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Background
It is difficult to obtain adequate tissue sample for diagnosing autoimmune pancreatitis (AIP) with the help of traditional EUS-guided FNA. As per ICDC guidelines, EUS-guided FNA is not recommended for diagnosing AIP(1). We herein present a report of 2 cases of using a new flexible 22 gauge (G) core biopsy needle (SharkCore, Medtronic, Sunnydale, Calif) for diagnosing AIP.Methods
This is a report of 2 cases reviewed retrospectively which had used 22G core biopsy needle for obtaining histo-pathological samples for diagnosing AIP. The cases were reviewed with both endoscopist and a pathologist to determine if the diagnostic criteria were met.Results
Both the cases had adequate tissue sample obtained to make a clear diagnosis of AIP. Pathology showed changes of chronic pancreatitis with atrophy and storiform pattern of fibrosis with a dense lymphoplasmacytic infiltrate in both cases along with identification of IgG4 cells.Conclusion
EUS-guided fine needle biopsy (FNB) using the SharkCore needle can be used reliably for diagnosing AIP. More studies need to be performed to validate this further. 相似文献Paroxysmal kinesigenic dyskinesia is an episodic movement disorder caused by dominant mutations in the proline-rich transmembrane protein PRRT2, with onset in childhood and typically with improvement or resolution by middle age. Mutations in the same gene may also cause benign infantile seizures, which begin in the first year of life and typically remit by the age of 2 years. Many details of PRRT2 function at the synapse, and the effects of mutations on neuronal excitability in the pathophysiology of epilepsy and dyskinesia, have emerged through the work of several groups over the last decade. However, the age dependence of the phenotypes has not been explored in detail in transgenic models. Here, we report our findings in heterozygous and homozygous Prrt2 knockout mice that recapitulate the age dependence of dyskinesia seen in the human disease. We show that Prrt2 deletion reduces the levels of synaptic proteins in a dose-dependent manner that is most pronounced at postnatal day 5 (P5), attenuates at P60, and disappears by P180. In a test for foot slippage while crossing a balance beam, transient loss of coordination was most pronounced at P60 and less prominent at age extremes. Slower traverse time was noted in homozygous knockout mice only, consistent with the ataxia seen in rare individuals with biallelic loss of function mutations in Prrt2. We thus identify three age-dependent phenotypic windows in the mouse model, which recapitulate the pattern seen in humans with PRRT2-related diseases.
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