Eosinophilic enteritis presenting as intestinal obstruction: case report and review of the literature.

Eosinophilic enteritis (EE) is characterized by intense eosinophilic infiltrate of the gastrointestinal tract. Clinical manifestations depend on the affected segment and intestinal layer. First-line treatment is systemic corticosteroids; surgery is reserved for complications. 84-year-old male patient with a history of right hemicolectomy and two episodes of intestinal obstruction presented to the ED with abdominal pain, distension, nausea, and vomiting. CBC showed leukocytosis and no eosinophilia. Contrast-enhanced CT revealed stenosis with thickening of the distal intestinal wall and partial intestinal obstruction. Colonoscopy found aphthous ulcers. Histopathology reported EE. The patient received budesonide and metronidazole, with resolution within 24 h.

La enteritis eosinofílica (EE) se caracteriza por infiltrado eosinofilico del tracto GI. Las manifestaciones clínicas dependen de la capa intestinal afectada. Se recomiendan esteroides sistémicos como primera línea de tratamiento, reservando la cirugía para complicaciones. Masculino de 84 años con antecedente de hemicolectomía derecha y dos episodios de oclusión intestinal acude al servicio de urgencias con dolor abdominal, distensión, náusea y vómito. Laboratorio reportó leucocitosis, sin eosinofilia. Tomografía con contraste evidenció estenosis, con engrosamiento de la pared del intestino delgado e imagen compatible con oclusión intestinal. La colonoscopía demostró ulceras en íleon terminal la cual reporto EE. Se inició tratamiento con budesonide y metronidazol, con adecuada respuesta y resolución a las 24 h.

Comparing fine needle biopsy techniques in solid pancreatic lesions: A prospective randomized study.

INTRODUCTION: Endoscopic ultrasound-guided fine-needle biopsies (EUS-FNB) are the best technique for sampling solid pancreatic lesions. However, the most appropriate biopsy technique has not been standardized using Fine Needle Biopsy (FNB) needles. The aim of this work was to identify the best biopsy technique to achieve the best tissue integrity and cause the least blood contamination. MATERIAL AND METHODS: Patients ≥18 years of age with solid pancreatic lesions who underwent EUS-FNB at our institution from January 2020 to May 2021 were consecutively selected. Three passes were performed with each of the threee techniques to obtain tissue: suction with 10 ml of vacuum, capillary, and wet. An independent pathologist evaluated the received tissue integrity and the degree of blood contamination of each sample according to scales. RESULTS: Seventy-five patients were recruited for our study. A superior tissue integrity was observed using the wet-suction technique in lesions located in the body and/or tail of the pancreas, and an average score of 4.40 (p = 0.027) was assigned for this technique. Regarding the contamination of the sample in the whole cohort, the simple-suction technique shown a higher contamination, 1.55 (p < 0.001). There was no statistically significant difference among the techniques when evaluating tissue integrity or contamination in lesions larger or smaller than 3 cm. CONCLUSION: When performing EUS-FNB for solid pancreatic lesions located in the head/uncinated process, the three methods provided similar diagnostic yields. The wet-suction technique had a higher score in tissue integrity when lesions were located in the body and/or tail of the pancreas.

Pancreatic cancer, autoimmune or chronic pancreatitis, beyond tissue diagnosis: Collateral imaging and clinical characteristics may differentiate them.

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies and is developing into the 2nd leading cause of cancer-related death. Often, the clinical and radiological presentation of PDAC may be mirrored by other inflammatory pancreatic masses, such as autoimmune pancreatitis (AIP) and mass-forming chronic pancreatitis (MFCP), making its diagnosis challenging. Differentiating AIP and MFCP from PDAC is vital due to significant therapeutic and prognostic implications. Current diagnostic criteria and tools allow the precise differentiation of benign from malignant masses; however, the diagnostic accuracy is imperfect. Major pancreatic resections have been performed in AIP cases under initial suspicion of PDAC after a diagnostic approach failed to provide an accurate diagnosis. It is not unusual that after a thorough diagnostic evaluation, the clinician is confronted with a pancreatic mass with uncertain diagnosis. In those cases, a re-evaluation must be entertained, preferably by an experienced multispecialty team including radiologists, pathologists, gastroenterologists, and surgeons, looking for disease-specific clinical, imaging, and histological hallmarks or collateral evidence that could favor a specific diagnosis. Our aim is to describe current diagnostic limitations that hinder our ability to reach an accurate diagnosis among AIP, PDAC, and MFCP and to highlight those disease-specific clinical, radiological, serological, and histological characteristics that could support the presence of any of these three disorders when facing a pancreatic mass with uncertain diagnosis after an initial diagnostic approach has been unsuccessful.

A rare case of emphysematous gastritis caused by Lactobacillus fermentum in a patient with diabetes.

We present the case of a 42-year-old male with a history of type-2 diabetes mellitus (complicated by end-stage renal disease on peritoneal dialysis) and chronic diarrhea was admitted to the emergency department due to an exacerbation in the number of evacuations.

Utility of endoscopic ultrasound in idiopathic acute recurrent pancreatitis.

Idiopathic acute recurrent pancreatitis (IARP) is defined as at least two episodes of acute pancreatitis with the complete or near-complete resolution of symptoms and signs of pancreatitis between episodes, without an identified cause. There is a paucity of information about the usefulness of endoscopic ultrasound (EUS) in IARP. OBJECTIVES: To determine the diagnostic yield of EUS in IARP. DESIGN: A retrospective study was performed in patients with IARP evaluated by EUS between January 2009 and December 2016. Follow-up assessments of acute pancreatitis recurrence were carried out. RESULTS: Seventy-three patients with 102 EUS procedures were included. EUS was able to identify the cause of IARP in 55 patients (75.3%). The most common findings were chronic pancreatitis in 27 patients (49.1%), followed by lithiasic pathology in 24 patients (43.6%), and intraductal papillary mucinous neoplasm in four patients (7.3%). A directed treatment against EUS findings had a protective tendency associated with the final resolution of recurrence. There were no complications reported. CONCLUSION: EUS performed in patients with IARP helped to identify a possible cause in 2/3 of the cases. The majority of patients have a treatable disease.

More fuel to the fire: some patients with non-celiac self-reported wheat sensitivity exhibit adaptive immunological responses in duodenal mucosa.

BACKGROUND: In contrast to the well-characterized Celiac Disease (CD), the clinical scenarios encompassed by the non-celiac self-reported wheat sensitivity (NCSRWS) might be related to different antigens that trigger distinct immune-inflammatory reactions. Although an increased number of intestinal intraepithelial lymphocytes is observed at the inception of both diseases, the subsequent immunopathogenic pathways seem to be different. We aimed to describe the cytokine profile observed in the duodenal mucosa of patients with NCSRWS. METHODS: In a blind, cross-sectional study, we included duodenal biopsies from 15 consecutive untreated patients with active CD, 9 individuals with NCSRWS and 10 subjects with dyspepsia without CD and food intolerances. Immunohistochemistry and flow-cytometry were used to determine the presence of pro-inflammatory cytokine expressing monocytes and monocyte-derived dendritic cells involved in innate immune activation, cytokine-driven polarization and maintenance of Th1 and Th17/Th 22, and anti-inflammatory/profibrogenic cytokines. RESULTS: The percentage of cells expressing all tested cytokines in the lamina propria and the epithelium was higher in CD patients than in the control group. Cytokines that induce and maintain Th1 and Th17 polarization were higher in CD than in NCSRWS and controls, also were higher in NCSRWS compared to controls. Similar differences were detected in the expression of IL-4 and TGF-1, while IL-10-expressing cells were lower in NCSRWS patients than in controls and CD subjects. CONCLUSIONS: NCSRWS patients exhibit components of both, innate and adaptive immune mechanisms but to a lesser extent compared to CD.

Steroid-responsive pancreatitides.

Autoimmune pancreatitis has received considerable attention, especially due to the marked effect of corticosteroid therapy on its clinical course. Knowledge, especially regarding type 1 autoimmune pancreatitis, has significantly increased over the last decades, and despite significant differences in pathophysiology and outcomes, both type 1 and 2 autoimmune pancreatitis are still considered different types of the same disease. Some have proposed a different nomenclature reflecting these differences. Although the term steroid-responsive pancreatitides may be interpreted as synonymous to type 1 and 2 autoimmune pancreatitis, these are not the only pancreatic conditions that show a response to steroid therapy. Acute pancreatitis caused by vasculitis and connective tissue diseases and acute pancreatitis secondary to checkpoint inhibitors or programmed cell death receptor antibody-mediated blockage cancer therapy may also benefit from steroid treatment. This review presents current concepts on these disorders, aiming to increase awareness, analyze similarities and differences, and propose a new nomenclature that reflects their specific particularities, clustering them under the term "steroid-responsive pancreatitides".

Increased Mortality from Extrapancreatic Infections in Hospitalized Patients with Acute Pancreatitis.

Nosocomial extrapancreatic infections in patients with acute pancreatitis (AP) are associated with a higher mortality even after adjusting the risk for the severity of the pancreatitis. The aim of this study was to describe the clinical features of hospitalized patients with AP who died during their hospitalization and to evaluate risk factors associated with mortality. We performed a descriptive study of the clinical features of adult patients who died from AP during their hospitalization and a case control study with a paired group of patients that survived AP during a 10-year period. Data of interest were collected from the medical records and are presented with appropriate measures of central tendency and dispersion. For the case control study, the primary outcome evaluated was death, and to evaluate associated clinical features and determine differences between groups, we performed the χ 2 or Fisher's exact tests for categorical variables and the Student t-test or Mann-Whitney U test for continuous variables as appropriate. We found 48 patients with acute pancreatitis who died within the period of the study during hospitalization; from these, 50% were men, mean age was 53.2 years, and the most common etiology was biliary obstruction by gallstones in 45.8%. The global mortality rate was of 2.5%. A total of 43.7% patients had infected pancreatic necrosis, and in 58.3%, some extrapancreatic infection was documented, being the most common urinary tract infection in 50%, bacteremia in 50% and pneumonia in 33.3%. Clinical features associated with mortality were the presence of organ failure (p < 0.001), nosocomial complications (p < 0.001), infected necrosis (p < 0.001), and extrapancreatic infections (p = 0.002). From the different extrapancreatic infections, only bacteremia (p = 0.001) and pneumonia (p = 0.011) were associated with higher mortality. In conclusion, extrapancreatic infections are associated with increased mortality among hospitalized patients with acute pancreatitis, in particular, bacteremia and pneumonia with an isolated pathogen.

Retroperitoneal fibrosis. Steroid treatment response seems to depend on its association to IgG4 related disease.

Retroperitoneal fibrosis (RF) is part of a rare fibrosclerotic disorder. Oral steroids are the initial treatment. Steroid combination with other immunosupressants is used in refractory cases. Steroids refractoriness has been observed in chronic cases. Some cases of RF represent a manifestation of the IgG4 related disease (IgG4-RD) that is associated to a dramatic response to steroid therapy. It is uncertain if RF́s treatment response differs according to its association with IgG4-RD. We hypothesize that RF́s treatment response to steroids depends on the association with IgG4-RD, thus, we collected and compared clinical data from 10 RF cases; 6 male, mean age 50.6 (±16.15 SD) years. Mean FU was 28 (±25.7 SD) months. According to IgG4 levels, patients were categorized as idiopathic RF (IRF n = 5) or RF-IgG4-RD (n = 5). Therapy response was categorized as complete, partial, stable disease, recurrence or non-response. Nine cases received initial therapy with prednisone; complete response was achieved in 4 RF-IgG4 RD. The remaining 5 cases (1 RF-IgG4RD and 4 IRF) underwent a 2nd line therapy; 4 prednisone + tamoxifen and 1 prednisone + azathioprine. Prednisone + tamoxifen combination achieved complete response in 1 case (RF-IgG4RD), partial response in 1 IRF; in 1 IRF case, disease remained stable and 1 did not respond. The prednisone + azathioprine treatment achieved complete response. At follow-up all patients remained stable and no recurrence was registered. These observations suggest and support the hypothesis that response to steroid monotherapy depends on the association of RF with IgG4, suggesting that IRF cases might benefit from initial combination therapies instead of steroid monotherapy.

Recombinant human hepatocyte growth factor provides protective effects in cerulein-induced acute pancreatitis in mice.

Acute pancreatitis is a multifactorial disease associated with profound changes of the pancreas induced by release of digestive enzymes that lead to increase in proinflammatory cytokine production, excessive tissue necrosis, edema, and bleeding. Elevated levels of hepatocyte growth factor (HGF) and its receptor c-Met have been observed in different chronic and acute pancreatic diseases including experimental models of acute pancreatitis. In the present study, we investigated the protective effects induced by the recombinant human HGF in a mouse model of cerulein-induced acute pancreatitis. Pancreatitis was induced by 8 hourly administrations of supramaximal cerulein injections (50 µg/kg, ip). HGF treatment (20 µg/kg, iv), significantly attenuated lipase content and amylase activity in serum as well as the degree inflammation and edema overall leading to less severe histologic changes such as necrosis, induced by cerulein. Protective effects of HGF were associated with activation of pro-survival pathways such as Akt, Erk1/2, and Nrf2 and increase in executor survival-related proteins and decrease in pro-apoptotic proteins. In addition, ROS content and lipid peroxidation were diminished, and glutathione synthesis increased in pancreas. Systemic protection was observed by lung histology. In conclusion, our data indicate that HGF exerts an Nrf2 and glutathione-mediated protective effect on acute pancreatitis reflected by a reduction in inflammation, edema, and oxidative stress.

Abnormal Cardiovascular Findings in Acute Pancreatitis: Are They Associated with Disease Severity?

BACKGROUND: Acute pancreatitis (AP), a disease that commonly requires in-hospital treatment, has been associated with a high incidence of abnormal cardiovascular findings (ACFs). We conducted a prospective study to explore the association of these findings with severity of the disease. METHODS: Adult patients with AP diagnosis were prospectively enrolled in an observational study during an 8-month period in a tertiary care center. AP and its severity were defined according to the Revised Atlanta Classification of AP. Subjects were submitted to electrocardiographic, echocardiographic, and serologic testing during the acute period and a 3-month follow-up. The incidence of ACF was compared between two groups: (1) Mild and (2) moderate/severe cases. RESULTS: Twenty-seven patients (mean age 48 ± 17 years) with AP were enrolled; 15 (55%) had mild and 12 (45%) had moderate/severe AP. During the acute episode, 67% had increased pro-brain natriuretic peptide levels; 52% had abnormal electrocardiographic findings; 48% had abnormal echocardiographic findings; and 18% had increased troponin I levels. There was no significant difference in the incidence of ACF between mild and moderate/severe groups. Nineteen patients (70%) had repeated follow-up testing, and most of the initial ACF did not persist. CONCLUSION: ACFs occur in an important proportion of patients during AP episodes. Future research should continue to focus in the association of ACFs and the severity of the disease.

Decrease in the Prevalence of Pancreatitis Associated with Primary Hyperparathyroidism: Experience at a Tertiary Referral Center.

BACKGROUND: Hypercalcemia is a rare but well recognized cause of acute and chronic pancreatitis. Hypercalcemia-related pancreatitis is mainly caused by primary hyperparathyroidism. The prevalence of pancreatitis in hyperparathyroidism varies worldwide and additional disease-modifying factors may play a role in its development. In 1988 the prevalence of pancreatitis secondary to primary hyperparathyroidism at the Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán (INCMNSZ), a referral center in Mexico City, was 12.1% (95% CI: 6.7-21). OBJECTIVE: To describe the current prevalence of pancreatitis secondary to primary hyperparathyroidism at the INCMNSZ. METHODS: We reviewed 385 cases of primary hyperparathyroidism seen at the hospital between 1987 and 2012. RESULTS: 26 cases with acute or chronic pancreatitis associated with primary hyperparathyroidism were documented, with a prevalence of 6.7% (95% CI: 4.6-9.7), which was lower than the 12.1% previously reported. In the present study, 20% had a history of alcohol consumption, 10% of gallstones, and 20% of ureteral calculi, compared with the previously reported 32.0, 34.6, and 40.0%, respectively. The average calcium levels were 13.1 and 13.8 mg/dl in the previous and current series, respectively. CONCLUSIONS: We found a decrease in the prevalence of pancreatitis associated with primary hyperparathyroidism from 12.1% (95% CI: 6.7-21) to 6.7% (95% CI: 4.6-9.7).

Serous Cystadenomas Follow a Benign and Asymptomatic Course and Do Not Present a Significant Size Change During Follow-Up.

BACKGROUND: Serous cystadenoma is a benign pancreatic cystic neoplasm. Conservative management is favored. We studied the clinical characteristics and course of serous cystadenoma in patients undergoing surgery or conservative management only at an academic referral center. METHODS: Patients presenting with serous cystadenoma in the years 2000-2013 were selected. Hospital records were evaluated for patient and serous cystadenoma characteristics. RESULTS: A total of 22 patients with serous cystadenoma were identified. Mean age at diagnosis was 63 years and 82% were women. Diagnosis was incidental in 59%, and 18% presented with unspecific abdominal pain, 14% unexplained weight loss, 4.5% gastrointestinal obstructive symptoms, and 4.5% cholangitis. Location was pancreas body 36%, head 32%, tail 23%, and uncinate 9%. Mean serous cystadenoma diameter at diagnosis was 37 ± 23 mm. After diagnosis five patients underwent surgery. Initial size was similar between surgical and follow-up groups (p = 0.9). Four cases were lost to follow-up; 13 continued conservative management with a mean follow-up time of 54 ± 27 months. The initial and last serous cystadenoma size in the follow-up group remained similar (p = 0.9). Six cases presented significant tumor growth during follow-up (p > 0.05). All patients remained asymptomatic throughout follow-up. No malignancy or serous cystadenoma-related death occurred. CONCLUSIONS: Size change of serous cystadenoma was minimal and patients remained asymptomatic during follow-up. Surgery should be limited to symptomatic and selected cases.

PRSS1 and SPINK1 mutations in idiopathic chronic and recurrent acute pancreatitis.

AIM: To identify gene mutations in PRSS1 and SPINK1 in individuals with early onset idiopathic chronic or recurrent acute pancreatitis. METHODS: The cationic trypsinogen gene (PRSS1; exons 2 and 3) and the serine protease inhibitor Kazal 1 gene (SPINK1; exon 3) were selectively amplified and sequenced from blood samples of 19 patients admitted to the Pancreas Clinic at our institution with chronic pancreatitis and/or idiopathic recurrent acute pancreatitis that were diagnosed or with onset before age 35. Fifty healthy volunteers served as controls. Whole blood samples were collected and gene specific sequences were amplified by polymerase chain reaction (PCR). All PCR products were subsequently sequenced in order to identify the presence of any mutations. RESULTS: Nineteen patients with pancreatitis (14 males; median age 24 years, range 15-48 years) were included in this study, of which five showed the presence of gene mutations. Direct sequencing results indicated the presence of two previously unidentified mutations in exon 2 of PRSS1 (V39E and N42S) in two patients with recurrent acute pancreatitis. Two cases had the N34S SPINK1 mutation. Analysis of the relatives of one patient homozygous for this mutation showed that five of the six family members carried the N34S SPINK1 mutation. Of these members, three were healthy heterozygous carriers and two were homozygotes (one sibling had diabetes, the other was healthy). Another patient was heterozygous for a novel SPINK1 mutation located on exon 3 (V46D). All members from this patient's family had normal genotypes, indicating that it was a de novo mutation. No mutations in either gene were present in the control subjects. CONCLUSION: Two novel PRSS1 mutations and one novel SPINK1 mutation were identified in Mexican patients with early onset idiopathic recurrent acute pancreatitis.

Interventional EUS guided cholangiography. First description in Mexico of a novel, secure and feasible technique. A case report.

Endoscopic retrograde cholangio pancreatography (ERCP) is the procedure of choice for biliary decompression in individuals with obstructive jaundice. In those cases when ERCP fails, the alternatives are to refer the case to a highly specialized center and repeat the procedure, or decompress the bile ducts either percutaneously or surgically. The proximity of the endoscopic ultrasound (EUS) probe from the stomach and duodenum to the hepatobiliar system and pancreas allows ultrasound-guided access into the bile and pancreatic duct. We present what to our knowledge is the first description in Mexico of a therapeutic interventional EUS guided cholangiography in a patient with cholecystitis and choledocolithiasis in whom initial ERCP failed to decompress de bile duct.

When should we be concerned about pancreatic necrosis? Analysis from a single institution in Mexico City.

BACKGROUND/AIM: Although pancreatic necrosis classifies acute pancreatitis (AP) as severe, many patients with tomographic evidence of necrosis never develop systemic complications. Our aim was to analyze the incidence of pancreatic necrosis, organ failure (OF), and the relationship between them. METHODS: Medical records from 165 patients with a first AP episode and in whom a contrast-enhanced computed tomography (CECT) was performed were analyzed. Pancreatic necrosis was diagnosed as non-enhancing areas of the pancreas on the CECT and was graded as <30%, 30%-50%, and >50%. Pancreatic infection was assessed by guided percutaneous aspiration. Organ failure was defined according to the Atlanta criteria. RESULTS: Of 165 patients (mean age 42 years, 85 men), 54 (33%) had pancreatic necrosis. Necrosis was graded as <30% in 25 subjects (46%), 30%-50% in 16 (30%), and >50% in 13 (24%). Pancreatic infection was diagnosed in 14 cases (26%). Organ failure occurred in 49 patients: in 20 patients (37%) with necrosis, and in 29 patients (26%) without necrosis (P = 0.20). Extensive pancreatic necrosis (>50%) (P < 0.05) and infected necrosis (P < 0.05) were significantly associated with OF. Eight patients, all of them with OF, died. In 6 of these cases infected pancreatic necrosis was present. CONCLUSIONS: Patients with pancreatic necrosis are not necessarily at risk of developing OF. However, it should be considered an important risk factor when the necrotizing process compromises more than 50% of the gland and is infected.

Intestinal involvement is not sufficient to explain hypertransaminasemia in celiac disease?

Chronic unexplained hypertransaminasemia is an isolated clinical manifestation of celiac disease (CD) and lacks of a clear physiopathological explanation. Since CD and tropical sprue (TS) have similar intestinal functional and histological pattern of injury and that an increased inflammatory response has been reported to occur in patients with irritable bowel syndrome (IBS), liver involvement might be expected to occur either in TS or IBS. However, according to author's prior observations, the frequency of hypertransaminasemia is significantly higher in CD than in TS and IBS-diarrhea predominant patients (IBS-D). Thus, based on current knowledge, intestinal mucosal damage, increased intestinal permeability and/or an active intestinal inflammatory response do not completely explain liver damage in CD. We hypothesize that other factors, unique to CD not present in TS or IBS-D, like gluten toxicity and the presence of tissular transglutaminase (tTG) an auto-antigen with pro-inflammatory and remodeling properties, act in addition to intestinal mucosal injury and account to hypertransaminasemia in CD. Further research focusing on the mechanisms of gluten and tTG hepatic toxicity, and/or the characterization of the expression, secretion and enteral-hepatic transport of certain pro-inflammatory cytokines is needed, to understand the possible links between intestinal and liver disorders seen in CD.