- Histopathology（Endhardt、Weber 等，苏黎世大学医院）：在脂肪性肝病（SLD）常规活检中反复见到脂质空泡阻塞肝窦，作者命名为「肝窦脂质性阻塞」（LOS）——形态类似肝移植后的假性紫癜样脂肪变，但发生在移植情境之外。
- 诊断：2019—2024 年标本中检出 8 例；常规 HE 即可提示，IV 型胶原染色显示肝窦双轮廓有助确认，Gomori、CD68 证实脂肪位于细胞外、肝窦受压。
- 临床意义：LOS 伴肝坏死与巨噬细胞活化，病程从亚临床到需肝移植甚至死亡；脂湖面积与最大径越大，临床越重。
- 读片提示：脂肪肝活检见大片细胞外「脂湖」压迫肝窦时，应在报告中指出并量化，提醒临床可能存在肝血流受损。本站仅获摘要。
收录范围：PubMed 结构式摘要中英对照。原文为 Wiley 开放获取（CC BY），但出版社页面被 Cloudflare 拦截，本站未获全文与图表。
摘要
引言：在对脂肪性肝病（SLD）患者标本的常规检查中，我们反复观察到一种特殊现象：肝窦被脂质空泡阻塞（肝窦脂质性阻塞，LOS）。这些改变令人联想到假性紫癜样脂肪变（PPS）——一种肝移植（LT）后的并发症，但值得注意的是，它们发生在移植情境之外。本研究旨在确定 LOS 的诊断指标并明确其临床意义。
方法：对 2019—2024 年间常规送至本研究所的 SLD 肝脏标本进行 LOS 检查。通过辅助染色（Gomori、CD68、IV 型胶原）证实脂肪位于细胞外以及肝窦受压。通过测量脂湖的面积和最大径来量化 LOS 的范围。回顾性评估 LOS 患者的临床病程，并与组织学所见进行关联分析。
结果：8 例患者观察到 LOS，范围从局灶到非常广泛的细胞外脂肪不等。诊断基于常规组织学，并辅以显示肝窦双轮廓的 IV 型胶原染色。形态学所见提示肝窦的脂质性阻塞是关键病理生理因素。LOS 与肝坏死及巨噬细胞活化相关。LOS 患者临床病程不一，从亚临床到严重不等，包括需要肝移植甚至死亡。脂湖范围与临床病程严重程度相关。
结论：我们建议用 LOS 一词指称一种特殊的肝损伤模式，它可发生于移植情境之外的 SLD，并可能导致肝血流受损。LOS 的临床表现多样，从亚临床到致死不等。临床医生和病理医生应了解 SLD 的这一并发症，其诊断依靠肝脏组织学。
- Histopathology (Endhardt, Weber and colleagues, University Hospital Zurich): in routine steatotic liver disease (SLD) biopsies the authors repeatedly saw hepatic sinusoids obstructed by lipid vacuoles — lipidic obstruction of sinusoids (LOS) — resembling post-transplant pseudopeliotic steatosis but outside transplantation.
- Diagnosis: 8 cases among 2019–2024 specimens; suspected on routine histology, supported by collagen IV showing sinusoidal double contours, with Gomori and CD68 confirming extracellular fat and sinusoidal compression.
- Clinical significance: LOS was associated with necrosis and macrophage activation; courses ranged from subclinical to transplantation or death, and fat-lake extent correlated with severity.
- Practice point: large extracellular fat lakes compressing sinusoids in a steatotic liver biopsy should be reported and quantified as a warning of impaired hepatic blood flow. Abstract only.
Scope: the structured PubMed abstract. The article is Wiley open access (CC BY), but the publisher page was blocked by Cloudflare for our fetcher, so the full text and figures were not obtained.
Abstract
Introduction: During routine examination of specimens from patients with steatotic liver disease (SLD), we repeatedly observed a peculiar phenomenon characterized by obstruction of the hepatic sinusoids by lipid vacuoles (lipidic obstruction of sinusoids, LOS). These changes were reminiscent of pseudopeliotic steatosis (PPS), a complication following liver transplantation (LT), but notably occurred outside this context. The aim of our study was to identify diagnostic indicators for LOS and to determine its clinical significance.
Methods: Liver specimens routinely sent to our institute between 2019 and 2024 with SLD were examined for LOS. The extracellular nature of the fat and the compression of the sinusoids were demonstrated by ancillary stains (Gomori, CD68, collagen IV). The extent of the LOS was quantified by measuring the area and maximum diameter of fat lakes. The clinical course of patients with LOS was retrospectively evaluated and correlated with the histological findings.
Results: LOS was observed in eight patients, ranging from focal to very extensive extracellular fat. The diagnosis was based on routine histology, supplemented by collagen IV stain highlighting double contours of sinusoids. The morphological findings suggested that lipidic obstruction of the hepatic sinusoids was a key pathophysiological factor. LOS was associated with liver necrosis and activation of macrophages. Patients with LOS exhibited a variable clinical course, ranging from subclinical to severe, including LT or even death. The extent of fat lakes correlated with the severity of the clinical course.
Conclusions: We suggest the term LOS for a particular pattern of liver damage that can occur in SLD outside the transplantation setting and may lead to impaired hepatic blood flow. LOS is associated with a variable clinical presentation, ranging from subclinical to fatal. Clinicians and pathologists should be aware of this complication of SLD, which is diagnosed by liver histology.