Is Gastric Involvement by Strongyloides stercoralis in an Immunocompetent Patient a Common Finding? A Case Report and Review of the Literature

Purpose Gastric infection with Strongyloides stercoralis (SS) usually occurs in immunocompromised patients. The unexpected observation of this parasite in an otherwise healthy young lady who had undergone upper endoscopy and biopsy sampling of the gastro-duodenal mucosa, prompted us to review the literature to ascertain the conditions favouring gastric colonization by SS. Methods Pathology files of gastroduodenal biopsies received at St. Mary’s hospital, Northern Uganda, between 2007 and 2017 were reviewed. Pubmed search was performed under the headings “Strongyloides stercoralis”, “Gastric parasitosis”. Results Histology of the only gastroduodenal biopsy with SS infection showed parasite eggs, immature rhabditiform larvae, and numerous adult worms in gastric pits and rhabditiform larvae in interepithelial parasitic tunnels, causing reactive changes of the glandular epithelium. There was no significant acute inflammatory cell infiltrate surrounding the parasites. Literature review showed that gastric SS infection appears to be very uncommon and was, as expected, largely prevalent in immunodeficient individuals (84.2% of published cases). The rare gastric SS infection is a complication of systemic strongyloidiasis, either hyperinfective, or disseminated form. It is also commonly associated with duodenal infection at microscopical examination. Conclusion Involvement of gastric mucosa in the absence of duodenal strongyloidiasis appears to be quite rare and false-negative histopathological exams are reported if only the stomach is biopsied.

P150 Histologic features predicting prognosis and their relationship with endoscopic findings in Ulcerative Colitis patients with mucosal healing

Background Mucosal healing (MH) is one of the treatment targets in patients with ulcerative colitis (UC). However, it has been suggested that even in patients with MH, disease prognosis depends on histologic activity. This study aimed to evaluate histologic features predicting disease prognosis and their relationship with endoscopic findings in UC patients with MH. Methods We retrospectively reviewed the data of patients with UC who underwent colonoscopy or sigmoidoscopy with biopsy and evaluated eight histological features, including chronic inflammatory infiltrate, neutrophils in epithelium, ulceration, acute inflammatory cell infiltrate, basal plasmacytosis and serrated architectural abnormalities, as well as Nancy index (NI). Histologic variables predicting disease progression defined as starting corticosteroid, biologics, or small molecule agent, or undergoing clinical relapse or surgical operation were evaluated, and correlated with endoscopic findings. Results A total 194 biopsy specimens of 103 patients were evaluated. The highest grades of each histologic item were analyzed when biopsies were performed at multiple sites in one patient. 30.6% showed NI ≤ 1 (no acute inflammatory infiltrate) in 49 patients with endoscopic remission. Among 68 patients with MH, only 24.8% achieved NI ≤ 1. Mucosal friability in endoscopic findings was significantly associated with moderate-to-severe active histologic status (NI ≥3) (46.2% vs 80.0%, P=0.013), and patients with NI ≥3 showed significantly higher rates of disease progression during 13.7-month follow-up period (5.1% vs 19.0%, P=0.21). Ulceration and serrated architectural abnormalities were significantly associated with disease progression, and serrated architectural abnormalities was an independent risk factor in multivariate analysis (odds ratio 2.691 (95% confidence interval: 1.047–6.915), P=0.04). Conclusion Mucosal friability in endoscopic findings reflects moderate-to-severe active histologic status, and presence of serrated architectural abnormalities predicts disease progression in UC patients with MH. These findings may help identify patients need closer monitoring.

Comparison of Ischemic Preconditioning and Systemic Piracetam for Prevention of Ischemia-Reperfusion Injury in Musculocutaneous Flaps

Background Ischemia-reperfusion injury plays an important role in flap failure. Ischemic preconditioning technique is the only proven method for preventing ischemia-reperfusion injury, but it is not used widely in daily practice because of difficulties such as prolonging the operation time, need for surgical experience, and increasing the risk of complications. This study has been performed with the assumption that piracetam may be a simple and inexpensive alternative to the preconditioning technique due to its antioxidant, antiaggregant, rheological, anti-inflammatory, antiapoptotic, cytoprotective, and immune modulating effects. Methods Thirty-two rats were divided into four groups and latissimus dorsi musculocutaneous flaps were raised. No extra procedure was applied, and no treatment was given to the control group. Four hours of ischemia was created by clamping the thoracodorsal pedicle in the second group. The animals in the third group were treated with 10 minutes of ischemia and reperfusion periods as a preconditioning procedure before the 4 hours of ischemia. Animals in the fourth group received systemic piracetam 30 minutes before and 6 days after reperfusion. Nitric oxide and myeloperoxidase levels in serum and tissue, acute inflammatory cell response, and vascular proliferation in tissue were examined at the postoperative 24th hour and 10th day. Results Myeloperoxidase activity in both preconditioning and piracetam groups, was significantly lower than the ischemia-reperfusion group. Acute inflammatory cell response was similarly decreased in both preconditioning and piracetam groups compared with ischemia-reperfusion group. Tissue measurements of nitric oxide were also significantly higher in both preconditioning and piracetam groups than in the ischemia-reperfusion group. However, vascular proliferation increased in the preconditioning group, while it did not show any significant change in the piracetam group. Conclusion This study shows that systemic piracetam treatment provides protection against ischemia-reperfusion injury in musculocutaneous flaps and can offer a simple and inexpensive alternative to the preconditioning technique.

Isolated intraventricular conduction delay in fulminant myocarditis: A case report

Introduction: Fulminant myocarditis is uncommon. Making the diagnosis in the emergency department is difficult due to the nonspecific clinical presentation and electrocardiogram results. Case presentation: A 58-year-old Chinese woman presented to an emergency department with dizziness and malaise for 2 days. She was hypotensive and afebrile. Initial electrocardiogram showed isolated nonspecific intraventricular conduction delay. Despite resuscitation, she rapidly deteriorated in the emergency department and eventually succumbed. Autopsy and histological examination of heart muscle found acute inflammatory cell infiltration and multifocal necrosis, suggestive of acute fulminant myocarditis. Discussion: There is a wide range of differential diagnosis of nonspecific intraventricular conduction delay. Clinical presentation of mycoarditis is also often non-specific. Rapid and accurate recognition of the condition is essential to save life. Conclusion: Fulminant myocarditis presenting with cardiogenic shock and isolated intraventricular conduction delay on electrocardiogram poses a diagnostic challenge as illustrated in this case report.

Inhibition of JNK activation prolongs survival after smoke inhalation from fires

Initial injury from smoke inhalation is mainly to the trachea and bronchi and is characterized by mucosal hyperemia and increased microvascular permeability, exfoliation of epithelial lining, mucous secretion, mucous plugging, and an acute inflammatory cell influx. In this study, we explore the role of the c-Jun N-terminal protein kinase (JNK) pathway in smoke inhalation lung injury using a rat model of exposure to smoke from burning cotton. Male Sprague-Dawley rats were exposed to smoke from burning cotton for 15 min, and 1 h after injury a JNK inhibitor (SP-600125) or vehicle was injected. We measured neutrophil influx, cytokine release, percent of apoptotic cells, airway plugging, and survival. Administration of a JNK inhibitor 1 h after smoke inhalation decreased airway apoptosis, mucous plugging, influx of inflammatory cells, and the release of cytokines and significantly prolonged animal survival ( P < 0.05). These in vivo data show that the JNK pathway plays a critical role in smoke-induced lung injury and offer an attractive therapeutic approach for this injury.