Thrombophlebitis complicating sternocostoclavicular hyperostosis

Haenel, Louis C.; Bradway, William; Costantini, Peter J.

doi:10.1080/00325481.1980.11715594

Cited by 16 publications

(6 citation statements)

References 4 publications

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“…Venous thrombosis in patients with thoracic hyperostosis and palmoplantar pustulosis was first noted by Kohler et al [8] and was subsequently mentioned by others [4,6]. Most affected patients are white.…”

Section: Discussionmentioning

confidence: 96%

Soft tissue involvement, mediastinal pseudotumor, and venous thrombosis in pustulotic arthro-osteitis

et al. 1989

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A syndrome of hyperostosis of the thoracic wall, nonspecific signs of inflammatory disease, and palmar and plantar pustulosis is described in eight patients (Table 1). Seven had intersternocostoclavicular ossification, and one had chronic recurrent multifocal osteomyelitis. This complex of findings has been called "pustulotic arthro-osteitis". This report emphasizes the periosseous soft tissue inflammation and the unexplained subclavian and mediastinal vein thrombosis seen in two patients. Inflammatory periosseous and mediastinal lesions were seen on plain films in all eight patients and on computed tomographic (CT) scans in seven. Radiographs of the spine showed a spondyloarthropathy in three patients. This was characterized by ossification of the vertebral ligaments and sclerosis of the vertebral bodies. Awareness of the radiologic features of pustulotic arthro-osteitis is important because the clinical, biochemical and pathologic findings are often nonspecific and misleading.

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Section: Discussionmentioning

confidence: 96%

Soft tissue involvement, mediastinal pseudotumor, and venous thrombosis in pustulotic arthro-osteitis

et al. 1989

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“…We found 11 articles published describing a total of 15 cases of venous thrombosis. [3][4][5][6][7][8][9][10][11][12][13] One was a retrospective series of 120 cases, and only describes a case of thrombosis of the subclavian vein. 3…”

Section: Review Of the Literaturementioning

confidence: 99%

Thrombotic Manifestations in SAPHO Syndrome. Review of the Literature

Carranco-Medina

Calleja

Calero-Paniagua

et al. 2015

Reumatología Clínica (English Edition)

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“…Bile acids are amphipathic molecules synthesized in hepatocytes as the major products of cholesterol catabolism and act as biological detergents that promote the absorption, transport, and distribution of lipids and fat-soluble vitamins 1 . Bile acids are also required to modulate metabolic pathways, including glucose metabolism, lipid metabolism, and energy expenditure 2 . Impaired bile flow, due to blockage of the biliary tract or genetic defects, causes the accumulation of bile acids in the liver and systemic circulation and results in cholestatic liver diseases such as cholestasis, which leads to progressive liver fibrosis and ultimately liver failure 3 – 5 .…”

Section: Introductionmentioning

confidence: 99%

Sestrin2 protects against cholestatic liver injury by inhibiting endoplasmic reticulum stress and NLRP3 inflammasome-mediated pyroptosis

Han

Kim

et al. 2022

Exp Mol Med

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Chronic exposure to bile acid in the liver due to impaired bile flow induces cholestatic liver disease, resulting in hepatotoxicity and liver fibrosis. Sestrin2, a highly conserved, stress-inducible protein, has been implicated in cellular responses to multiple stress conditions and the maintenance of cellular homeostasis. However, its role in cholestatic liver injury is not fully understood. In this study, we investigated the role of hepatic Sestrin2 in cholestatic liver injury and its underlying mechanisms using in vivo and in vitro approaches. Hepatic Sestrin2 expression was upregulated by activating transcription factor 4 (ATF4) and CCAAT/enhancer-binding protein-β (C/EBP-β) after treatment with bile acids and correlated with endoplasmic reticulum (ER) stress responses. Bile-duct ligation (BDL)-induced hepatocellular apoptosis and liver fibrosis were exacerbated in Sestrin2-knockout (Sesn2−/−) mice. Moreover, Sestrin2 deficiency enhanced cholestasis-induced hepatic ER stress, whereas Sestrin2 overexpression ameliorated bile acid-induced ER stress. Notably, the mammalian target of rapamycin (mTOR) inhibitor rapamycin and the AMP-activated protein kinase (AMPK) activator AICAR reversed bile acid-induced ER stress in Sestrin2-deficient cells. Furthermore, Sestrin2 deficiency promoted cholestasis-induced hepatic pyroptosis by activating NLRP3 inflammasomes. Thus, our study provides evidence for the biological significance of Sestrin2 and its relationship with cholestatic liver injury, suggesting the potential role of Sestrin2 in regulating ER stress and inflammasome activation during cholestatic liver injury.

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Thrombophlebitis complicating sternocostoclavicular hyperostosis

Cited by 16 publications

References 4 publications

Soft tissue involvement, mediastinal pseudotumor, and venous thrombosis in pustulotic arthro-osteitis

Soft tissue involvement, mediastinal pseudotumor, and venous thrombosis in pustulotic arthro-osteitis

Thrombotic Manifestations in SAPHO Syndrome. Review of the Literature

Sestrin2 protects against cholestatic liver injury by inhibiting endoplasmic reticulum stress and NLRP3 inflammasome-mediated pyroptosis

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