{"title":"Autoimmune pancreatitis: Biopsy interpretation and differential diagnosis","authors":"Yoh Zen","doi":"10.1053/j.semdp.2024.01.001","DOIUrl":"10.1053/j.semdp.2024.01.001","url":null,"abstract":"<div><p><span>Autoimmune pancreatitis<span> (AIP) is classified into type 1 (IgG4-related) and type 2 (IgG4-unrelated) and the interpretation of pancreatic biopsy findings plays a crucial role in their diagnosis. </span></span>Needle biopsy<span><span> of type 1 AIP in the acute or subacute phase shows a diffuse lymphoplasmacytic infiltrate, storiform fibrosis, obliterative phlebitis, and the infiltration of many IgG4-positive plasma cells. In a later phase, changes become less inflammatory and more fibrotic, making interpretations more challenging. Confirmation of the lack of ‘negative’ findings that are unlikely to occur in type 1 AIP (e.g., neutrophilic infiltration, abscess) is important to avoid an </span>overdiagnosis<span>. The number of IgG4-positive plasma cells increases to >10 cells/high-power field (hpf), and the IgG4/IgG-positive plasma cell ratio exceeds 40 %. However, these are minimal criteria and typical cases show >30 positive cells/hpf and a ratio >70 % even in biopsy specimens. Therefore, cases with a borderline increase in this number or ratio need to be diagnosed with caution. In cases of ductal adenocarcinoma, the upstream pancreas rarely shows type 1 AIP-like changes; however, the ratio of IgG4/IgG-positive plasma cells is typically <40 %. Although the identification of a granulocytic epithelial lesion (GEL) is crucial for type 2 AIP, this finding needs to be interpreted in conjunction with a background dense lymphoplasmacytic infiltrate. An isolated neutrophilic duct injury can occur in peritumoral or obstructive pancreatitis. Drug-induced pancreatitis in patients with inflammatory bowel disease often mimics type 2 AIP clinically and pathologically. IL-8 and PD-L1 are potential ancillary immunohistochemical markers for type 2 AIP, requiring validation studies.</span></span></p></div>","PeriodicalId":49548,"journal":{"name":"Seminars in Diagnostic Pathology","volume":"41 2","pages":"Pages 79-87"},"PeriodicalIF":2.3,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139095341","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Caitlin A. Noble, Andrew P. Biesemier, Sarah McClees, Aljunaid Alhussain, Stephen E. Helms, Robert T. Brodell
{"title":"The History of the Microscope Reflects Advances in Science and Medicine","authors":"Caitlin A. Noble, Andrew P. Biesemier, Sarah McClees, Aljunaid Alhussain, Stephen E. Helms, Robert T. Brodell","doi":"10.1053/j.semdp.2024.01.002","DOIUrl":"https://doi.org/10.1053/j.semdp.2024.01.002","url":null,"abstract":"<p>Microscopes, more than any other instrument, reflect advances in clinical medicine over the past several hundred years. As the primary tool of the pathologist, they were, and continue to be, a key connector between the bedside and basic sciences. One specific example is the science of clinical dermatology, which relies on clinical-pathologic correlation to make a definitive diagnosis. The microscopes used by pathologists, however, are more than scientific artifacts. Many antique microscopes are hand-crafted works of art. Recognizing that light microscopes may soon be obsolete as scanned slides and computer joy-sticks replace optical instruments in patient care and teaching, their significance is not diminished. The microscope will never be forgotten in the history, art, and science of medicine, for these instruments set the social and cultural stage for modern, scientific patient care.</p>","PeriodicalId":49548,"journal":{"name":"Seminars in Diagnostic Pathology","volume":"17 1","pages":""},"PeriodicalIF":2.3,"publicationDate":"2024-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139460334","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Mark Wick contributions to pathology of the mediastinum","authors":"Horacio Maluf","doi":"10.1053/j.semdp.2024.01.006","DOIUrl":"https://doi.org/10.1053/j.semdp.2024.01.006","url":null,"abstract":"<p>Mark Wick made a wide range of contributions to the field of mediastinal pathology. Early papers amplified the spectrum of neuroendocrine carcinomas of the thymus and brought attention to the aggressive nature of this tumor, also highlighting the occurrence of coexisting carcinoid tumor and small cell carcinoma of this organ. The controversial issue of thymoma classification was addressed in several papers and editorial comments, while also reporting a case of metastatic thymoma. A series of thymic carcinomas as well a report on the unusual clear cell variant bear his name as one of the authors. He summarized the topic of mediastinal cyst in a review published in 2005. Sarcomas arising in mediastinal germ cell tumors were also within the purview of his interests, with a publication of series of seven cases. He reviewed the topic of inflammatory myofibroblastic tumor of the heart and added a case to the existing literature. Two books dedicated to different aspect of mediastinal pathology also carry his name in the front cover in association with Drs Taazelar in one and Marchevsky in the other.</p>","PeriodicalId":49548,"journal":{"name":"Seminars in Diagnostic Pathology","volume":"84 1","pages":""},"PeriodicalIF":2.3,"publicationDate":"2024-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139373855","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
C. Alexis Noble, Chinmoy Bhate, Buu Duong, Allison Cruse, Robert T. Brodell, Riley Hanus
{"title":"Clinical-pathologic Correlation: The Impact of Grossing at the Bedside","authors":"C. Alexis Noble, Chinmoy Bhate, Buu Duong, Allison Cruse, Robert T. Brodell, Riley Hanus","doi":"10.1053/j.semdp.2024.01.007","DOIUrl":"https://doi.org/10.1053/j.semdp.2024.01.007","url":null,"abstract":"<p>The unenlightened clinician may submit a skin specimen to the lab and expect an “answer.” The experienced clinician knows that in performing skin biopsies, it is critical to select the most appropriate: 1) anatomic location for the biopsy<span><sup>1</sup></span><sup>,</sup><span><sup>2</sup></span>; 2) type of biopsy<span><sup>1</sup></span><sup>,</sup><span><sup>2</sup></span>; 3) depth and breadth of the biopsy; and 4) medium for hematoxylin and eosin staining (formalin) or direct immunofluorescence (Michel's Transport Medium or normal saline)<span><sup>2</sup></span>. Demographic information, anatomic location, clinical context, and differential diagnosis are all critical components of a properly completed requisition form<span><sup>3</sup></span><sup>,</sup><span><sup>4</sup></span><sup>,</sup><span><sup>5</sup></span>. Proper biopsy design and appropriate grossing of the tissue at the bedside should be added to this list. In this article, we review the basics of gross pathologic examination and then provide four examples to demonstrate that optimal clinical-pathologic correlation requires the clinician consider the needs of the pathologist when tissue is presented to the lab.</p>","PeriodicalId":49548,"journal":{"name":"Seminars in Diagnostic Pathology","volume":"28 1","pages":""},"PeriodicalIF":2.3,"publicationDate":"2024-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139373870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Contributions of Dr. Wick to the pathology of diseases of the lung and pleura.","authors":"Saul Suster","doi":"10.1053/j.semdp.2024.01.005","DOIUrl":"https://doi.org/10.1053/j.semdp.2024.01.005","url":null,"abstract":"<p>The curriculum vitae of Dr. Mark R. Wick contains 57 peer-reviewed publications, 3 editorials, 6 book chapters and a whole book dedicated to diseases of the lung and pleura. It is remarkable that such productivity should represent only a small portion of the overall output of Dr. Wick, which includes (at last count) 341 original peer-review publications, 119 invited review articles, 93 book chapters, 42 editorials, 3 society-related position papers, 18 books and 2 interactive video disks. Yet, his contributions to the literature in pulmonary and pleural pathology have been significant and influential and have established for him a national and international reputation as one of the leading experts in pulmonary pathology. Herein, it is my privilege to recount the various publications contributed by Dr. Wick to this topic, which span the gamut from transplant pathology to neoplastic diseases of the lung and pleura.</p>","PeriodicalId":49548,"journal":{"name":"Seminars in Diagnostic Pathology","volume":"49 2 1","pages":""},"PeriodicalIF":2.3,"publicationDate":"2024-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139373856","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Hereditary succinate dehydrogenase-deficient renal cell carcinoma","authors":"Joanna Rogala , Ming Zhou","doi":"10.1053/j.semdp.2023.11.001","DOIUrl":"10.1053/j.semdp.2023.11.001","url":null,"abstract":"<div><p>Succinate dehydrogenase (SDH), formed by four subunits SDHA, SDHB, SDHC, SDHD, and an assembly factor SDHAF2, functions as a key respiratory enzyme. Biallelic inactivation of genes encoding any of the components, almost always in the presence of a germline mutation, causes loss of function of the entire enzyme complex (so-called SDH deficiency) and subsequent development of SDH-deficient neoplasms which include pheochromocytoma/paraganglioma, gastrointestinal stromal tumor, and renal cell carcinoma (RCC). These tumors may occur in the same patient or kindred. SDH-deficient RCC shows distinctive morphological features with vacuolated eosinophilic cytoplasm due to distinctive cytoplasmatic inclusions containing flocculent material. The diagnosis is confirmed by loss of SDHB on immunohistochemistry with positive internal control. The majority of tumors occur in the setting of germline mutations in one of the <em>SDH</em> genes, most commonly <em>SDHB</em>. The prognosis is excellent for low-grade tumors but worse for high-grade tumors with high-grade nuclei, sarcomatoid change, or coagulative necrosis. Awareness of the morphological features and low-threshold for applying SDHB immunohistochemistry help identify patients with SDH-deficient RCC and hereditary SDH-deficient tumor syndromes. In this review we summarize recent development on the clinical and genetic features, diagnostic approach, and pitfalls of SDH-deficient syndrome, focusing on SDH-deficient renal cell carcinomas.</p></div>","PeriodicalId":49548,"journal":{"name":"Seminars in Diagnostic Pathology","volume":"41 1","pages":"Pages 32-41"},"PeriodicalIF":2.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135516526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"TABLE OF CONTENTS (p/u from previous issue w/updates)","authors":"","doi":"10.1053/S0740-2570(24)00015-7","DOIUrl":"https://doi.org/10.1053/S0740-2570(24)00015-7","url":null,"abstract":"","PeriodicalId":49548,"journal":{"name":"Seminars in Diagnostic Pathology","volume":"41 1","pages":"Page ii"},"PeriodicalIF":2.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0740257024000157/pdfft?md5=6b02b535c507563baa2302cab55c6932&pid=1-s2.0-S0740257024000157-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139487297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Hereditary papillary renal cell carcinoma","authors":"Isa Mulingbayan Jacoba, Zhichun Lu","doi":"10.1053/j.semdp.2023.12.002","DOIUrl":"10.1053/j.semdp.2023.12.002","url":null,"abstract":"<div><p>Hereditary papillary renal cell carcinoma (HPRCC) is an autosomal dominant syndrome characterized by the occurrence of bilateral and multifocal, classic type papillary renal cell carcinomas. In the recent decades, extensive molecular studies have narrowed the molecular underpinnings of this syndrome to missense mutations in tyrosine kinase domain of MET proto-oncogene. Although MET mutations are specific to HPRCC, it has been found in sporadic papillary renal cell carcinomas and as recently reported, in biphasic squamoid alveolar variant of papillary renal cell carcinoma. Dual MET/VEGFR2 kinase inhibitor and tyrosine kinase inhibitors have shown promising results in systemic therapy for HPRCC.</p></div>","PeriodicalId":49548,"journal":{"name":"Seminars in Diagnostic Pathology","volume":"41 1","pages":"Pages 28-31"},"PeriodicalIF":2.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0740257023001132/pdfft?md5=afe25686463bb80fe4933d12ed8c6cbb&pid=1-s2.0-S0740257023001132-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138715919","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Miranda E. Machacek, Chin-Lee Wu, Kristine M. Cornejo
{"title":"Pathology of hereditary renal cell carcinoma syndromes: Tuberous sclerosis complex (TSC)","authors":"Miranda E. Machacek, Chin-Lee Wu, Kristine M. Cornejo","doi":"10.1053/j.semdp.2023.09.001","DOIUrl":"10.1053/j.semdp.2023.09.001","url":null,"abstract":"<div><p><span>Tuberous sclerosis<span> complex (TSC) is an autosomal dominant genetic disease characterized by hamartomatous tumors involving multiple organs such as the brain, skin, heart, lung and kidney. TSC is caused by inactivating mutations in </span></span><em>TSC1/TSC2</em><span><span><span>, which encodes hamartin and </span>tuberin, respectively, and forms a complex that regulates </span>mechanistic target of rapamycin complex 1<span><span> (mTORC1), resulting in cell overgrowth and oncogenesis. Since a leading cause of morbidity and mortality in TSC relates to chronic kidney disease and the ability to preserve renal function, this review describes the important pathologic findings in TSC-associated renal neoplasms and their correlating sporadic counterparts. The most common </span>renal tumor<span><span> in TSC patients are AMLs, followed by a heterogeneous spectrum of renal </span>epithelial tumors, which may provide clues to establishing a diagnosis of TSC.</span></span></span></p></div>","PeriodicalId":49548,"journal":{"name":"Seminars in Diagnostic Pathology","volume":"41 1","pages":"Pages 8-19"},"PeriodicalIF":2.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135388098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}