Mid‐dermal elastolysis associated with Hashimoto's thyroiditis

Gambichler, Thilo; Linhart, Carola; Wolter, M.

doi:10.1111/j.1468-3083.1999.tb01038.x

Cited by 25 publications

(2 citation statements)

References 35 publications

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“…Gambichler et al found increased histiocyte activity—the natural producer of MMPs—in MDE lesions as well as objective upregulation of MMPs and elastophagocytosis. This is accompanied by downregulation of tissue inhibitor of metalloproteinase 1, which is responsible for the physiological negative feedback of MMPs.…”

Section: Discussionmentioning

confidence: 99%

“…2,3 These peptidases are naturally responsible for extracellular matrix degradation; overactivity causes pathologic elastin destruction and therefore decreased skin resilience and wrinkling. 3 Gambichler et al 1,4 found increased histiocyte activitythe natural producer of MMPs-in MDE lesions as well as objective upregulation of MMPs and elastophagocytosis. This is accompanied by downregulation of tissue inhibitor of metalloproteinase 1, which is responsible for the physiological negative feedback of MMPs.…”

Section: Observation Middermal Elastolysis-a Possible End Stage Of Gr...mentioning

confidence: 99%

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Middermal Elastolysis—A Possible End Stage of Granuloma Annulare

2020

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samples, there were deposits of complement including C5b-9, suggesting a critical role for complement activation in the pathogenesis of the thrombotic diathesis. Coagulopathy in the context of severe inflammation (elevated D-dimer, fibrinogen, or C-reactive protein levels) has been reported in patients with COVID-19. 3 Because of the increased incidence of thrombotic events reported in severely ill patients with COVID-19 4 and recent data suggesting a survival benefit in such patients who receive anticoagulants, 5 treatment algorithms for severely ill patients with COVID-19 are including therapeutic anticoagulation at many institutions. 6 Despite initiation of prophylactic anticoagulation therapy at admission for all 4 patients, all developed cutaneous thrombosis and a clinically suspected pulmonary embolism.The limitations of this report include our inability to confirm the precise timing of rash onset owing to limited full skin examinations. In addition, we did not perform imaging for pulmonary emboli because of efforts to minimize staff exposure.The findings suggest that clinicians caring for patients with COVID-19 should be aware of livedoid and purpuric rashes as potential manifestations of an underlying hypercoagulable state. If these skin findings are identified, a skin biopsy should be considered because the result may guide anticoagulation management. Even in the absence of other thrombotic events, consultation with hematology staff, along with escalation of anticoagulation, should be considered.

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Section: Discussionmentioning

confidence: 99%

Section: Observation Middermal Elastolysis-a Possible End Stage Of Gr...mentioning

confidence: 99%

Middermal Elastolysis—A Possible End Stage of Granuloma Annulare

2020

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A novel MGP mutation in a consanguineous family: Review of the clinical and molecular characteristics of Keutel syndrome

Hur

Raymond

Kahler

et al. 2005

American J of Med Genetics Pt A

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Keutel syndrome (KS) [OMIM 245150] is a rare autosomal recessive condition, characterized by abnormal cartilage calcification. Mutations in the matrix Gla protein gene (MGP) have been previously reported in three unrelated KS families. MGP is an extracellular matrix protein that acts as a calcification inhibitor by repressing bone morphogenetic protein 2 (BMP2). Loss-of-function mutations of MGP result in abnormal calcification of the soft tissues, a cardinal feature of KS. We report the fourth MGP mutation (IVS2 + 1G > A) in a consanguineous Arab family, which results in the loss of the consensus donor splice site at the exon 2-intron 2 junction. In addition to the typical manifestations, we observed abnormalities in the white matter of the brain, optic nerve atrophy, and mid-dermal elastolysis in the affected individuals of this family. This report broadens the clinical phenotype observed in patients with KS. The effect of the IVS2 + 1G > A mutation is consistent with the previously reported loss-of-function mutations of MGP.

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