Biomedical subjects

M Jablonská

Publications and source records attributed to M Jablonská.

At least 19 recordsLinked to original sources

PubMed2005

[Protective mechanism of the gastric mucosa].

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.

Bicarbonates↗

PubMed2004

[Helicobacter pylori infection and diseases of the stomach and duodenum].

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.

Duodenal Diseases↗

PubMed2004

[Indication for the treatment of Helicobacter pylori infection].

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.

Drug Therapy, Combination↗

PubMed1999

The role of the host versus the environment in duodenal ulcer disease.

Gastric functions can be understood only in the context of a network including the brain gut axis, neuro-endocrine and paracrine mechanisms and growth factors. These host factors including parietal cell sensitivity (PCS) may well interact with an important environmental factor, Helicobacter pylori (Hp), and help to explain its actions. The aim of this study was to investigate PCS related to Hp status and duodenal ulcer (DU). PCS was assessed by constructing dose-response curves after pentagastrin and calculating the D50. Five groups of patients were studied: I) active DU, Hp pos. (8); II) history of DU, Hp pos. (8); III) asymptomatic Hp pos. (8); IV) asymptomatic Hp neg. (10); V) DU on maintenance H2 blocker therapy, Hp pos. (20). PCS was repeated after Hp eradication. PCS was lowest in group IV, and in Hp pos. groups, was significantly higher, with insignificant differences among them, irrespective of DU. PCS declined significantly after Hp eradication. Group V showed an insignificant decline in PCS during treatment, not preventing recurrence. A higher PCS in Hp infection irrespective of DU, declining after eradication, suggests that this may be a reversible epiphenomena related to Hp infection. This may offer an explanation as to why DU develops only in some subjects with Hp, suggesting the importance of the host in the pathogenesis of DU.

Adult↗

PubMed1997

[Viruses and primary hepatocellular carcinoma].

The etiological association between primary hepatocellular carcinoma (PHCC) and chronic viral hepatitis has been proved by now beyond doubt in the hepatitis B virus (HBV) and C virus (HCV). PHCC develops most frequently in cirrhotic livers, sometimes also in the absence of cirrhosis. Extensive epidemiological studies provided convincing evidence of this etiological relationship which is also supported by observations and animal experiments. An important factor in hepatocarcinogenesis due to the influence of HBV is integration of the viral genoma into the liver cell genoma. In the tumourous part of the liver integrated HBV sequences are more frequent than in the non-tumourous part. The integration can produce changes in the genome of the liver cell which may sometimes lead to malignant transformation. The mechanisms of this process are not quite clear so far. Their outcome--the development of carcinoma--can be summarized as the peak effect of factors leading to the disorganization of DNA with participation of chromosomal changes, the action of transactivation of HBs protein, transformation growth factors and the important influence of mutations of the suppressor gene p 53 on the 17th chromosome which is probably the target of HBV. HCV produces chronic live: disease developing into cirrhosis and PHCC, even more frequent than HBV; however its integration into the liver cell does not take place. The genetic variability of this gene is great. Its transformating action is probably implemented rather as a co-carcinogen on the background of cirrhosis of the liver which alone regardless of its cause is an increased risk for the development of PHCC. In clinical practice these findings imply the necessity of optimal prevention of chronic viral hepatic infection (vaccination, so far available for HBV, transfusions) and the necessity to assess the virological status in patients with chronic liver disease and early detection of small tumourous liver lesions where nowadays due to modern therapeutic approaches the prognosis has improved greatly.

Animals↗

PubMed1995

Healing of gastric body ulcer with gastroprotective versus antisecretory treatment.

The aim of this study was to compare the healing effect of a gastroprotective agent and antisecretory drugs in gastric body ulcer where failure of the mucosal defense might be an important factor. Eighty-five patients with benign gastric ulcer were divided into four groups: treated with antacids (I), cimetidine (II), ranitidine (III), and colloidal bismuth subcitrate (De-Nol) (IV). Endoscopically confirmed complete healing was achieved in 57, 61, and 63% in groups I, II, and III, respectively, and in 88% in group IV (P < 0.05). Gastric secretion did not change significantly. Relapses during the next three years occurred several times more frequently in groups I, II, and III than in group IV. Helicobacter pylori was positive in about half the relapsing patients in groups I, II, and III but negative in those of group IV. It is concluded that De-Nol treatment of gastric body ulcer was more efficient than antisecretory drugs both initially and in reducing relapses.

Adult↗

PubMed1995

Clinical implications of recognition of the hereditary non-polyposis colon cancer syndrome (HNPCC) for the early detection of colorectal cancer.

UNLABELLED: Hereditary non-polyposis colon cancer (HNPCC), also known as the Lynch syndrome or, previously, as the cancer family syndrome (CFS) is a recently defined autosomal cancer syndrome which is different from familial adenomatous polyposis and accounts for a considerable proportion of colorectal cancer (CRC). The main features of HNPCC include familial aggregation of CRC (either solely or combined with other, particularly gynaecological cancer sites- Lynch I or II, resp.), very frequent localization of the cancer in the right colon, a considerably lower age at the time of occurrence and a high risk of synchronous and metachronous tumours. Recognition of the syndrome through family history offers an important chance to detect CRC at a presymptomatic stage with a positive effect on the prognosis. In 1981/82 we started a prospective follow-up of symptom-free subjects conforming with the criteria of HNPCC. Up to 1994 we found 364 subjects of this type coming from 38 families. After initial colonoscopy these subjects entered a system of colonoscopic surveillance built up according to the individual degree of risk. Initial colonoscopy revealed cancer in 61 and adenomas in 122 subjects, both in more than 70% in the right colon. The mean age at this time was 47.5 in cancer and 45.3 in adenomas. More cancers and adenomas were found on repeated colonoscopies during surveillance. All the cancers were well resectable, a 5 year survival in all. During this course in a group of 239 non-screened symptomatic cases of the HNPCC syndrome, detected only at the time of colonoscopy, cancer was found in 146 and adenomas in 71 patients. Five year survival was 65% in this group. The cancers in the screened group were Dukes A and B (mostly A) in 82% and C in 18%, in the symptomatic group Dukes A or B (mostly B) in 67%, C in 18 and D in 15%. - CONCLUSIONS: The results show more favourable colonoscopic findings and better prognosis in symptom-free, colonoscopally screened cases of HNPCC than in symptomatic ones and fully justify an active approach based on colonoscopic surveillance of HNPCC subjects prior to diagnosis.

Adenocarcinoma↗

PubMed1993

[Early diagnosis of colorectal carcinoma in the familial carcinoma syndrome (Lynch I and II)].

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)

Adult↗

PubMed1993

[Risk of development of colorectal carcinoma in patients with ulcerative colitis].

In patients with ulcerative colitis of prolonged duration and major extent there is according to the majority of investigations an increased risk of development of colorectal carcinoma; the magnitude of the risk which is of major importance for clinical practice, however, differs according to different authors. The present study comprises 189 patients with ulcerative colitis, 103 men and 86 women, perspectively followed up for a period of 12.5 years (8.0-24.5). In 60 patients the distal form was present, in 68 left-sided colitis and in 61 pancolitis. The patients were monitored systematically--clinically colonoscopically and endoscopically. The intervals between these check-ups were gradually shorter when the disease persisted for 10 or 12 years, i.e. the patients were checked once to twice a year. The endoscopic findings were focused in particular on evidence of dysplasia. The follow-up system was modified with regard to individual conditions. In the course of the follow-up colorectal carcinoma was detected in 9 patients (4.8%) with a persistence of the disease for 9-25 years (in one patient after 9 years, in 5 after 10-20 years and in 3 after longer periods). In three instances the left-sided form was involved, in 6 pancolitis. Dysplastic changes were mostly medium grade and were found at least once in all patients. The preoperative diagnosis of carcinoma was established for certain in three patients, there was major suspicion in four patients. In two patients the carcinoma was detected only on operation (in active forms of the disease). All carcinomas were resectable, 4 times DUKES A, 4 times B, once C. As to the remaining 180 patients, 32 were operated on account of colitis; in 28 at least once dysplasia was proved, with a rising trend as the disease had a prolonged duration. These results confirm the increased risk of carcinoma in ulcerative colitis with a long duration and with a major extent and justify systematic colonoscopic and endobioptic follow-up of these patients.

Adolescent↗

PubMed1992

[Significance of the detection of the familial carcinoma syndrome (Lynch I and II) in the early diagnosis of colorectal carcinoma].

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.

Adenocarcinoma↗

PubMed1992

Resistance to medical ulcer therapy--possible reasons and management.

UNLABELLED: In 112 patients with duodenal ulcer (males, mean age 29, range 18-35) with a history of at least 3 years, and never being treated with H2-antagonists, maintenance therapy with Tagamet was started. All of them had ulcer recurrence when entering the study. The first two months a full dose was applied, after this bedtime doses up to 24 months. Endoscopy was performed at the beginning, after the first and second months and then every two-month period. Gastric secretion was measured every 2-3 months. A resistant ulcer was defined as one 1/not healing within the two initial months, 2/recurring on maintenance treatment. RESULTS: in 78% the ulcer was healed within one month, in 96% within two months, in the rest within the following 3-4 weeks. Relapses occurred in 21 patients, altogether 27 times. Factors likely to contribute to recurrence included a large ulcer size, longer duration, an inflamed mucosa and--most frequently--heavy smoking. Patients with relapses had higher initial secretory values and smaller decrease during maintenance treatment. Helicobacter pylori (examined in a subgroup) was not clearly associated with ulcer recurrence.

Adolescent↗

PubMed1987