Diagnostic yield of endoscopic ultrasound-guided tissue acquisition for small solid pancreatic lesions

Background and study aims Endoscopic ultrasound (EUS)-guided tissue acquisition is sometimes required to diagnose small solid pancreatic lesions. The aim of this study was to evaluate the diagnostic yield of EUS-guided tissue acquisition for small solid pancreatic lesions and the differences in diagnostic yield among different needles. Patients and method We retrospectively analyzed consecutive patients who had undergone EUS-guided tissue acquisition for solid pancreatic lesions less than 2 cm between November 2012 and June 2019. Three types of needles were evaluated in this study: a 22-gauge fine-needle aspiration (FNA) Lancet needle, a 20-gauge fine-needle biopsy (FNB) Menghini needle with a lateral forward bevel, and a 22-gauge FNB Franseen needle. We evaluated the diagnostic yield and safety of the procedure using these needles. Results We analyzed 160 patients with 163 lesions. The overall sensitivity, specificity, and accuracy were 92.0 %, 100 %, and 92.6 %, respectively. In the histological plus cytological diagnosis, accuracies of the Lancet, Menghini, and Franseen needles were 92.7 %, 97.0 %, and 85.7 %, respectively (P = 0.10). In the histological diagnosis alone, the negative predictive values (NPVs) of the Lancet, Menghini, and Franseen needles were 13.3 %, 53.3 %, and 27.3 %, respectively (P = 0.08). Adverse events occurred in four cases (2.5 %): one postprocedural bleeding, two cases of pancreatitis, and one pancreatic abscess. Conclusions EUS-guided tissue acquisition for small solid pancreatic lesions has a high diagnostic yield and safety. This study suggested a difference in the diagnostic yield of each needle for small solid pancreatic lesions.

Duodenal duplication cyst masquerading as a pancreatic abscess in a cat

This report details a cat with a duodenal duplication cyst in the region of the right distal pancreas. The cat presented with vomiting, anorexia, pancreatitis and a palpable abdominal mass that was visible on abdominal ultrasound as a thick-rimmed, cavitated structure with echogenic contents. As such, an initial clinical diagnosis of pancreatic abscess or cyst was suspected. After an exploratory coeliotomy to assess the lesion, a definitive diagnosis of duodenal duplication cyst was determined based on the histopathological findings of a wall with features of the intestinal tract and no communication with the intestinal lumen. The clinical signs, physical examination findings and advanced imaging characteristics of pancreatic abscess and duodenal duplication cyst are discussed in this report to aid clinicians with differentiating between these two rare lesions.

Asparaginase-Associated Pancreatitis in ALL: Results from the NOPHO ALL2008 Treatment of Patients 1-45 Years

Premature discontinuation of asparaginase reduces cure rate in contemporary acute lymphoblastic leukemia (ALL) treatment. One of the commonest causes of asparaginase truncation is asparaginase-associated pancreatitis (AAP). We prospectively registered AAP during treatment of 2,448 consecutive Nordic/Baltic ALL patients aged 1.0-45.9 years treated according to the Nordic Society of Pediatric Hematology and Oncology (NOPHO) ALL2008 protocol (7/2008-10/2018). The Day 280 cumulative incidence of first-time AAP (including 99% (167/168) of AAP events at this time point) was 8.3% (95% confidence interval (CI) 7.0-9.9) with a median time of 104 days (interquartile range (IQR) 70-145) from ALL diagnosis to AAP, with a median of 10 days (IQR 6-13) from last asparaginase exposure, and after a median number of five asparaginase doses (IQR 3-7, max 14 doses). All patients received polyethylene glycol conjugated Escherichia coli-derived asparaginase as standard treatment. Eighty-five percent (140/164, unknown in N=4) of AAP events were severe (AAP-associated symptoms and/or pancreatic enzymes >3x upper normal limit lasting >72 hours or with hemorrhagic pancreatitis, pancreatic abscess, or pseudocyst). Four age groups were defined: 1.0-4.9, 5.0-8.9, 9.0-16.9, and 17.0-45.9 years-each containing approximately 25% of the AAP events. Compared with patients aged 1.0-4.9 years, adjusted (sex, immunophenotype, and white blood cell count) hazard ratios (HR) of AAP were associated with higher age (5.0-8.9 years: HR 2.3, 95% CI 1.5-3.6, P<.0001; 9.0-16.9 years: HR 2.5, 95% CI 1.6-3.8, P<.0001; and 17.0-45.9 years: HR 2.5, 95% CI 1.6-3.8, P<.0001). When analyzing the odds of developing any AAP-related complication among patients with ≥100 days of follow-up after the AAP diagnosis, older children (≥5.0 years) and adolescents had increased odds of developing any complication compared with younger children aged 1.0-4.9 years, notably a more than six-fold increase among adolescents (5.0-8.9 years: odds ratio (OR) 2.67, 95% CI 1.07-6.68, P=.04 and 9.0-16.9 years: OR 6.52, 95% CI 2.35-18.1, P=.0003)-including acute and permanent insulin need; intensive care unit admission; pancreatic pseudocyst development; recurrent abdominal pain; elevated pancreatic enzymes at last-follow-up; imaging compatible with pancreatitis (pancreatic inflammation/edema/pseudocysts/hemorrhage) at last follow-up; and AAP-related death. Adult age was not associated with development of any AAP-related complication (17.0-45.9 years: OR 2.3, 95% CI 0.9-5.9, P=.07). Three patients aged 8.6, 17.3, and 18.6 years died of first-time AAP within 0-29 days from AAP diagnosis. Of 168 AAP patients, 34 (20%) were re-challenged with asparaginase. Fifty percent (17/34) developed a second episode of AAP-41% being severe (7/17). The median time to a second AAP event from asparaginase re-exposure was 29 days (IQR 16-94) and occurred after a median of two asparaginase doses (range 0-7). Neither age group nor severity of the first AAP was associated with increased hazard of a second AAP event. None of the patients with a second AAP were further re-exposed to asparaginase, and none died of the second AAP. Among a total of 196 ALL relapses, 21 patients have had AAP including 17 patients with asparaginase truncation. However, the hazard of relapse (age- and sex-adjusted) was not increased among AAP patients with asparaginase truncation versus AAP patients with asparaginase re-exposure (5.0-year cumulative incidence of relapse: 13.2% versus 14.2%) (HR 1.0, 95% CI 0.3-3.1, P=1.0). When analyzing time to relapse among AAP patients versus non-AAP patients, no difference in hazard of relapse was found (HR 2.0, 95% CI 0.8-4.9, P=.2). In conclusion, adolescents and young adults tolerated asparaginase treatment as well as children; however, the risk of AAP was higher for patients older than 5.0 years of age with no difference with increasing age. Despite a low AAP-related mortality, the morbidity was considerable and most profound for patients aged 9.0-16.9 years. Since asparaginase re-exposure was associated with a high risk of a second AAP event and neither AAP development nor AAP-related asparaginase truncation was associated with increased relapse risk, asparaginase re-exposure should be attempted only in patients with a high risk of leukemic relapse. Finally, there is an unmet need for preventive strategies toward AAP. Disclosures Wolthers: Novo Nordisk: Employment.