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Presents a case of a 66-year-old man with epigastric pain and jaundice. Rarity of traumatic neuroma; Difficulty of removing the common bile duct stones during endoscopic retrograde cholangio-pancreatography; Description of neuroma.

Amyloidosis is a group of disorders caused by deposition of misfolded proteins as aggregates in the extracellular tissues of the body, leading to impairment of organ function. Correct identification of the causal amyloid protein is absolutely crucial for clinical management in order to avoid misdiagnosis and inappropriate, potentially harmful treatment, to assess prognosis and to offer genetic counselling if relevant. Current diagnosticmethods, including antibody-based amyloid typing, have limited ability to detect the full range of amyloid forming proteins. Recent investigations into proteomic identification of amyloid protein have shown promise. This paper will review the current state of the art in proteomic analysis of amyloidosis, discuss the suitability of techniques based on the properties of amyloidosis, and further suggest potential areas of development. Establishment of mass spectrometry aided amyloid typing procedures in the pathology laboratory will allow accurate amyloidosis diagnosis in a timely manner and greatly facilitate clinical management of the disease. [ABSTRACT FROM AUTHOR]

Background: Correct identification of the amyloidosis-causing protein is crucial for clinical management. Recently the Mayo Clinic reported laser-capture microdissection (LCM) with liquid chromatography-coupled tandem mass spectrometry (MS/MS) as a new diagnostic tool for amyloid diagnosis. Here, we report an independent implementation of this proteomic diagnostics method at the Princess Alexandra Hospital Amyloidosis Centre in Brisbane, Australia. Results: From 2010 to 2014, 138 biopsies received from 35 different organ sites were analysed by LCM-MS/MS using Congo Red staining to visualise amyloid deposits. There was insufficient tissue in the block for LCM for 7 cases. An amyloid forming protein was ultimately identified in 121 out of 131 attempted cases (94 %). Of the 121 successful cases, the Mayo Clinic amyloid proteomic signature (at least two of Serum Amyloid P, ApoE and ApoA4) was detected in 92 (76 %). Low levels of additional amyloid forming proteins were frequently identified with the main amyloid forming protein, which may reflect co-deposition of fibrils. Furthermore, vitronectin and clusterin were frequently identified in our samples. Adding vitronectin to the amyloid signature increases the number of positive cases, suggesting a potential 4th protein for the signature. In terms of clinical impact, amyloid typing by immunohistochemistry was attempted in 88 cases, reported as diagnostic in 39, however, 5 were subsequently revealed by proteomic analysis to be incorrect. Overall, the referring clinician's diagnosis of amyloid subtype was altered by proteomic analysis in 24 % of cases. While LCM-MS/MS was highly robust in protein identification, clinical information was still required for subtyping, particularly for systemic versus localized amyloidosis. Conclusions: This study reports the independent implementation and evaluation of a proteomics-based diagnostic for amyloidosis subtyping. Our results support LCM-MS/MS as a powerful new diagnostic technique for amyloidosis, but also identified some challenges and further development opportunities. [ABSTRACT FROM AUTHOR]

We report an unusual case of fibrillary glomerulonephritis (FGN) presenting as rapidly progressive renal failure and extensive crescent formation along with linear staining of capillary walls of the glomeruli on immunofluorescence, mimicking anti-glomerular basement membrane (anti-GBM) antibody-mediated disease. Laboratory results for circulating anti-GBM antibodies were negative. The subsequent electron microscopic findings were that of presence of electron-dense deposits in the glomerular mesangium and capillary walls, comprising of non-branching fibrils with an average diameter of 16 nm consistent with a diagnosis of FGN. This case illustrates the crucial role of electron microscopy in differential diagnosis of crescentic glomerulonephritis. [ABSTRACT FROM PUBLISHER]