Old and New Aspects of H. pylori-Associated Inflammation and Gastric Cancer

H. pylori is involved in the development of 80% of gastric cancers and 5.5% of all malignant conditions worldwide. Its persistence within the host’s stomach causes chronic inflammation, which is a well-known hallmark of carcinogenesis. A wide range of cytokines was reported to be involved in the initiation and long-term persistence of this local and systemic inflammation. IL-8 was among the first cytokines described to be increased in patients with H. pylori infection. Although, this cytokine was initially identified to exert a chemoattracting effect that represents a trigger for the activation of inflammatory cells within H.-pylori-infected mucosa, more recent studies failed in encountering any association between IL-8 and H. pylori infection. IL-6 is a multifunctional, pleiotropic and multipotent cytokine involved in mediating the interaction between innate and adaptive immunity with a dichotomous role acting as both a proinflammatory and an anti-inflammatory cytokine depending on the signaling pathway. IL-1α functions as a promoter of angiogenesis and vascular endothelial cell proliferation in gastric carcinoma since it is closely related to H.-pylori-induced inflammation in children. IL-1β is an essential trigger and enhancer of inflammation. The association between a low IL-1β level and an increased TNF-α level might be considered a risk factor for peptic ulcer disease in the setting of H. pylori infection. IL-10 downregulates both cytotoxic inflammatory responses and cell-mediated immune responses. H. pylori uses the immunosuppressive role of IL-10 to favor its escape from the host’s immune system. TGFβ is a continuous inflammatory mediator that promotes the adherence of H. pylori to the host’s cells and their subsequent colonization. The role of H.-pylori-induced inflammatory responses in the onset of gastric carcinogenesis seems to represent the missing puzzle piece for designing effective preventive and therapeutic strategies in patients with H.-pylori-associated gastric cancer

ANEMIA APLASTICĂ – ASPECTE TERAPEUTICE ŞI DEONTOLOGICE

Anemia aplastică este o patologie hematologică severă, potenţial fatală, caracterizată prin citopenie periferică şi măduvă osoasă hipocelulară, cu o prevalenţă de 2-6 cazuri la 1 milion locuitori. Prezentarea actuală ilustrează cazul unui copil de 9 ani, fără antecedente personale patologice cunoscute, şi cu debut brusc, aparent în plină stare de sănătate, diagnosticat cu anemie aplastică idiopatică severă şi cu evoluţie fulminantă. Lipsa de complianţă a părinţilor la actul medical, precum şi lipsa unei legislaţii care să protejeze copilul, au dus la decesul pa cientului într-un interval foarte scurt de timp

Not Every Dyspepsia Is Related to <i>Helicobacter pylori</i>—A Case of Esophageal Inlet Patch in a Female Teenager

Helicobacter pylori infection is one of the main causes of dyspepsia, but it is not the only cause. Esophageal inlet patches are areas of heterotopic gastric mucosa within the esophagus and are commonly located in the cervical part of the esophagus. We report the case of a 16-year-old female, previously known to display symptoms of anxiety, who was admitted to our clinic for dyspeptic symptoms lasting for approximately 1 month in spite of the treatment with proton pump inhibitors. The clinical exam revealed only abdominal tenderness in the epigastric area, while routine laboratory tests showed no abnormalities. The upper digestive endoscopy revealed a well-circumscribed salmon-pink-colored oval lesion of approximately 10 mm in the cervical esophagus, along with hyperemia of the gastric mucosa and biliary reflux. The histopathological exam established the diagnosis of esophageal inlet patch with heterotopic antral-type gastric mucosa and also revealed regenerative changes within the gastric mucosa. We continued to treat the patient with proton pump inhibitors, as well as ursodeoxycholic acid, with favorable evolution. Although rare or underdiagnosed, esophageal inlet patches should never be underestimated and all gastroenterologists should be aware of their presence when performing an upper digestive examination in a patient with dyspeptic symptoms

ABORDAREA TERAPEUTICĂ A BOLII DIAREICE ACUTE LA PACIENTUL PEDIATRIC

Obiective. În abordarea problematicii bolii diareice acute (BDA) la pacientul pediatric, ne-am fixat ca obiectiv principal o evaluare amănunţită a etiologiei şi factorilor de risc şi, pe de altă parte, evaluarea raportului risc/ beneficiu în ceea ce priveşte justificarea antibioterapiei în tratamentul BDA la pacientul pediatric. Material şi metodă. Am efectuat un studiu analitic descriptiv, retrospectiv, pe un lot de 125 pacienţi, internaţi în Clinica Pediatrie I Tg. Mureş pe parcursul anului 2016 (ianuarie-decembrie) cu diagnosticul de boală diareică acută (BDA). Rezultate. Din totalul de 125 de pacienţi, s-a identificat o etiologie bacteriană a BDA în 23 de cazuri (18,4%). Pe de altă parte, s-a observat faptul că 84 de pacienţi au primit tratament antibiotic (67,2%), 110 pacienţi (88%) tratament simptomatic iar în 60% din cazuri (75 pacienţi) s-a asociat şi tratament probiotic. Durata medie de spitalizare a fost de 5 zile, durată influenţată de prezenţa/absenţa unor factori de risc precum febra, sindromul inflamator, tulburările hidroelectrolitice sau sindromul de deshidratare acută, factori care au prelungit perioada de spitalizare cu până la 2 zile (p<0,05). Concluzii. Antibioterapia trebuie utilizată raţional şi justificat în tratamentul BDA, analizând foarte atent raportul risc/beneficiu. Considerând caracterul autolimitant şi prognosticul favorabil al bolii, concluzionăm prin faptul că ne aflăm în faţa unui abuz de antibiotice în cazul pacienţilor pediatrici cu BDA

EVALUAREA TROMBOCITOZEI REACTIVE POSTSPLENECTOMIE LA PACIENTUL PEDIATRIC

Trombocitoza reprezintă creşterea numărului de trombocite peste 500.000/mm³. Obiectiv. Obiectivul acestui studiu este de a evalua frecvenţa şi severitatea trombocitozei reactive la pacienţii pediatrici splenectomizaţi. Material şi metodă. Am realizat un studiu retrospectiv în care au fost incluşi 20 de pacienţi (4-16 ani) care au suferit o intervenţie de splenectomie în intervalul 2006-2015. Criteriile de includere în studiu au fost: pacienţi cu vârsta sub 18 ani, care au fost splenectomizaţi şi care au dezvoltat trombocitoză ulterior intervenţiei. Rezultate. În lotul studiat, 80% dintre pacienţii splenectomizaţi (16) au dezvoltat o formă de trombocitoză; în 4 cazuri formă severă (trombocite > 1milion/mm3), iar în 7 cazuri formă uşoară. Nu s-au observat diferenţe semnificative în repartiţia pe sexe a pacienţilor (9 de sex feminin şi 11 de sex masculin). La 13 dintre pacienţi trombocitoza s-a remis după 30 de zile şi doar în 3 dintre cazuri episodul a durat >360 de zile. Fenomene trombotice s-au observat la un singur pacient din lotul studiat. Toţi pacienţii au beneficiat de măsuri de tromboprofilaxie şi hidratare, iar 2 cazuri au necesitat asociere terapeutică de Hidoxiuree. Concluzii. Studiul nostru relevă o frecvenţă crescută a trombocitozei după splenectomie (80%), cu un vârf maxim de incidenţă la 2-10 zile postchirurgical, trombocitoza fiind în general benignă şi cu remisie spontană; evenimente trombotice s-au semnalat într-un singur caz, iar trombocitoza severă a fost mai frecventă după splenectomia de cauză traumatică

<i>Helicobacter pylori</i>—The Bridge between Local and Systemic Inflammation in Children

Helicobacter pylori (H. pylori)-associated inflammatory status is no longer a debatable topic in children. The aim of our study was to to compare the inflammatory status in pediatric patients with H. pylori gastritis and non-H. pylori gastritis versus control group. We performed a prospective study on 68 children with dyspeptic symptoms which were divided into 3 groups: 14 children with H. pylori gastritis (group 1), 26 children with non-H. pylori gastritis (group 2) and 28 children with no pathological findings—control group (group 3). Several laboratory parameters, histopathological and immunohistochemistry tests were performed in all children for detecting inflammatory status. We noticed a significant difference in terms of rural area between the three groups (p = 0.0404). Comparing the laboratory parameters between the three groups, we noticed significant differences in terms of serological tests (p = 0094), and NLR (p = 0.0253), the latter being significantly higher in children with H. pylori-induced gastritis as compared to those with non-H. pylori gastritis (0.0107). According to the Dunn’s Multiple Comparison Test, we noticed a significantly elevated neutrophil level in children with H. pylori-induced gastritis when compared to non-H. pylori gastritis group (p = 0.0146), as well as a significantly increased eosinophil count in patients with non-H. pylori gastritis as compared to control group (p = 0.0417). The immunohistochemistry method pointed out no significant variation concerning interleukin (IL 6) between children with gastritis and control group [RR = 1.283, IC (95%): 0.9404–1.751, p = 0.0988]. Additionally, children with gastritis regardless of the etiology have a significant risk of associating increased gastric expression of tumor necrosis factor alpha (TNF α) [RR = 3.967; CI (95%): 1.283–12.263; p = 0.0063]. Moreover, TNF α was significantly associated with presence of H. pylori gastritis (p = 0.0002). The early detection of local inflammation triggered by this infection might preempt gastric carcinogenesis, while identifying H. pylori-induced systemic inflammation lowers the risk of severe extraintestinal manifestations