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11. Shanmugam V, Geraghty B, DeSimone R. Diagnostic value of positive urinary cytology in the detection of recurrent urothelial carcinoma: 10-year experience at the Papanicolaou Cytology Laboratory. Diagn Cytopathol. 2016; 44: 975-9.
12. Sun X, Song M, Bai R, Cheng S, Xing Y, Yuan H et al. Ileal interposition surgery-induced improvement of hyperglycemia and insulin resistance in Goto-Kakizaki rats by upregulation of TCF7L2 expression. Exp Ther Med. 2013; 5:1511-1515.
13. Van der Aa F, Joniau S, Van Den Branden M, Van Poppel H. Metabolic Changes after Urinary Diversion. Adv Urol. 2011; 2011: 764325. http://dx.doi.org/10.1155/2011/764325
14. Vasdev N, Moon A, Thorpe AC. Metabolic complications of urinary intestinal diversion. Indian J Urol. 2013; 29 (4): 310-5. doi: 10.4103/ 0970-1591.120112.
Реферпin
ДИНАМ1ЧН1 ЗМ1НИ КЛ1ТИННОГО СКЛАДУ ОСАДУ СЕЧ1 АРТИФЩ1ЙНОГО
СЕЧОВОГО М1ХУРА Савчук Р.В., Костев Ф.1., Вгг В.В.
Метою роботи було ощнити динамiчнi змши клтнного складу осаду артифщшного сечового мiхура. Виявлена динамка структурних змш осаду сечi тсля оперативного втручання свщчить про те, що, при наявност позитивних клтачних результата операцп, завершуються процеси перебудови епiтелiального вистилання пересадженого замють сечового мiхура фрагмента кишечника, спрямоват на виконання шших функцш. На пiдставi отриманих даних можна припустити можливють використання в клшщ цитолопчного дослщження для встановлення динамки процесу тсля оперативного лкування, виявлення ступеня ексфолiащI еттелто пересадженого кишечника, а також корекцп окремих ланок процесу адаптацп в нових умовах функщонування пересадженого фрагмента кишечника, яю принципово вiдрiзняються.
Ключовi слова: артифщшний сечовий мiхур, клiтинний склад, адаптащя.
Стаття надiйшла 20.04.2019 р.
ДИНАМИЧЕСКИЕ ИЗМЕНЕНИЯ КЛЕТОЧНОГО СОСТАВА ОСАДКА МОЧИ АРТИФИЦИАЛЬНОГО МОЧЕВОГО ПУЗЫРЯ Савчук Р.В., Костев Ф. И., Вит В.В.
Целью работы было оценить динамические изменения клеточного состава осадка артифициального мочевого пузыря. Выявленная динамика структурных изменения осадка мочи после оперативного вмешательства свидетельствует о том, что, при наличии положительных клинических результатов операции, завершаются процессы перестройки эпителиальной выстилки пересаженного вместо мочевого пузыря фрагмента кишечника, направленные на выполнение других функций. На основании полученных данных можно предположить возможность использования в клинике цитологического исследования для установления динамики процесса после оперативного лечения, выявления степени эксфолиации эпителия пересаженного кишечника, а также коррекции отдельных звеньев процесса адаптации в новых условиях функционирования пересаженного фрагмента кишечника, которые принципиально отличаются.
Ключевые слова: артифициальный мочевой пузырь, клеточный состав, адаптация.
Рецензент Старченко 1.1.
DOI 10.26724/2079-8334-2020-1-71-120-124 UDC 616.329-006.66-091.816
T.V. SitIi;i. O.ll. Kiiryk'. V.O. Yiikovenko2. R.P. I knchenko' Boigomoiels Nalional Medical I niversily. 'SI "Research and Practical Centre of Preventive and Clinical Medicine" Stale Administrative Deparlmenl. 2Medical Centre "Oberih" Clinic. Kyiv
RISK OF ADENOCARCINOMA IN BARRETT'S ESOPHAGUS
e-mail: O_Kurik@ukr.net
The total of 7396 videoesophagogastroscopy cases were analyzed. The presence of metaplastic columnar epithelium of esophagus was found in 2910 patients (39.4%) at pathohistological examination. The gastric metaplasia was evaluated in 876 cases (11.9%), the specialized intestinal metaplasia without dysplasia - in 1970 (26.6%), the low-grade dysplasia - in 48 (0.65%), the high-grade dysplasia - in 16 (0.22%). Esophageal adenocarcinoma was evaluated in four patients (0.05%, CI 0.01 - 0.12%). Low probability of esophageal adenocarcinoma formation in all types of metaplasia was demonstrated. Only the presence of dysplasia of metaplastic epithelium should cause increased alertness for the occurrence of esophageal adenocarcinoma. Exaggerated value of Barrett's esophagus may result in additional traumatization of mucosa, increase the risk of bleeding and stenosis.
Keywords: Barrett's esophagus, metaplasia, dysplasia, esophageal adenocarcinoma.
The work is a fragment of the research project "Differential - diagnostic criteria for tumors and pre - tumor changes and their value in a prognosis ", state registration No. 0120U1006.
Barrett's esophagus (BE) is the condition in which metaplastic columnar epithelium replaces the stratified squamous epithelium that normally lines the distal esophagus. BE predisposes to cancer development. In addition to Barrett's mucosa, a source of esophageal adenocarcinoma (EAC) may be cardiac or submucosal glands. Estimates of the prevalence of BE in the general population have varied widely from 0.4 to more than 20 percent, although the large majority of cases go unrecognized [12, 13].
© T.V. Serha, O.H. Kuryk, 2020
EAC is a type of cancer that has been increasing in incidence in many Western societies over recent decades [14]. There is some evidence to suggest that EAC arise from BE, however the details of pathogenesis of it remain unknown. In surveillance programs of BE only a minority of patients develop EAC raising the question of what factors are implicated in the development of EAC from BE [2, 15].
In the National Cancer Registry № 20 "Cancer in Ukraine 2017-2018" incidences of esophageal adenocarcinoma are not separated from other forms of malignant neoplasms of the esophagus and its level is unknown.
It is estimated that the risk of cancer progression for patients with nondysplastic BE is ~ 0.20.5% per year, for patients with low-grade dysplasia the annual risk of BE progression to cancer is ~ 0.7% per year, for patients with high-grade dysplasia the annual risk of neoplastic progression is ~ 7% per yeaer [8, 10].
In spite of this at Clinical Guideline of American College of Gastroenterology (ACG) is reported that the majority (>90%) of patients diagnosed with BE die of causes other than EAC [14].
The purpose of the study was to estimate the number of patients who developed EAC among patients with the different types of BE in unselected cohort of subjects.
Materials and methods. We analyzed 7396 cases of videoesophagogastroscopies for the period from January 2010 to December 2018 in the Medical Centre "Oberih" clinic, Kyiv, Ukraine. Among them 2910 patients had histologically proven BE and were 10 to 79 years old. Patients' endoscopic findings (endoscopically suspected esophageal metaplasia), and pathological findings (the type of metaplasia, degree of dysplasia) were collected for further analysis.
Esophagogastroscopies were made by gastroscopes Olympus Q160-Z, Olympus EVIS EXERA II, with using NBI and 115 magnification according to the sampling protocol. Target biopsies were performed from all areas of suspected metaplasia, as well as from 4 quadrants of esophageal wall and every 2 cm along the metaplastic segment.
Diagnosis of BE was set endoscopically by visualization of a columnar lined epithelium at least 1 cm above the gastroesophageal junction. BE was divided into short- and long-segment BE. Short-segment BE had a maximal length less than 3 cm, whereas long-segment had a length more than 3 cm. In previous studies it was shown that long-segment BE had a higher risk for development of EAC. The length of the BE segment is known to be associated with risk of progression to neoplasia.
Statistical analysis was performed with using MedStat programme. To estimate the prevalence of changes in the esophagus a 95% confidence interval was calculated with using the Fisher angular transformation method. The data was analyzed with using the Student's Z-test for continuous variables, and Chi-square test for categorical variables. The difference between the mean values was considered significant at p <0.05.
Results of the study and their discussion. In order to detect the BE we used endoscopic studies with biopsy and morphological verification. We analyzed 7396 cases of videoesophagogastroscopies in the period from 2010 to 2018. The study was conducted at the Medical Centre "Oberih" clinic in Kyiv, Ukraine.
There was an equal number of male and female patients included in the study (3684 men and 3708 women).
The age of the patients was from 10 to 79. In the statistical evaluation of the results revealed low peaks of gastric metaplasia at the age of 20 - 29 and high frequency of intestinal metaplasia at the age of 60 - 69. For gastric metaplasia, the rate was 2 times lower in this age category. For intestinal metaplasia
- 1.25 times higher in the category of 60 - 69 years old.
The presence of columnar lined metaplasia with forming the columnar-lined esophagus was demonstrated in 2910 patients (39.4% of 7396, CI 38.3 - 40.5%). Long-segment BE was present in 54 patients (1.8%, CI 1.4 - 2.3%) in other 2856 cases the short-segment BE was present (98.2%, CI 97.7 -98.6%).
Among all the cases (7396) the gastric metaplasia was evaluated in 876 cases (11.9%, CI 11.1 -12.6%), in 1970 cases the specialized intestinal metaplasia without dysplasia was found (26.6%, CI 25.6
- 27.6%). From all the cases (7396) in 48 cases the low-grade dysplasia of the specialized intestinal metaplasia (Fig. 1) was detected (0.65%, CI 0.48 - 0.85%), in 16 cases the high-grade dysplasia of the specialized intestinal metaplasia (0.22%, CI 0.12 - 0.34%) was found. Esophageal adenocarcinoma was evaluated in four patients (0.05%, CI 0.01 - 0.12%) (fig. 1).
Fig. 1. BE with low-grade dysplasia. Stained with hematoxylin and eosin. x100 magnification.
Fig. 2. The results of videoesophagogastroscopies of esophageal mucosa.
Fig. 3. EAC in the setting hematoxylin-eosin. x200 magnification.
of BE. Stained with
It the study the frequency of EAC detection was 0.05%. All those four cases of EAC were primarily diagnosed (fig. 3). There was no data of the previous changes in esophageal epithelium for the further analysis. It can be expected that there might be a couple of possible sources for EAC. Among them there are cells from the area of epithelium metaplasia, esophageal cardiac glands and their ducts, esophageal stem cells.
The probability of cancer progression for patients with nondysplastic BE with gastric type of metaplasia is 0.5% per year, for patients with nondysplastic BE with intestinal type of metaplasia is 0.2% per year. For patients with low-grade dysplasia the probability of progression of BE to cancer is 8.33% per year, for patients with highgrade dysplasia the probability of neoplastic progression is 25% per year and for patients without metaplasia - 0.09% per year. Noteworthy is the high probability of transformation of metaplasic epithelium with dysplasia into adenocarcinoma.
BE is the condition in which a metaplastic columnar epithelium replaces the stratified squamous epithelium that normally lines the distal esophagus.The metaplastic epithelium is acquired as a consequence of chronic gastroesophageal refluxe disease, and is a predisposing factor for the development of EAC.
Frequency of detection of Barrett's esophagus depends on the frequency of biopsy taking and the level of informative videoesophagogastroscopy. Incidence rates of esophageal adenocarcinoma among patients with the different types of BE are variable.
Recent studies have indicated a lower incidence rate of EAC in individuals with BE than earlier
studies.
Holmberg D. et al. found that among 7932 participants with BE and 18,415 person-years of follow-up, the overall incidence of EAC was 1.47 (95% CI 0.91-2.02) per 1000 person-years [5].
Liu S. et al. presented large-scale longitudinal clinical and histological data on 5401 esophageal cancers patients diagnosed during the 10-year period. All 217 EAC patients from these 5401 esophageal cancers patients were examined for better understanding of the relationship between BE and EAC. They found that EAC was relatively rare and accounted for approximately 5% of all esophageal cancers each year during 2002-2011. Only 10 out of 217 (4.6%) EAC cases had any evidence of BE [9].
In western countries BE is generally considered to be the premalignant condition for EAC. The risk of malignant progression has been examined in over 8,500 patients with BE with using the Northern Ireland BE Register and followed-up for a mean of 7 years [1]. Patients with specialized intestinal metaplasia had the combined incidence 0.38% per year.
In a nationwide population-based cohort study that included all patients with BE collected in Denmark in the period from 1992 to 2009 the relative risk of EAC among patients with BE, compared with the risk in the general population, was 11.3 and the annual risk of esophageal EAC was 0.125 [6]. Some large population-based studies indicated that BE remained a strong risk factor for EAC, but the absolute
annual risk was remarkably lower than the previously assumed risk of 0.5%, and suggested that current surveillance guidelines should be revised [7].
Our data provide the evidence of the rare occurrence of EAC.
Mortality in the overwhelming majority of BE patients is not related to EAC but is rather due to non-esophageal malignancies and cardiovascular disorders [3, 11].
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According to the data we have received, the range of EAC was 0.5%. Low probability of esophageal adenocarcinoma formation in all types of metaplasia was demonstrated. Therefore, only the presence of dysplasia of metaplastic epithelium should cause increased alertness for the occurrence of esophageal adenocarcinoma.
Consequently, the Barrett's esophagus without dysplasia should not be qualified as a pre-malignant condition. The wrong evaluation of this condition leads to misguided patients' management with additional biopsies, mini-endoscopic surgeries. Those procedures may result in additional traumatization of mucosa, increase the risk of bleeding and stenosis, lead to financial expenses and have psycho-emotional load for patients.
1. Bhat S, Coleman HG, Yousef F, Johnston BT, McManus DT, Gavin AT, Murray LJ. Risk of malignant progression in Barrett's esophagus patients: results from a large population-based study. J Natl Cancer Inst. 2011; 103(13): 1049-57. https://doi. org/10.1093/j nci/dj r203
2. Desai TK, Krishnan K, Samala N, Singh J, Cluley J, Perla S, Howden CW. The incidence of oesophageal adenocarcinoma in non-dysplastic Barrett's oesophagus: a meta-analysis. Gut. 2012; 61(7): 970-6. https://doi.org/10.1136/gutjnl-2011-300730
3. Erichsen R, Horvath-Puho E, Lund JL, Dellon ES, Shaheen NJ, Pedersen L, Davey Smith G, Sorensen HT. Mortality and cardiovascular diseases risk in patients with Barrett's oesophagus: a population-based nationwide cohort study. Aliment Pharmacol Ther. 2017; 45(7): 973-982. https://doi.org/10.1111/apt.13962
4. Fitzgerald RC, di Pietro M, Ragunath K, Ang Y, Kang JY, Watson P, et al. British Society of Gastroenterology guidelines on the diagnosis and management of Barrett's oesophagus. Gut. 2014; 63(1): 7-42. https://doi.org/10.1136/gutjnl-2013-305372
5. Holmberg D, Ness-Jensen E, Mattsson F, El-Serag H.B., Lagergren J. Risk of oesophageal adenocarcinoma in individuals with Barrett's oesophagus. Eur J Cancer. 2017; 75: 41-46. https://doi.org/10.1016Zj.ejca.2016.12.037
6. Hvid-Jensen F, Pedersen L, Drewes AM, Sorensen HT, Funch-Jensen P. Incidence of adenocarcinoma among patients with Barrett's esophagus. N Engl J Med. 2011; 365(15): 1375-83. https://doi.org/10.1056/NEJMoa1103042
7. Kahrilas PJ. The problems with surveillance of Barrett's esophagus. N Engl J Med. 2011; 365(15): 1437-8. https://doi.org/10.1056/NEJMe1108435.
8. Kestens C, Leenders M, Offerhaus GJ, van Baal JW, Siersema PD. Risk of neoplastic progression in Barrett's esophagus diagnosed as indefinite for dysplasia: A nationwide cohort study. Endoscopy. 2015; 47: 409-414. https://doi.org/10.1055/s-0034-1391091
9. Liu S, Dai JY, Yao L, Li X, Reid B, Self S et al. Esophageal Adenocarcinoma and Its Rare Association with Barrett's Esophagus in Henan, China. PLoSOne. 2015; 10(4): e0127135. https://doi.org/10.1371/journal.pone.0110348
10. Ma M, Shroff S, Feldman M, DeMarshall M, Price C, Tierney A, Falk GW. Risk of malignant progression in Barrett's esophagus indefinite for dysplasia. Dis. Esophagus. 2017; 30: 1-5. https://dx.doi.org/10.1093%2Fdote%2Fdow025
11. Pines G, Dickman R, Niv Y, Kashtan H, Birkenfeld S. Extraesophageal malignancies among patients with Barrett esophagus. J ClinGastroenterol. 2014; 48: e8-e11. https://doi.org/10.1097/MCG.0b013e31828bf26f
12. Sami SS, Dunagan KT, Johnson ML, Schleck CD, Shah ND, Zinsmeister AR et al. A randomized comparative effectiveness trial of novel endoscopic techniques and approaches for Barrett's esophagus screening in the community. Am J Gastroenterol. 2015; 110(1): 148-58. https://doi.org/10.1038/ajg.2014.362
13. Shaheen NJ, Falk GW, Iyer PG, Gerson LB. American College of Gastroenterology. ACG Clinical Guideline: Diagnosis and Management of Barrett's Esophagus. Am J Gastroenterol 2016; 111(1): 30-50. https://doi.org/10.1038/ajg.2015.322
14. Solaymani-Dodaran M, Card TR, West J. Cause-specific mortality of people with Barrett's esophagus compared with the general population: a population-based cohort study. Gastroenterology. 2013; 44(7): 1375-83. https://doi.org/10.1053/j.gastro.2013.02.050
15. Watanabe N, Shimizu M, Kochi T, Shirakami Y, Tanaka T. Esophageal carcinogenes. Op J Pathol. 2014; 4(4): 151-170. http://dx.doi.org/10.4236/ojpathology.2014.44021
1\'фер:ми
РИЗИК ВИНИКНЕННЯ АДЕНОКАРЦИНОМИ ПРИ СТРАВОХОД1 БАРРЕТТА Серга Т.В., Курик О.Г., Яковенко В.О., Ткаченко Р.П.
Проаналiзовано дат 7396
вщеоезофагогастроскопш. При патопстолопчному дослщжент шдтверджено наявшсть метаплазй ештелш стравоходу у 2910 обстежених (39,4%). Шлункова метаплазiя була виявлена у 876 пащентв (11,9%), у 1970 випадках виявлена спецiалiзована кишкова метаплазiя ештелто стравоходу без дисплазй (26,6%), у 48 випадках виявлена дисплазiя низького ступеня (0,65%), у 16
РИСК ВОЗНИКНОВЕНИЯ АДЕНОКАРЦИНОМЫ ПРИ ПИЩЕВОДЕ БАРРЕТТА Серга Т.В., Курик Е.Г., Яковенко В.А., Ткаченко Р.П.
Проанализированы данные 7396
видеоэзофагогастроскопий. При патогистологическом исследовании подтверджено наличие метаплазии эпителия пищевода у 2910 обследованных (39,4%). Желудочная метаплазия была выявлена у 876 пациентов (11,9%), в 1970 случаях определена специализированная кишечная метаплазия эпителия пищевода без дисплазии (26,6%), в 48 случаях определена дисплазия низкой степени (0,65%), в 16
випадках - дисплазiя високого ступеня (0,22%). Аденокарциному стравоходу встановлено у 4 пащентсв (0,05%, Д1 0,01-0,12%). Продемонстровано низьку ймовiрнiсть виникнення аденокарциноми при вах типах метаплазп еттелто стравоходу. Лише наявшсть дисплазп метаплазованого еттелто повинна викликати пiдвищену настороженiсть щодо виникнення аденокарциноми. Стравохiд Барретта без дисплазй не повинен розцiнюватися як передраковий стан. Перебшьшення його значення призводить до додатково! травматизацп слизово!, пiдвищення ризику кровотеч та стенозiв.
Ключовi слова: стравохiд Барретта, метаплазiя, дисплазiя, аденокарцинома стравоходу.
Стаття надшшла 15.03.2019 р.
случаях - дисплазия высокой степени (0,22%). Аденокарциному пищевода диагностировано у 4 пациентов (0,05%, ДИ 0,01-0,12%). Была продемонстрирована низкая вероятность возникновения аденокарциномы при всех типах метаплазии. Только наличие дисплазии метаплазированного эпителия должно вызывать повышенную настороженность в отношении возникновения аденокарциномы. Пищевод Барретта без дисплазии не должен оцениваться как предраковое состояние. Преувеличение его значения приводит к дополнительной травматизации слизистой, повышению риска кровотечений и стенозов.
Ключевые слова: пищевод Барретта, метаплазия, дисплазия, аденокарцинома пищевода.
Рецензент Срошенко Г. А.
DOI 10.26724/2079-8334-2020-1-71-124-128 UDC 616.31:615.24
P.N. Skrypnykov. T.P. Skrypnikova. G.A. Lobaii. O.V. (¡audio, L.M. Khavalkina, S.V. Zezekalo
I k|ainian Medica| Slomalo|ogica| \iademv. I o|lava
EFFECT OF NATURAL MINERAL BISCHOFITE CONTAINING PREPARATION
ON THE ORAL MICROFLORA
e-mail: ludmila_khavalkina@dentaero.com
The oral cavity can be considered as an ecological system complex in which external factors (biological, individual, social) interact with internal ones (periodontium, bacterial community, local immune system, oral epithelium). If the favorable conditions arise, one or another disease of the oral mucosa may be developed and must be adequately treated. The arsenal of drugs is large and requires the doctor's knowledge, skills in using of the most optimal means and providing the appropriate recommendations to the patient. We studied the efficacy of the oral care product Antiqua Mare MAX, containing natural mineral Poltava's Bischofite, on the representatives of the oral microflora. To achieve this goal, museum strains of E. coli ATCC 25922, S. aureus ATCC 25923, S. epidermidis ATCC 14990, E. faecalis ATCC 29212, M. lysodeicticus ATCC 4698 and C. albicans ATCC1023 were used. As a control, a well-known antimicrobial agent 0.02% aqueous solution of chlorhexidine bigluconate was used. The ability of the Antiqua Mare MAX drug to inhibit the growth of museum cultures of the yeast-like fungi, colon bacilli, enterococci, micrococci, epidermal and golden staphylococci in the liquid medium was shown to coincide completely in three repeated determinations during the study of the effect of Bischofite containing oral care product. The fungiostatic activity of the studied preparation Antiqua Mare MAX exceeded the effect of 0.02% solution of chlorhexidine bigluconate by 4 times (p<0,001), but the fungicidal effect did not differ.
Keywords: OCMM microflora, chlorhexidine bigluconate, Antiqua Mare MAX.
The work is a fragment of the research project "Dental health restoration in patients with underlying diseases and their rehabilitation", state registration No. 0116U004191.
Oral mucosa diseases are common lesions of the human body among dental diseases. They reflect changes in organs and tissues of the body. Notwithstanding the diversity of causes, mechanisms of development and clinical course of the disease, the majority of these diseases are characterized by some common features that can be combined into separate related groups.
The oral microflora is represented by numerous types of aerobic and anaerobic bacteria, among which anaerobes dominate (in dental plaque the anaerobic/aerobic ratio is 1000/1) [7]. The permanent oral microflora is composed of representatives of several groups of microorganisms: bacteria, fungi, spirochetes, protozoa, viruses. The role of microorganisms in the development of periodontitis, candidiasis, ulcerative necrotic gingivitis, etc., is undoubtful [5]. The development of oral inflammatory diseases alters composition of the microflora of different biotopes that are part of the oral cavity [10].
The oral cavity can be considered as a complex ecological system in which the external factors (biological, individual, social) interact with internal ones (periodontal, bacterial community, local immune system, oral epithelium) [9]. Similar to the outer environment, all components of the system are in dynamic equilibrium.
In case of favorable conditions, any of the oral diseases, which required treatment, may develop [9]. The drug arsenal is large and requires the dental professional to be expert in their usage and giving recommendations.
Jardin Cosmetics LLC (Ukraine) has developed the oral care product Antiqua Mare MAX that is composed from natural products only: Poltava's Bischofite mineral complex, propolis, decoctions of stevia leaves, liquorice, oak bark (Sanitary-Hygienic Official Letter No. 602-123-20-1/781 as of 21.01.2019).
© P.N. Skrypnykov, T.P. Skrypnikova, 2020 124
