Articles

Acute pancreatitis is inflammation of the pancreas that may be accompanied by a systemic inflammatory response which results in impairment of the functioning of various organs, systems. Pancreatitis associated vascular complications very often cause morbidity and mortality. There are various cardiovascular complications like shock, hypovolemia, pericardial effusion, and sometimes ST–T changes in the electrocardiogram (ECG) presenting as acute myocardial infarction (AMI). Acute myocardial infarction complicating acute pancreatitis has rarely been studied and the exact process of myocardial injury still remains unclear. We here report a case of Acute Pancreatitis associated with acute myocardial Infarction.

There is growing evidence that gastroesophageal disease is influenced by the esophageal microbiome, and that commensal bacteria of the oropharynx, stomach, and colon are thought to have a role in modulatiing pathogenesis. These emerging hypotheses are based on observed changes in the composition of the esophageal flora, notably, repeated observations: 1. There is an abundance of gram-positive bBacteria in the healthy esophagus. are more gram positive prevalent 2. The esophageal bacterial population becomes increasingly gram negative with disease progression. Associated with this shift to a more gram negative prevalence is an increase in the potential for the presence of antigenic lipopolysaccharide (LPS). The immunoreactivity of LPS endotoxin thought to promote susceptibility to inflammation and disease. The pathogenesis of the more common diseases of the esophagus e.g. gastroesophageal reflux disease (GERD), esophageal dysmotility (achalasia), eosinophilic esophagitis (EoE), Barrett’s esophagus (BE), and esophageal cancer, are well-established. Emerging data suggest however, that these are all characterized by an immune-mediated inflammatory cascade, propogated by a dysbiotic state. Thereby, the ability of the healthy “normative state” to protect against foreign bacteria is compromised. This dysbiosis thereby can create adverse inflammatory or immunoregulatory responses with progression of disease. In the normal healthy state, the esophageal microbiome is constituted in-part, by a multitude of gram positive bacteria, many of which produce antibacterial peptides called bacteriocins. Bacteriocins are selective and used to maintain population integrity by killing off foreign bacteria. When the “normative biome” is interrupted (e.g. antibiotics, medications, diet, environmental factors), the constitutional changes may allow a more hospitable imbalance favoring the proliferation of opportunistic pathogens. Therefore it seems rational that defining, perhaps that defining, perhaps cultivating, a protective bacterial community that could help prevent or mitigate inflammatory diseases of the esophagus. Furthermore, in conjunction with evidence demonstrating that some bacteriocins are cytotoxic or antiproliferative toward cancer cell lines, further exploration might provide a rich source of effective peptide-based drug targets. Therapeutic options targeting the microbiome, including prebiotics, probiotics, antibiotics and bacteriocins, have been studied, albeit the attributable effects on the esophagus for the most part, have been unrecognized by clinicians. This review focuses on the current knowledge of the involvement of the microbiome in esophageal diseases (most notably GERD/Barrett’s esophagus/esophageal cancer) and identifies emerging new concepts for treatment.

Familial adenomatous polyposis is an autosomal dominant syndrome of variable penetration and constitutes the second frequent inherited syndrome enunciating the emergence of a colorectal carcinoma. The syndrome is accompanied by exemplification of defective adenomatous polyposis coli (APC) gene located upon chromosome 5q21 with a prototypic denomination of colonic adenomatous polyps usually exceeding a > 100. Incriminated individuals develop innumerable colonic and rectal polyps, particularly during early teenage years and are accompanied by an almost 100% possible emergence of colorectal carcinoma within 40 years in untreated subjects [1]. Prophylactic colectomy is advisable to substantially reduce possible occurrence of colorectal carcinoma. Familial adenomatous polyposis is concurrent with associated neoplasms such as gastric or duodenal cancer, hepatoblastoma or desmoid tumour along with a probable emergence of extra-colonic carcinomas [1,2].

Celiac disease affects 1% of the world population; however it is under diagnosed in UAE. The disease has many clinical manifestations, ranging from severe malabsorption to minimally symptomatic or non-symptomatic presentation. Hypocalcaemia is a common finding in celiac disease and could be the only presentation of the disease; however hypercalcemia has been previously reported in patients with celiac disease either due to primary hyperparathyroidism or tertiary hyperparathyroidism due to prolonged hypocalcaemia. A normal calcium level on the other hand in patients with untreated celiac disease who also have primary hyperparathyroidism can be due to interplay of these two conditions and may delay the diagnosis of primary Hyperparathyroidism. We report the very first case from our practice in UAE with untreated celiac disease and normal calcium level at presentation, where a diagnosis of primary hyperparathyroidism was not entertained initially. Patient went on gluten free diet which then caused normalization of intestinal abnormalities and likely calcium absorption manifesting as hypercalcemia on subsequent labs. This led to further work up and finally the diagnosis of Primary hyperparathyroidism due to parathyroid adenoma.

Introduction: Pancreatic pseudocysts (PPs) are mostly delayed complications of acute or chronic pancreatitis and trauma. Pancreatic pseudocysts are usually managed by supportive medical treatment without surgical procedure. All the surgical interventions (percutaneous, endoscopic or surgical approaches) are based on the location, size, symptoms, complications of the pancreatic pseudocyst and medical condition of the patients. Recently, laparoscopic cystogastrostomy has become most appropriate approach especially for retrogastric pancreatic pseudocysts. In this study, we would like to report results of laparoscopic anterior transgastric cystogastrostomy by using linear articulated endo GIA stapler (Covidien medium thick purple) and versa-lifter (versa lifter®, laparoscopic retractor, manufactured by protomedlabs, France) in 14 pancreatic pseudocysts patients. Methods: We retrospectively analyzed data of patients with pancreatic pseudocysts treated by laparoscopic anterior transgastric cystogastrostomy from September 2010 to October 2014. All of the patients were controlled for the recurrence of pancreatic pseudocysts in February 2017. Results: 14 patients with pancreatic pseudocysts were managed by laparoscopic anterior transgastric cysto-gastrostomy. Conversion was performed in only one patient (7%). There were no symptoms and signs of recurrence of pancreatic pseudocyst during on average 43.6 months follow up time. Conclusion: Laparoscopic cystogastrostomy by using articulated linear endo-GIA stapler and versa-lifter is a safe and effective method for management of appropriate retro-gastric pancreatic pseudocysts.

Heterotopic gastric mucosa (HGM) is an islet of gastric mucosa within the esophageal mucosa. These lesions can sit throughout the digestive tract and rarely in the upper third of the esophagus. The pathophysiology of HGM remains poorly understood. Our study aims to estimate the prevalence of HGM, clinical signs, endoscopic, microscopic aspects and different epidemiological factors associated. All patients from a single endoscopy center with HGM of the upper third of the esophagus were included over a 5-month evaluation period. All lesions seen in endoscopy were confirmed by histological analysis. The prevalence was 1.3% with a clear male predominance. 80% of patients were symptomatic and received medical treatment, clinical evolution was good. No case of dysplasia was identified and no complication was observed. Due to insufficient data in the evolutionary literature, the management of HGM remains debated and could resemble that of Barett’s esophagus for monitoring and therapeutic management, particularly in the event of symptoms or dysplasia.

Introduction: Fluid management is the cornerstone of treatment for acute pancreatitis (AP), but the proper rate and volume is still controversial. We aim to evaluate the role of aggressive hydration in AP patients. Methods: We retrospectively reviewed and analyzed 279 hospitalized patients of AP. Severity was determined by the Revised Atlanta classification; validated clinical scores were also calculated based on clinical information upon presentation. We extracted amount of fluid received by at 6, 12, 24 and 48 hours after presentation. Aggressive hydration was defined as amount higher than 10 ml/kg bolus followed by infusion at 1.5 ml/kg/h. After direct comparison between aggressive versus non-aggressive hydration groups, propensity-score match was performed to control severity, APACHE II and BISAP score. Post-match comparison as well as a subgroup comparison were conducted. Results: At 24 hours, 125 (44.8%) patients received aggressive hydration averaged at 5.1 L (2-18 L), while 154 (55.2%) patients received non-aggressive hydration averaged at 2.5 L. Post-match comparison showed that aggressive hydration group had longer hospital stay (MAP: 5.3 vs 4.5, p = 0.145, MSAP/SAP: 8.3 vs 4.8 d, p = 0.007), and higher rate of intensive care unit admission (mild: 12.9% vs 4.4%, p = 0.042, moderately severe or severe: 36.8% vs 3.1%, p = 0.001), while showed no difference in rate of mortality or re-admission by 1 year. In patients who presented without organ failure, aggressive hydration did not change the rate of development of organ failure (14.1% vs 12.5%, p = 0.731), but the aggressive hydration group had a trend towards longer hospital stay (5.5 vs 4.6 d, p = 0.083) and higher rate of MICU admission (12.1% vs 4.8%, p = 0.051)

Background: This article reviews current knowledge of Gaucher’s disease (GD) and liver involvement and reports our experience: how many patients with chronic liver disease of unknown origin could be affected by Gaucher’s disease. Patients and methods: Over 24 months, we tested 75 sine causa chronic liver disease patients (30 women and 45 men, mean age 55 years, range 15 to 77). Results: None of the 75 patients was affected by Gaucher’s disease. Conclusion: We believe that the chronic liver disease patient is unlikely to be affected by Gaucher’s disease. Probably this disease is to be found in cases of coexistence of hepatic disease and other symptoms of Gaucher’s disease (bone, neurological, bone marrow involvement).

Hepatitis C Virus (HCV) infection is usually treated with direct acting antivirals (DAAs) for 12 weeks. In treatment naive patients with genotype (GT) 1 infection without cirrhosis and baseline viral load < 6 million, 8 weeks of Ledipasvir/Sofosbuvir (LDV/SOF) is an option. Eight weeks with Glecaprevir/Pibrentasvir (GLE/PIB) is an option for patients with GT 1 through 6 without cirrhosis. Our objective was to evaluate achievement of Sustained Virologic Response (SVR) after 8 weeks of LDV/SOF or GLE/PIB in our HCV-infected veterans. Patients with HCV infection that received GLE/PIB or LDV/SOF for a planned 8 weeks of therapy in the past four years were reviewed (January 2015-September 2018). Treatment outcomes were evaluated through medical record review. Two hundred sixty-five veterans were initiated on 8 weeks of therapy with either GLE/PIB or LDV/SOF. Of these, 231 (87%) were initiated on 8 weeks of LDV/SOF and 34 (13%) were initiated on 8 weeks of GLE/PIB. The majority of patients had GT 1 (93%) infection. One hundred and ninety-five veterans who completed 8 weeks of LDV/SOF and 30 veterans on GLE/PIB had follow-up viral loads. The overall SVR was 95%. Treatment with GLE/PIB resulted in a higher SVR rate (100%) compared to LDV/SOF (95%). Elderly patients had similar SVR rates. Treatment with 8 weeks of DAA is effective in our veteran population and showed an SVR rate similar to literature reports. The SVR for patients treated with 8 weeks LDV/SOF was slightly lower than the SVR for GLE/PIB; however, the GLE/PIB population was smaller

Introduction: Erdheim-Chester disease (ECD) is a rare and difficult-to-treat non-Langerhans cell histiocytosis characterized by the excessive production and accumulation of histiocytes. This study reports a case of ECD, emphasizing both its diagnosis, assessment and treatment of the pain associated with the disease. Case Report: Six years ago, a 39-year-old male patient presented with generalized pain of moderate intensity in the lower limbs that involved periods of greater intensity associated with ambulation. The diagnosis of histiocytosis associated with panhypopituitarism and adrenal insufficiency was proposed. For a specific diagnosis, a bone lesion biopsy was performed, revealing the presence of histiocytic proliferation that was CD1 negative, S100 protein positive, and CD68 negative. Therefore, the diagnosis of non-Langerhans histiocytosis known as ECD was confirmed. During the two years that followed, the patient presented with severe bone pain, particularly in the lower limbs and cranial vault, and the pain subsided to a certain extent with the use of tramadol and paracetamol. Because of the pain, the patient was unable to walk and became bedridden As the patient remained in severe pain, even after the administration of morphine, the opioid was changed from morphine (60mg/day) to oxycodone (30mg/day) for a convenient dosing schedule; furthermore, the oxycodone dosage was scheduled to increase to 40mg/day that same week. The patient experienced significant pain reduction, requiring rescue analgesia only once or twice a week. Conclusion: To the best of our knowledge, this is the first case report on the characterization and treatment of pain specific to ECD, and we highlight that the patient had a good response to treatment.