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Collagenous Gastritis: a Case Report Kolagenozni Gastritis – Prikaz Primera

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Collagenous Gastritis: a Case Report Kolagenozni Gastritis – Prikaz Primera Klinični primer Metabolne in hormonske motnje METABOLNE IN HORMONSKE MOTNJE Collagenous gastritis: A case report Kolagenozni gastritis – Prikaz primera Marija Malgaj, Nina Zidar,1 Nejc Sever2 1 Inštitut za patologijo, Abstract Medicinska fakulteta Background: Collagenous gastritis is a rare disease defined histologically by the subepithelial de- Ljubljana position of collagen bands thicker than 10 μm and the infiltration of inflammatory mononuclear 2 Klinični oddelek za cells in the lamina propria. There are approximately 60 reported cases of collagenous gastritis in the gastroenterologijo, English literature. Univerzitetni klinični center Ljubljana Case report: We present a 41-year-old female patient with weight loss, postprandial abdominal dis- comfort, early satiety, flatulence and a change in bowel habits. Her current laboratory investigation Korespondenca/ reports showed mild sideropenic anemia. Esophagogastroduodenoscopy and the corresponding his- Correspondence: tological examination showed findings, typical for collagenous gastritis. Gastric emptying scintigra- Marija Malgaj, phy and SPECT/CT of the abdomen revealed gastroparesis. e: [email protected] Conclusion: Collagenous gastritis is a diagnostically challenging disease and its exact etiology re- Ključne besede: mains unclear. Even though collagenous gastritis is a histological diagnosis, the combination of other odlaganje kolagena; key clinical and endoscopic findings should prompt consideration of this entity. No safe and effective hujšanje; dispepsija; treatment has been established. Therefore, better understanding of the disease and study of a larger anemija; nodularna number of patients will help to establish diagnostic criteria and therapeutic strategies. želodčna sluznica Key words: Izvleček collagen deposition; weight loss; dyspepsia; Izhodišča: Kolagenozni gastritis je redka bolezen, pri kateri najdemo v histološki sliki pomnoženo anemia; nodular gastric kolagenizirano vezivo pod epitelom (debeline vsaj 10 μm) in monojedrnocelični infiltrat v lamini mucosa propriji. V angleški literaturi je do sedaj opisanih približno 60 primerov kolagenoznega gastritisa. Citirajte kot/Cite as: Prikaz primera: V prispevku je prikazan primer 41-letne bolnice, obravnavane zaradi hujšanja, ne- Zdrav Vestn. 2016; lagodja po jedi, prezgodnjega občutka sitosti, napenjanja in sprememb v odvajanju blata. Laborato- 85: 296–302 rijski izvidi so razkrili sideropenično anemijo. Izvida ezofagogastroduodenoskopije in pripadajoče histološke preiskave sta bila značilna za kolagenozni gastritis. Scintigrafija hitrosti praznjenja želod- Prispelo: 24. mar. 2016, ca in SPECT/CT trebuha sta pri bolnici odkrili še gastroparezo. Sprejeto: 12. maj 2016 Zaključek: Kolagenozni gastritis je diagnostično zahtevna bolezen, njegova etiologija pa ostaja ne- pojasnjena. Čeprav je diagnoza kolagenoznega gastritisa histološka, moramo nanjo pomisliti, če od- krijemo ključne klinične in endoskopske znake. Zaenkrat še ne poznamo varnega in učinkovitega zdravljenja. Za oblikovanje diagnostičnih meril in razvoj učinkovitega zdravljenja bi bilo potrebno boljše razumevanje bolezni in raziskave na večjem številu bolnikov. Background Collagenous gastritis (CG) is a rare of inflammatory mononuclear cells in disease defined histologically by the su- the lamina propria.1,2 CG has similar bepithelial deposition of collagen bands histological characteristics as collageno- thicker than 10 μm and the infiltration us colitis and collagenous sprue and are 296 Zdrav Vestn | april 2016 | Letnik 85 KLinični PRIMER cal therapy so far. She was referred to a gastroenterologist for further evaluation. On examination a decreased body mass index of 16.8 was found. Her la- boratory values showed a mild sidero- penic anemia. We diagnosed lactose intolerance (low lactase levels in duode- nal mucosa and a positive blood lactose tolerance test) and she was given proper diet counseling. We excluded celiac dise- ase and other immune-related disorders. Previously reported elevated total IgE levels were now normal. She underwent esophagogastroduodenoscopy, which showed nodularity (Fig. 1) and oedema of the gastric corpus and antrum. Duo- denal bulb mucosa exhibited a diffuse cobblestone appearance. Biopsies were taken from the stomach according to Figure 1: Nodular thought to be part of the same disease the Sydney protocol and from the duo- appearance of the stomach mucosa on entity – collagenous gastroenteritides.1 denum. Histological examination of ga- gastroscopy. While there are many published cases of stric biopsies showed a thickened sube- collagenous colitis, there are only 60 re- pithelial layer in the corporal and antral ported cases of CG in the English litera- mucosa (Fig. 2) with associated gastritis. ture since the disease was first identified The inflammatory infiltrate was predo- by Colletti and Trainer in 1989.1,3 In con- minantly lymphoplasmacytic. The sube- trast to collagenous colitis, the course of pithelial collagenous layer stained blue CG is unpredictable and the optimal tre- with Masson trichrome stain (Fig. 3) and atment has yet to be defined. We present was more than 20 μm thick, suggesting a patient with CG. the diagnosis of CG. Immunohistoche- mistry for Helicobacter pylori was negati- Case report ve. Histological examination of the duo- denal biopsies showed a non-specific A 41-year-old Caucasian woman chronic inflammation, but staining with presented with a history of progressive Masson trichrome stain did not show a weight loss, postprandial abdominal di- thickened subepithelial layer of connec- scomfort, early satiety, flatulence and a tive tissue. In addition to esophagoga- change in bowel habits. She has previo- stroduodenoscopy, she also underwent usly been diagnosed with an eating di- colonoscopy: macroscopic appearance sorder (anorexia nervosa) and has been of the mucosa was normal, however, treated by a psychiatrist with cognitive histological examination of the biopsy behavioral therapy. While her treatment samples showed mild inflammation, but was reported successful and she mana- it was not diagnostic for collagenous co- ged to gain some weight and menstru- litis. Furthermore, we performed gastric al cycle (although irregular) her other emptying scintigraphy and SPECT/CT symptoms mainly persisted. She has not of the abdomen, which revealed delayed been maintained on any pharmacologi- emptying from the fundus and corpus of Collagenous gastritis: A case report 297 METABOLNE IN HORMONSKE MOTNJE mens before starting a more aggressive therapeutic approach (e.g. steroids). We plan to do the first follow-up endosco- pic investigation in about one year after the initial diagnosis. The lack of possi- ble etiopathogenic factors remains the main problem, which disables us to start causal treatment (e.g. treatment of concurrent immune-related disorders, discontinuation of certain drugs). Our current conclusion is that the patient’s symptoms and clinical findings are most likely multifactorial – a combi- nation of the relapsing eating disorder, functional gastrointestinal disorder (ir- ritable bowel syndrome), gastroparesis and CG. The correlation and causality between these entities, if any at all, is unclear and will be hard to prove. Mul- Figure 2: Increased the stomach, thus suggesting gastropare- tidisciplinary approach will be needed collagenous fibrous tissue beneath the sis. in the future to form a proper treatment surface epithelium in After reviewing the literature and strategy. the biopsy sample from excluding all potentially reversible fac- the antral mucosa. Hematoxylin and eosin, tors, which might influence and/or ca- Discussion orig. magn. 20x. use CG (e.g. immune-related disorders, specific drugs), we have decided to start Etiology and pathogenesis of CG a trial with a proton pump inhibitor is unknown, but autoimmune mecha- for symptom relief. Treatment of side- nisms, drugs and infection have been ropenic anemia with oral iron supple- postulated as possible etiopathoge- ments was ineffective, but was resolved nic factors.2,4,5 CG has been descri- after parenteral iron supplementation. bed in patients with immune-related Because of suspected gastroparesis she disorders, including celiac disease,6,7 was also started on a short-term the- Sjögren syndrome,8 systemic lupus rapy with a prokinetic agent: first with erythematosus,9 common variable im- metoclopramide and later with dom- mune deficiency (CVID),10 lymphocytic peridone. She discontinued the use gastritis, lymphocytic colitis and ulcera- of both shortly after receiving each of tive colitis,2 Hashimoto thyroiditis and them because of adverse effects. Over a polymyositis,11 juvenile arthritis, rheu- few weeks of follow-up, her symptoms matoid arthritis, Graves disease and dia- have not improved. She still complains betes mellitus type 1.12 Collectively, these of postprandial abdominal discomfort, associations support the hypothesis that while her weight is now stable. Because collagenous gastroenteritides might be of the unclear natural history of CG and related to immune mechanisms.13,14 A no standard therapy regimens, we have subset of CG cases may be attributed to decided to do follow-up esophagoga- drugs, such as olmesartan, an angioten- stroduodenoscopies with a histological sin II receptor blocker,15 and venlaflaxi- examination of corresponding speci- ne, an antidepressant.12 298 Zdrav Vestn | april 2016 | Letnik 85 KLinični PRIMER Interestingly, the nodular lesions repre- sent the undamaged mucosa, and the depressed areas surrounding
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