectively. Endoscopy was performed between January and June 2005 at the Endoscopic center of the 4th Medical Department of the University Hospital in Prague. CONCLUSIONS: Presented study has shown that in patients who underwent endoscopy, hiatal hernia occurs in 16.6%, more frequently in men (53.6%). The most common type is an axial hiatal hernia with incidence of 94.58%. In 50% of patients with hiatal hernia the reflux oesophagitis of various degrees was diagnosed.


Subject(s)
Endoscopy, Gastrointestinal , Hernia, Hiatal/diagnosis , Adult , Aged , Aged, 80 and over , Esophagitis, Peptic/complications , Esophagitis, Peptic/diagnosis , Female , Gastroesophageal Reflux/complications , Gastroesophageal Reflux/diagnosis , Hernia, Hiatal/complications , Humans , Male , Middle Aged
5.
Cas Lek Cesk ; 145(6): 480-3, 2006.
Article in Czech | MEDLINE | ID: mdl-16836002

ABSTRACT

BACKGROUND: The diagnosis of chronic pancreatitis is based on the imaging methods. These imaging methods show the main morphological changes in the pancreatic ducts and its parenchyma, but they do not define the function of the pancreas. The aim of our study was Faecal Elastase I. determination in patients with chronic pancreatitis. The test is a simple, non-invasive method of the investigation of the pancreatic exocrine insufficiency. The Faecal Elastase I occurring in the stool was correlated with the level of the damage of pancreatic tissue together with the control group of the patients with different diagnoses. METHODS AND RESULTS: Faecal Elastase I (mean values in ug/g of stool) detection is a simple, non-invasive method which correlates well with the damage of pancreatic tissue, stemming from chronic pancreatitis. This test is routinely used especially in the diagnosis of chronic pancreatitis. The classification of chronic pancreatitis currently depends on the morphological changes of the pancreatic duct system (the patho-morphological changes). We are currently missing the classification describing simultaneously the morphological changes of the gland and the function of the pancreas. In our studies we have used a newly proposed classification system, which was put together in Bern, 2000 (1). This new system encompasses morphological and functional changes. Faecal Elastase I was determined by a microplate ELISA method using monoclonal antibody to human pancreatic protein. The Faecal Elastase I. was tested in the stool of the 196 patients with chronic pancreatitis stemming from alcoholism. The occurrence of Faecal Elastase I. was classified according to the levels assigned by the classification system. The control group used in this study included 144 patients with different diagnoses. The results demonstrate a very good correlation of Faecal Elastase I. with the grading of the newly proposed classification system of chronic pancreatitis. Patients with the highest levels of the damage of the pancreas had a significantly lower occurrence of Faecal Elastase I. in comparison with the non-pancreatic control group and in patients with chronic pancreatitis who had no clinical complications or damage of endocrine and exocrine functions of the pancreas. CONCLUSIONS: Feacal Elastase I performance plays an important role in diagnosing of the severe cases of chronic pancreatitis and in the follow-up of the chronic pancreatitis in the patients with the intermediate damage of the pancreas.


Subject(s)
Feces/enzymology , Pancreatic Elastase/analysis , Pancreatitis, Chronic/diagnosis , Biomarkers/analysis , Female , Humans , Male , Middle Aged , Pancreas/pathology , Pancreatic Function Tests , Pancreatitis, Chronic/pathology , Sensitivity and Specificity
6.
Cas Lek Cesk ; 144 Suppl 1: 40-3, 2005.
Article in Czech | MEDLINE | ID: mdl-15981985

ABSTRACT

The gastric mucosa represents a masterpiece in the functional design. As the tissue lining the stomach, it secretes aggressive combination of digestive fluids, powerful enough to digest any tissue. Nonetheless, the gastric mucosa remains undamaged by the effect of its inherent protective mechanisms. The possibility of development of gastric erosions and ulcers remains vivid evidence that the gastric mucosa is not always resistant to injury.


Subject(s)
Gastric Mucosa/physiology , Bicarbonates/metabolism , Gastric Mucosa/metabolism , Gastric Mucosa/physiopathology , Humans , Mucus/metabolism , Prostaglandins/metabolism , Stomach Ulcer/physiopathology
7.
Cas Lek Cesk ; 144 Suppl 1: 63-6, 2005.
Article in Czech | MEDLINE | ID: mdl-15981990

ABSTRACT

Portal hypertension is an unavoidable complication of liver cirrhosis, which usually limits the survival (bleeding from esophageal varices, ascites). Increase in portal pressure is not only due to mechanical obstruction of portal circulation, but there is also a dynamic component (endothelial dysfunction of hepatic microcirculation) and increased blood flow through the splanchnic circulation. For the long-term treatment of portal hypertension two groups of medicaments are available at present: non-selective betablockers (vasoconstriction in splanchnic bed) and nitrates (lowering of intrahepatic resistance). Long-term treatment is necessary in these situations: Primary prophylaxis of bleeding from esophageal varices (in patients, who never bled, but with "risk" varices)--non-selective betablockers; secondary prophylaxis (in patients after variceal bleeding)--non-selective betablockers (possibly with nitrates) or endoscopic treatment. It is clearly documented, that this treatment lowers the risk of the first or repeated bleeding from varices and hence lowers the mortality and morbidity due to this complication in patients with liver cirrhosis. Another serious complication of liver cirrhosis is the spontaneous bacterial peritonitis. All patients after that infection have to receive prophylactic treatment with antibiotics. This treatment should be long life, till the disappearance of ascites or till the liver transplantation.


Subject(s)
Hypertension, Portal/drug therapy , Esophageal and Gastric Varices/etiology , Esophageal and Gastric Varices/prevention & control , Gastrointestinal Hemorrhage/etiology , Gastrointestinal Hemorrhage/prevention & control , Humans , Hypertension, Portal/complications , Peritonitis/etiology , Peritonitis/prevention & control
8.
Cas Lek Cesk ; 143(2): 97-100, 2004.
Article in Czech | MEDLINE | ID: mdl-15077571

ABSTRACT

BACKGROUND: The aim of the present study was to evaluate the relationship between Pancreatic Cancer and Type 2 Diabetes Mellitus, which represents a higher risk of many human tumors. In patients with Pancreatic Cancer, Type 2 Diabetes Mellitus occurs approximately in 30%. METHOD AND RESULTS: Fifty patients with newly diagnosed Pancreatic Cancer were analysed in a retrospective pilot study where the staging of the tumor and the case history of the patients were studied. This data were compared in three groups of patients: the control group without diabetes, one with Impaired Fasting Glucose, and patients with Diabetes Mellitus. Incidence of Diabetes Mellitus and that of Impaired Fasting Glucose were also followed in patients with Pancreatic Cancer and Colorectal Cancer. The retrospective study confirmed the late diagnosis of Pancreatic Cancer. The tumors were actually in clinical stage IV in 50% of the patients. Diabetes Mellitus was present in 34% of patients with Pancreatic Cancer; in 44% of these patients the Impaired Fasting Glucose was also diagnosed while the normal glucose status was seen in 22% of patients. Incidence of Impaired Fasting Glucose and that of Diabetes Mellitus in groups of patients with Pancreatic Cancer and Colorectal Cancer was studied. Diabetes Mellitus was present in 12.5% patients with Colorectal Cancer. CONCLUSIONS: In spite of modern diagnostic methods, the early diagnosis of Pancreatic Cancer remains a great problem. Incidence of Diabetes Mellitus in patients with Pancreatic Cancer was significantly higher in comparison with the Colorectal Cancer group (P0.01). A significant number of patients with Impaired Fasting Glucose were also present in the group with Pancreatic Cancer. Analysis of the relationships between Pancreatic Cancer and Impaired Glucose Metabolism could contribute to the early diagnosis of this serious malignant disease.


Subject(s)
Carcinoma/complications , Diabetes Complications , Pancreatic Neoplasms/complications , Adult , Aged , Aged, 80 and over , Colorectal Neoplasms/complications , Diabetes Mellitus, Type 2/complications , Female , Humans , Male , Middle Aged , Pancreatic Neoplasms/diagnosis
9.
Vnitr Lek ; 50(11): 842-5, 2004 Nov.
Article in Czech | MEDLINE | ID: mdl-15648964

ABSTRACT

UNLABELLED: Primary biliary cirrhosis is a chronic liver disease, characterized by the destruction of the epithelial cells of the sublobular, interlobular and septal bile ducts and with the development of cirrhosis. The presence of anti-mitochondrial antibodies against the subunits of mitochondrial 2-oxoacids dehydrogenases is characteristic for patients with primary biliary cirrhosis. The aim of this work was to study the effect of anti-mitochondrial antibodies upon activity of the isolated mitochondrial pyruvate dehydrogenase complex after the incubation with serum from patients with primary biliary cirrhosis. GROUP OF PATIENTS AND METHODS: The activity of the purified bovine pyruvate dehydrogenase complex was studied spectrophotometrically in presence of the serum (1: 1000) from five patients with primary biliary cirrhosis and from ten disease free controls. RESULTS: The activity of the pyruvate dehydrogenase was decreased after incubation with the serum from patients with primary biliary cirrhosis. No similar inhibitory effect was found after incubation with serum from controls. DISCUSSION: The inhibitory effect of the anti-mitochondrial antibodies upon activity of pyruvate dehydrogenase may broaden the spectrum of diagnostic methods in patients with primary biliary cirrhosis. Further investigations are necessary to assess the possible application of this method for monitoring of changes during the course of the disease and for assignation of the disease prognosis.


Subject(s)
Autoantibodies/analysis , Liver Cirrhosis, Biliary/immunology , Mitochondria/immunology , Adult , Aged , Antibody Specificity , Female , Humans , Middle Aged , Pyruvate Dehydrogenase Complex/immunology
10.
Cas Lek Cesk ; 143(12): 850-3, 2004.
Article in Czech | MEDLINE | ID: mdl-15730218

ABSTRACT

Helicobacter pylori is a microorganism that is thought to play a role in the etiopathogenesis of peptic ulcer disease. Eradication of this microorganism is valuable clinical cure of infected patients. Efficacious regimens generally include an antisecretory agent combined with two antimicrobials. The main determinant of overall cost of treatment is the rate of eradication of the microorganism. Resistance can occur to the commonly used antibiotics but can usually be overcome with an altered regimen. It is important for care physicians to clearly understand indication and how to select appropriate therapy against Helicobacter pylori infection.


Subject(s)
Gastrointestinal Diseases/drug therapy , Helicobacter Infections/drug therapy , Helicobacter pylori , Drug Therapy, Combination , Gastrointestinal Diseases/microbiology , Humans
11.
Cas Lek Cesk ; 143(11): 734-7, 2004.
Article in Czech | MEDLINE | ID: mdl-15628566

ABSTRACT

The last twenty years have been the witness of the major revolution in the medical science and practice. Pathogenesis of gastric ulcer disease has probably undergone the most serious change both in the conception and in practice. Though the number of information concerning Helicobacter pylori (Hp) is rising explosively, our understanding of the specific and detailed role of Hp infection in the pathogenesis of various Hp related diseases remains modest.


Subject(s)
Duodenal Diseases/microbiology , Helicobacter Infections/complications , Helicobacter pylori , Stomach Diseases/microbiology , Helicobacter Infections/diagnosis , Humans
12.
Cas Lek Cesk ; 142(8): 483-6, 2003 Aug.
Article in Czech | MEDLINE | ID: mdl-14626564

ABSTRACT

Helicobacter pylori is an organism that is thought to be important in the pathophysiology of ulcer disease and gastritis. Eradication of the organism is useful in the treatment of infected patients. Efficacious regimens generally include an antisecretory agent combined with two antimicrobials. The main determinant of the overall cost of treatment is the eradication of H. pylori in the microorganism. Resistance to the commonly used antibiotics can occur but it can be usually overcome with regimen changes. It is important for care physicians to clearly understand when and how to test and how to select appropriate therapy for Helicobacter pylori infection.


Subject(s)
Helicobacter Infections/drug therapy , Helicobacter pylori , Peptic Ulcer/microbiology , Drug Therapy, Combination , Helicobacter Infections/complications , Humans , Peptic Ulcer/therapy
13.
Cas Lek Cesk ; 142(12): 751-4, 2003.
Article in Czech | MEDLINE | ID: mdl-14746225

ABSTRACT

BACKGROUND: It has been proven that damage to the gastric mucosa is the result of the combined effects of acidopeptic agents including infection with Helicobacter pylori and insufficient protective mechanisms of the mucosa. Thickness of gastric mucus is very important protective factor. We can hypothetically expect that fasting may cause changes in the thickness of gastric mucus layer, which may in certain circumstances contribute to the conditions for mucosal injury. We have therefore conducted an experimental study on laboratory rats, aiming to assess the changes in the thickness of gastric mucus after 8 and 24-hour periods of fasting. METHODS AND RESULTS: We measured gastric mucus thickness with the aid of microelectrodes in 279 laboratory rats (group I) after 8 hours of fasting (2 measurements each, total of 558 measurements), followed by the same measurement in 70 laboratory rats (group II) after a 24-hour fasting. Group I had a gastric mucus thickness of 595 +/- 10 (mean +/- SD, microns); in group II the thickness was 502 +/- 10 (mean +/- SD, microns). After statistical analysis of the homogeneity of the two populations (Fisher's analysis), it has been proven that both groups belong to the same basic population sample. The statistical evaluation of the thickness of gastric mucus in both groups showed thinning of the mucus layer to 1% of the significant statistical difference. The difference between both groups is statistically significant. CONCLUSIONS: The thickness of gastric mucus is reduced after 24 hours' fasting in laboratory rats. This change is statistically significant (P < 0.01). It can be hypothesized that--under the specific conditions--this process can facilitate the injury of gastric mucosa.


Subject(s)
Gastric Mucosa/pathology , Animals , Fasting , Male , Rats , Rats, Sprague-Dawley
14.
Bratisl Lek Listy ; 94(6): 302-7, 1993 Jun.
Article in Czech | MEDLINE | ID: mdl-8124589

ABSTRACT

The hereditary form of colorectal cancer (Lynch syndrome, cancer family syndrome "nonpolyposis hereditary colorectal cancer"), which is different from familial adenomatous polyposis, represents probably 5-8% of the development of this malignancy. The main characteristics of the syndrome include an autosomal dominant hereditary type, frequent familial occurrence of colorectal cancer (either solely at this site--Lynch variant I--or in combination with other, particularly gynecological sites of cancer-Lynch variant II), younger age at the time of diagnosis, more frequent localization in the right colon and more frequent occurrence of synchronic and metachronic cancer. During the years 1982-1992, we found 339 asymptomatic members of families meeting the criteria of the syndrome. After initial colonoscopy these individuals entered a long-term surveillance system with repeated colonoscopies; intervals between them where organized according to the individual degree of risk and to at the initial finding. Results of initial colonoscopy showed colorectal cancer in 16.2% and adenomas in 32.1% of the whole group. The right colon was affected in 74.5% of the cancers and in 64% of the adenomas; the mean age of the probands with these findings was 46.4% years. The Lynch variant I was found in 34%, the variant II in 66%. Cancer in relatives of the variant II was mostly in the colorectal, followed by the gynecological region. The highest number of cancers detected on initial colonoscopy was found in probands with the highest degree of genetic risk-with 3 or more than 3 direct relatives. On repeated colonoscopies a new cancer was found in 7 further probands. All the cancers were well resectable, mostly DUKES A and B.(ABSTRACT TRUNCATED AT 250 WORDS)


Subject(s)
Colorectal Neoplasms, Hereditary Nonpolyposis/diagnosis , Adult , Colonoscopy , Female , Humans , Male , Middle Aged
15.
Cas Lek Cesk ; 131(11): 329-33, 1992 Jun 05.
Article in Czech | MEDLINE | ID: mdl-1638599

ABSTRACT

In 1982-1991 at the Fourth Medical Clinic 309 asymptomatic family members meeting the criteria of the hereditary form of colorectal carcinoma (Lynch syndrome--syndrome of familial cancer, also "non-polypous" hereditary colorectal carcinoma) which differs from familial polyposis (adenomatosis) of the colon. The syndrome is characterized by autosomal dominant heredity and by familial incidence of colorectal carcinoma (Lynch I) or colorectal carcinoma and carcinoma of other, in particular gynaecological areas (Lynch II) and a younger age of the affected subjects, a more frequent localization in the right colon, synchronous and metachronous neoplasia. In the authors group 34% were type I, the remainder type II. Initial total coloscopy revealed carcinoma in 51 subjects (78% in the right colon), adenomatous polyps in 99 (73% in the right colon). The mean age of the patients with carcinoma was 47.5 years, of those with adenoma 46.5 years. The majority of cases were recorded in subjects with three or more than three direct relatives with carcinoma (highest risk grade). During subsequent coloscopic check-up examinations at intervals depending on individual risk, colorectal carcinoma was detected in another six subjects. In 30 patients it was carcinoma Dukes A, in 12 B and in 3 Dukes C. These results indicate that identification of asymptomatic cases of Lynch syndromes via the family-history and coloscopic follow-up contributes to the early diagnosis of colorectal carcinoma.


Subject(s)
Colorectal Neoplasms, Hereditary Nonpolyposis/diagnosis , Adenocarcinoma/diagnosis , Adenocarcinoma/genetics , Adenoma/diagnosis , Adenoma/genetics , Adult , Colonoscopy , Colorectal Neoplasms, Hereditary Nonpolyposis/genetics , Female , Humans , Male , Middle Aged , Risk Factors
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