Stellate cell nodule

Single-cell necrosis Single-cell necrosis (s. pp 400, 545) becomes manifest as the destruction of fatty liver cells and as hyaline necrosis. The latter is either drained haematogenically or removed by stellate cells, which may generate stellate cell nodules. When disposing of fatty liver cells, the stellate cells take in lipoid from the necrotic epithelium and become foam-like. This may result in the formation of lipophagic granulomas, (s. p. 398) However, leucocytes also participate, sometimes even exclusively, in the removal of fatty hepatocytes. 

Mesenchymal reaction shows an activation of the stellate cell system the stellate cells and the mononuclear phagocytosis system proliferate, (s. p. 397) Stellate cell nodules form. (s. fig. 22.3) This process spreads from the sinusoids at the site of the lesion to include neighbouring parenchymal cells. The reticular lattice fibre is damaged and sometimes even destroyed. In a more massive lesion, the inflammatory process spreads to the portal zone histiocytes, lymphocytes and eosinophilic leucocytes lead to portal zone cellulations with oedematous dilations, in some cases subsequent to portal fibrosis (s. fig. 21.14), or to cholangitis of the PBC type (s. fig. 29.5) as well as of the PSC type. 

Y. N. Park, C. P. Yang, O. Cubukcu, S. N. Thung, and N. D. Theise, Hepatic stellate cell activation in dysplastic nodules Evidence for an alternate hypothesis concerning human hepatocarcinogenesis, Liver 17 271-274 (1997). 

The earliest histological feature is proliferation of Langerhans cells found around terminal and respiratory bronchioles (3,21). These early cellular lesions expand to form nodules that are typically 1 to 6 mm in diameter (21). These bronchiolo-centric nodules characteristically have a stellate configuration (Fig. la). The morphology of the nodules varies with the activity of the lesions. Early lesions are cellular. The peribronchiolar interstitium and adjacent alveolar septa are thickened by clusters of Langerhans cells admixed with variable numbers of eosinophils, neutrophils, lymphocytes, macrophages, and fibroblasts. Eosinophils are often numerous and can form eosinophilic abscesses but may be absent in up to 20% of... 

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