Innate immunity and nonalcoholic fatty liver disease.

Nonalcoholic fatty liver disease (NAFLD), recently renamed as metabolic (dysfunction)-associated fatty liver disease (MAFLD), is a complex, multifactorial disease that progresses via nonalcoholic steatohepatitis (NASH) towards severe liver complications. MAFLD/NAFLD affects up to a third of the global population. It is connected with metabolic syndrome parameters and has been increasing in parallel with the rates of metabolic syndrome parameters worldwide. This disease entity exhibits a strong immune-inflammatory dimension. In MAFLD/NAFLD/NASH, a vast network of innate immune cells is mobilized that can provoke liver damage, leading to advanced fibrosis, cirrhosis and its complications, including hepatocellular carcinoma. However, our understanding of the inflammatory signals that drive the onset and progression of MAFLD/NAFLD/NASH is fragmented. Thus, further investigation is required to better understand the role of specific innate immune cell subsets in the disease, and to aid the design of innovative therapeutic agents to target MAFLD/NAFLD/NASH. In this review, we discuss current concepts regarding the role of innate immune system involvement in MAFLD/NAFLD/NASH onset and progression, along with presenting potential stress signals affecting immune tolerance that may trigger aberrant immune responses. A comprehensive understanding of the innate immune mechanisms involved in MAFLD/NAFLD/NASH pathophysiology will help the discovery of early interventions to prevent the disease, and lead to potential innovative therapeutic strategies that may limit its worldwide burden.

Controlling the Impact of Helicobacter pylori-Related Hyperhomocysteinemia on Neurodegeneration.

Helicobacter pylori infection consists a high global burden affecting more than 50% of the world's population. It is implicated, beyond substantiated local gastric pathologies, i.e., peptic ulcers and gastric cancer, in the pathophysiology of several neurodegenerative disorders, mainly by inducing hyperhomocysteinemia-related brain cortical thinning (BCT). BCT has been advocated as a possible biomarker associated with neurodegenerative central nervous system disorders such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, and/or glaucoma, termed as "ocular Alzheimer's disease". According to the infection hypothesis in relation to neurodegeneration, Helicobacter pylori as non-commensal gut microbiome has been advocated as trigger and/or mediator of neurodegenerative diseases, such as the development of Alzheimer's disease. Among others, Helicobacter pylori-related inflammatory mediators, defensins, autophagy, vitamin D, dietary factors, role of probiotics, and some pathogenetic considerations including relevant involved genes are discussed within this opinion article. In conclusion, by controlling the impact of Helicobacter pylori-related hyperhomocysteinemia on neurodegenerative disorders might offer benefits, and additional research is warranted to clarify this crucial topic currently representing a major worldwide burden.

Retroperitoneal Liposarcoma Masquerading as an Impending Rupture of Inflammatory Abdominal Aortic Aneurysm.

BACKGROUND: We present a unique case scenario of a periaortic liposarcoma masquerading as an impending rupture of an inflammatory abdominal aortic aneurysm (AAA). METHODS AND RESULTS: A 57-year-old man was referred to our unit for an emergency endovascular repair of "an inflammatory AAA with computed tomography (CT) features of impending rupture." He underwent an uneventful endovascular repair with a bifurcated endograft (C3; Gore, Flagstaff, AZ). Seven weeks later, CT showed that the periaortic "mass" grew larger and asymmetric, and a CT-guided needle biopsy suggested the presence of a high-grade malignant mesenchymal tumor. He underwent laparotomy and excision of the retroperitoneal tumor en bloc with the anterior wall of the infrarenal aorta. The endograft acted as an excellent "safety net" providing adequate hemostatic control and obviating the need for aortic cross-clamping and repair of the aortic defect with a patch or tube graft. CONCLUSIONS: The learning point from the present case is that when faced with an inflammatory AAA and/or retroperitoneal fibrosis, the rare possibility of a retroperitoneal neoplasm should be kept in mind.

The Effect of Iloprost in the Healing of Colonic Anastomosis in Rats under Chemotherapy with Irinotecan.

PURPOSE: We have investigated the possible positive effect of iloprost in the healing of colonic anastomosis, in rats under intraperitoneal chemotherapy with irinotecan. METHOD: Forty male Wistar rats have been divided into four groups. They underwent a partial colectomy and a termino-terminal anastomosis. They were administered, intraperitoneally, saline (group 1), irinotecan (group 2), iloprost (group 3), or irinotecan and iloprost (Group 4). After the sacrifice of the animals what followed was an autopsy, a macroscopic examination and the measurement of the anastomotic rupture pressure. A portion of the anastomosis was sent over for histological examination and determination of hydroxyproline levels. Results: The frequency of the leakage from the anastomosis was considered as significantly increased in group 2 compared with the other groups. In group 2, a significantly greater degree of adhesions, compared to all the remaining groups, was observed. The bursting pressure of the anastomosis was significantly lower in group 2, as compared with all the remaining groups, and significantly increased in the group 4 compared with group 2. Leukocytosis, fibroblasts, the neocollagen and the levels of hydroxyproline in group 4 showed significantly increased values, compared with group 2. The angiogenesis was significantly increased in groups 3 and 4 compared with group 2. Conclusions: Intraperitoneal administration of iloprost after colectomy, termino-terminal anastomosis and intraperitoneal administration of irinotecan promotes the healing process of the colon anastomoses as it competes the inhibitory effect of irinotecan.

Vitamin B12 Deficiency and Hemoglobin H Disease Early Misdiagnosed as Thrombotic Thrombocytopenic Purpura: A Series of Unfortunate Events.

We herein would like to report an interesting case of a patient who presented with anemia and thrombocytopenia combined with high serum Lactic Dehydrogenase where Thrombotic Thrombocytopenic Purpura was originally considered. As indicated a central venous catheter was inserted in his subclavian vein which led to mediastinal hematoma and finally intubation and Intensive Care Unit (ICU) hospitalization. After further examination patient was finally diagnosed with B12 deficiency in a setting of H hemoglobinopathy. There have been previous reports where pernicious anemia was originally diagnosed and treated as Thrombotic Thrombocytopenic Purpura but there has been none to our knowledge that was implicated with hemothorax and ICU hospitalization or correlated with thalassemia and we discuss the significance of accurate diagnosis in order to avoid adverse reactions and therapy implications.

Histological presence of Helicobacter pylori bacteria in the trabeculum and iris of patients with primary open-angle glaucoma.

PURPOSE: To investigate the role of Helicobacter pylori in primary open-angle glaucoma (POAG) pathophysiology by detecting its presence in eye biopsies of POAG patients during trabeculectomy. PATIENTS AND METHODS: Fifty-one consecutive patients who underwent trabeculectomy for POAG not responsive to antiglaucoma therapy, and 35 consecutive anemic controls were examined for H. pylori presence mainly by gastric mucosa histology. In POAG patients, eye biopsies were also obtained and stained for H. pylori presence in situ. RESULTS: Forty-three of 51 (84.3%) POAG patients and 17 of 35 (48.6%) controls were tested H. pylori positive (p = 0.0004). In 5 H. pylori-positive POAG patients, H. pylori bacteria were identified in the trabeculum and iris specimens. CONCLUSION: For the first time, H. pylori bacteria have been detected histologically in eye biopsies of POAG patients.

A rare case of femoral hydatidosis.

BACKGROUND: We present a case of a hydatid cyst located in the left thigh. CASE REPORT: A 67-year-old man was admitted to our department with a 10 × 5 × 4 cm mass in the medial compartment of the left thigh. Computed tomography scan indicated possible hydatidosis. Serological testing (indirect hemagglutination) was positive for hydatidosis. The patient was operated seven years ago for liver hydatidosis. RESULTS: The patient, after evaluation, underwent surgical excision of the cyst under epidural anesthesia. The cyst was located in the left quadriceps muscle; had a soft, elastic substance; was firmly attached to the muscle fibers; and contained transparent fluid and daughter cysts. Histologic examination confirmed the initial diagnosis. The patient was discharged on the fifth postoperative day. CONCLUSIONS: The diagnosis of muscular hydatidosis is difficult and the usual diagnostic methods are the serological tests for hydatidosis and imaging (e.g., ultrasound, computed tomography, and magnetic resonance imaging). In every soft tissue mass with benign characteristics the existence of a hydatid cyst should always be considered. Careful surgical excision of the intact cyst is the treatment of choice, but complementary control for liver-or other organ-hydatidosis should be performed.