Midenin Nonneoplastik Hastalıklarında Patoloji
Özet
Mide hastalıkları klinik pratikte sık karşılaşılan inflamatuar ve neoplastik süreçleri kapsamakta olup, doğru tanı için klinik, endoskopik ve histopatolojik bulguların birlikte değerlendirilmesi esastır. Günümüzde gastritlerin sınıflandırılmasında morfolojik, topografik ve etiyolojik kriterleri esas alan "Güncelleştirilmiş Sydney Sistemi" yaygın olarak tercih edilmektedir. Akut hemorajik ve eroziv gastrit, alkol, NSAİİ kullanımı veya ağır stres faktörlerine bağlı olarak gelişen geçici inflamatuar süreçleri ve epitel hasarını tanımlar. Kronik gastrit vakalarının en önemli etiyolojik ajanı olan Helicobacter pylori, mukoza ilişkili lenfoid doku (MALT) lenfoması ve mide kanseri gelişimi ile yakından ilişkilidir. Bu enfeksiyon, mukoza epitelinde nötrofilik ve lenfoplazmositer infiltrasyonun yanı sıra lenfoid folikül oluşumuna yol açar. Diğer taraftan, otoimmün gastrit, parietal hücreleri ve intrinsik faktörü hedef alarak oksintik mukozanın diffüz atrofisine, hipergastrinemiye ve B12 vitamini eksikliğine (pernisiyöz anemi) neden olan kronik iltihabi bir hastalıktür. Mide biyopsilerinde nadiren saptanan granülomatöz, eozinofilik ve lenfositik gastritler ise spesifik etiyolojik faktörlere veya sistemik hastalıklara bağlı olarak gelişim gösterir. Peptik ülser hastalığı ise çoğunlukla H. pylori enfeksiyonu ve NSAİİ kullanımı zemininde, asit-pepsin etkisi ile mukozal savunma arasındaki dengesizliğin submukozaya uzanan lokal epitel defektleri oluşturmasıyla karakterizedir.
Gastric diseases encompass inflammatory and neoplastic processes frequently encountered in clinical practice, and a definitive diagnosis strictly requires the concurrent evaluation of clinical, endoscopic, and histopathological findings. Today, the "Updated Sydney System," which bases its criteria on morphological, topographic, and etiological features, is widely preferred for classifying gastritis. Acute hemorrhagic and erosive gastritis describes transient inflammatory processes and epithelial injury triggered by alcohol, NSAID use, or severe stress factors. As the primary etiological agent in chronic gastritis cases, Helicobacter pylori is closely linked to the development of mucosa-associated lymphoid tissue (MALT) lymphoma and gastric cancer. This infection leads to neutrophilic and lymphoplasmacytic infiltration in the mucosal epithelium, as well as the formation of lymphoid follicles. Conversely, autoimmune gastritis is a chronic inflammatory disorder that targets parietal cells and intrinsic factor, leading to diffuse atrophy of the oxyntic mucosa, hypergastrinemia, and vitamin B12 deficiency (pernicious anemia). Granulomatous, eosinophilic, and lymphocytic gastritis, which are rarely detected in gastric biopsies, develop due to specific etiological factors or systemic diseases. Lastly, peptik ulcer disease is characterized by local epithelial defects extending into the submucosa, caused by an imbalance between acid-pepsin activity and mucosal defense, mostly secondary to H. pylori infection and NSAID use.
Referanslar
Strickland RG, Mackay I. A reappraisal of the nature and significance of chronic atrophic gastritis.Am J Dig Dis 1973;18:426-440.
Wyatt JI , Dixon MF. Chronic gastritis--a pathogenetic approach. J Pathol 1988;154:113-124.
Dixon MF, Genta RM, Yardley JH, Correa P. Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994. Am J Surg Pathol 1996;20:1161–81.
Appelman HD. Gastritis: Terminology, etiology, and clinicopathological correlations: Another biased view. HUMAN PATHOLOGY 1994;25;1006-1019.
Chamberlain CE. Acute hemorrhagic gastritis. Gastroentero Clin North Am 1993;22:843-873.
Marshall B, Armstrong J, McGechie D, Glancy R. Attemptto fulfill Koch’s postulate for pyloric Campylobacter. Med J Austr 1985;142:436–9.
Ozaydin N, Turkyilmaz SA, Cali S. Prevalence and risk factors of helicobacter pylori in Turkey: a nationally-representative, cross-sectional, screening with the 13C-Urea breath test. BMC Public Health 2013;13:1215.
Veijola L, Oksanen A, Linnala A et al. Persisting chronic gastritiis and elevated helicobacter pylori antibodies after successful eradication therapy. Helicobacter. 2007;12:605-608 .
Moss SF, Legon S, Bishop AE, et al. Effect of helicobacter pylori on gastric somatostatin in duodenal ulcer dissease. Lancet. 1992;340:930-932.
Uemura N, Okamoto S, Yamamoto S, et al. Helicbacter pylori infection and development of gastric cancer. N.Engl J Med 2001;345:784-789.
Ohkusa T, Fujiki K, Takashimizu I, et al. İmprovement atrophic gastritis and intestinal metplasia in patients in whom Helicobacter pylori was eradicated. Ann Intern Med 2001;134:380-386 .
Oliva MM, Lazenby AJ, Perman JA. Gastritis associated with Gastrospirillum hominis in children. Comparison with helicobacter pylori and review of the literature. Mod Pathol 1993;6:513-515.
Singhal AV, Sepulveda AR. Helicobacter heilmannii gastritis: a case study with review of literature. Am J Surg Pathol 2005;29:1537-1539.
Kusters JG, van Vliet AH, Kuipers EJ. Pathogenesis of helicobacter pylori infection. Clin Microbiol Rev 2006;19:449-490.
Lahner E , Conti L , Cicone F et al. Thyro-entero-gastric autoimmunity: Pathophysiology and implications for patient management. Best Pract Res Clin Endocrinol Metab 2020;34(1):101373.
Torbenson M, Abrahan SC, Boitnott J, et al. Autoimmun gastritis: distinct histological and immunohistochemical findings before complete lose of oxyntic glands. Mod Pathol 2002;15:102-109.
Sirivastava A, Lauwers GY. Pathology of non infective gastritis. Histopathology 2007;50:15-29.
Park JY, Cornish TC, Lam-Himlin D, et al. Gastric lesions in patients with autoimmune metaplastic atrophic gastritis (AMAG) in a tertiary care setting. Am J Surg Pathol 2010;34:1591-1598.
Maeng L, Lee A, Choi K, et al. Granulomatous gastritis: a clinicopathologic analysis of 18 biopsy cases. Am J Surg Pathol. 2004;28:941-945.
Rashid AM, Williams RM. A new differential diagnosis in granulomatous gastritis. Histopathology 1992;20:280-281.
