scholarly journals Bullous pemphigoid in a 3-month-old infant: case report and literature review of this dermatosis in childhood

2013 ◽  
Vol 88 (6) ◽  
pp. 961-965 ◽  
Author(s):  
Eugenio Galdino de Mendonça Reis-Filho ◽  
Tainah de Almeida Silva ◽  
Luiza Helena de Lima Aguirre ◽  
Carmelia Matos Santiago Reis

Bullous pemphigoid is an autoimmune subepidermal blistering dermatosis that is uncommon in childhood. We report a case of a female infant, 3 months old, which presented clinical and laboratory data for the confirmatory diagnosis of bullous pemphigoid. The authors used immunohistochemical staining for collagen type IV that allowed the differentiation of bullous pemphigoid from other subepidermal bullous diseases. Opportunely we review the clinical, immunological, therapeutic and prognostic features of this pathology in children.

1996 ◽  
Vol 84 (6) ◽  
pp. 1013-1019 ◽  
Author(s):  
Masashi Tamaki ◽  
Warren McDonald ◽  
Rolando F. Del Maestro

✓ Type IV collagen is a major protein component of the vascular basement membrane and its degradation is crucial to the initiation of tumor-associated angiogenesis. The authors have investigated the influence of cell density on the release of collagen type IV degrading activity by C6 astrocytoma cells in monolayer culture. The release of collagen type IV degrading activity was assessed biochemically, immunocytochemically, and by Western blot analysis. The results demonstrate that increasing plating density and increasing cell density are associated with decreased collagen type IV degrading activity released per tumor cell. These findings indicate the existence of regulatory mechanisms dependent on cell—cell communication, which modulate release of collagen type IV degrading activity. The extrapolation of these results to the in vivo tumor microenvironment would suggest that individual and/or small groups of invading tumor cells, distant from the main tumor mass, would release substantial collagen type IV degrading activity, which may be crucial to their continued invasion and to angiogenesis.


2000 ◽  
Vol 32 (7) ◽  
pp. 1785 ◽  
Author(s):  
K Utsumi ◽  
T Sawada ◽  
E Adachi ◽  
S Horita ◽  
T Tojimbara ◽  
...  

2021 ◽  
Vol 74 (7) ◽  
pp. 1722-1727
Author(s):  
Vira I. Bobrova ◽  
Anastasia O. Horobets ◽  
Julia I. Proshchenko ◽  
Ludmila O. Levadna ◽  
Zoriana V. Selska

The aim: To study peculiarities of morphological and immunohistochemical changes of stomach’s mucosa in eosinophilic gastritis in children Materials and methods: 64.1±6.0% patients with eosinophilic gastritis and 35.9±6.0% patients with lymphocytic gastritis participated in our investigation. In order to verify the diagnosis morphological and immunohistochemical diagnostics of the stomach’s mucosa was performed in all children. To assess morphological changes in tissues the specimens were colored with hematoxylin, eosin and picrofuchsin by van Gieson’s. Indirect streptavidin-peroxydase staining method was used for immunohistochemical investigation and the following indexes were assessed: proliferating cell nuclear antigen – PCNA, Bcl – 2, Вax, Collagen Type ІV, TGFβ and NF-κβ. Results: Comparative analysis of morphologic investigation has demonstrated that eosinophilic gastritis is characterized by fibrosis and fibroblasts proliferation into basal and superficial parts of mucosa’s lamina propria, multiple hemorrhages, thrombosis and erosions on the background of eosinophilic infiltration. Immunohistochemical indexes of cellular restoration in eosinophilic gastritis are characterized by increased proliferative activity and decreased indexes of proapoptotic and antiapoptotic activity. Prevalence of the reaction with the use of monoclonal antibodies to Collagen Type IV in majority of children with eosinophilic gastritis was characterized by separate fragmented foci in basal membranes of superficial epithelium. Remarkable TGFβ immune coloration was detected in majority of children on the background of fibrosis and eosinophilic infiltration of lamina propria. NF-κβ expression in epitheliocytes’ cytoplasm and nuclei was uneven. Homogenous remarkable coloration was detected in majority of patients with lymphocytic infiltration of mucosa. Conclusions: Eosinophilic gastritis course in children is characterized by remarkable inflammation, decreased regeneration of the mucosa, impairment of cellular restoration which is prognostic index of fibrous remodeling development.


1999 ◽  
Vol 276 (5) ◽  
pp. F684-F690 ◽  
Author(s):  
Margo P. Cohen ◽  
Fuad N. Ziyadeh ◽  
Gregory T. Lautenslager ◽  
Jonathan A. Cohen ◽  
Clyde W. Shearman

Albumin modified by Amadori-glucose adducts induces coordinate increases in the expression of extracellular matrix proteins, transforming growth factor (TGF)-β1, and the TGF-β type II receptor in glomerular mesangial cells. Because activation of protein kinase C (PKC) accompanies the increased mesangial cell expression of matrix proteins and TGF-β1 induced by high ambient glucose, we postulated that glycated albumin (GA) modulates PKC activity and that PKC participates in mediating the GA-induced stimulation of matrix production. To test this hypothesis, we examined the effects of PKC inhibitors on collagen type IV production by mouse or rat mesangial cells incubated with GA, and the influence of GA on PKC activity in these cells. Increased collagen type IV production evoked by GA in 5.5 and 25 mM glucose in mouse mesangial cells was prevented by both general (GF-109203X) and β-specific (LY-379196) PKC inhibitors. Total PKC activity, measured by phosphorylation of a PKC-specific substrate, increased with time after exposure of rat mesangial cells to GA compared with the nonglycated, glucose-free counterpart. GA caused an increase in PKC-β1 membrane-bound fraction and in total PKC activity in media containing physiological (5.5 mM) glucose concentrations in rat mesangial cells, confirming that the glucose-modified protein, and not a “hyperglycemic” milieu, was responsible. The findings indicate that Amadori-modified albumin stimulates mesangial cell PKC activity, and that activation of the PKC-β isoform is linked to the stimulation of collagen type IV production.


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