Diagnosis of Prostatic Carcinoma After Therapy

Abstract Context.—Prostate cancer is the most common cancer of men in the United States and is third only to lung and colon cancer as a cause of cancer death. In 2006, 27 350 Americans will die of prostate cancer, and 234 460 new cases will be diagnosed. Treatment changes in the benign and cancerous prostate create diagnostic challenges in pathologic interpretation, particularly in needle biopsy specimens and in evaluation of extraprostatic metastases. Objective.—To summarize therapy-related pathologic findings in the prostate with emphasis on recognition of treated adenocarcinoma. Data Sources.—Extensive review of published literature and the authors' experience. Conclusions.—Following therapy for prostate cancer, it is critical that the clinician provide the pertinent history of androgen deprivation or radiation therapy to assist the pathologist in rendering the correct diagnosis.</jats:p

Atypical Small Acinar Proliferation in the Prostate: Clinical Significance in 2006

Abstract About 2% of contemporary prostate needle biopsy specimens contain collections of small acini that are suspicious for cancer but that fall below the diagnostic threshold and are reported as atypical small acinar proliferation suspicious for but not diagnostic of malignancy. Prostate cancer has been identified in specimens from subsequent biopsies in up to 60% of cases of atypical small acinar proliferation, indicating that this finding is a significant predictor of cancer. Identification of atypical small acinar proliferation warrants repeat biopsy for concurrent or subsequent invasive carcinoma.</jats:p

Histologic Patterns and Clues to Autoinflammatory Diseases in Children: What a Cutaneous Biopsy Can Tell Us

Autoinflammation is defined by aberrant, antigen-independent activation of the innate immune signaling pathways. This leads to increased, pro-inflammatory cytokine expression and subsequent inflammation. In contrast, autoimmune and allergic diseases are antigen-directed immune responses from activation of the adaptive immune system. The innate and adaptive immune signaling pathways are closely interconnected. The group of ‘complex multigenic diseases’ are a result of mutual dysregulation of both the autoinflammatory and autoimmune physiologic components. In contrast, monogenic autoinflammatory syndromes (MAIS) result from single mutations and are exclusively autoinflammatory in their pathogenesis. Studying the clinical and histopathological findings for the various MAIS explains the phenotypical correlates of their specific mutations. This review aims to group the histopathologic clues for autoinflammation into three recognizable patterns. The presence of these histologic patterns in a pediatric patient with recurrent fevers and systemic inflammation should raise suspicion of an autoinflammatory component in MAIS, or, more frequently, in a complex multigenic disease. The three major histopathological patterns seen in autoinflammation are as follows: (i) the ‘neutrophilic’ pattern, seen in urticarial neutrophilic dermatosis, pustular psoriasis, aseptic neutrophilic folliculitis, and Sweet’s syndrome; (ii) the ‘vasculitic’ pattern seen in small vessel-vasculitis (including hypersensitivity/leukocytoclastic vasculitis, thrombosing microangiopathy and lymphocytic vasculitis), and intermediate-sized vessel vasculitis, mimicking polyarteritis nodosa; and (iii) the ‘granulomatous’ pattern. Beyond these three patterns, there are additional histopathologic clues, which are detailed below. It is important for a dermatopathologist to recognize the patterns of autoinflammation, so that a diagnosis of MAIS or complex multigenic diseases may be obtained. Finally, careful histopathologic analyses could contribute to a better understanding of the various clinical manifestations of autoinflammation.</jats:p

Histologic patterns and clues to autoinflammatory diseases in children: What a cutaneous biopsy can tell us

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Eruption annulaire centrifuge prurigineuse

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