Wound Healing in Pyoderma Gangrenosum

AbstractEvaluation of skin diseases can be challenging for non-dermatologists. Even obvious well-characterized skin pathologies might be misleading and thus treatment can fail. Particularly the differentiation of surgical treated entities is important, for example the management of a wound healing disturbance profoundly differs from that of a pyoderma gangrenosum. This article outlines several easily mistaken pairs of dermatologic entities on one hand and surgical on the other. For example, a livedo vasculopathy can be confused with a leg ulcer, a nail melanoma with a simple hematoma and finally a hidradenitis suppurativa with an axillary abscess. Typical clinical signs and anamnestic data may often lead to the right diagnosis also assisted by the simple fact to “keep it in mind“.

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Ustekinumab for the treatment of recalcitrant pyoderma gangrenosum: A case report

SAGE Open Medical Case Reports ◽

10.1177/2050313x19845206 ◽

2019 ◽

Vol 7 ◽

pp. 2050313X1984520 ◽

Cited By ~ 2

Author(s):

Isabelle A Vallerand ◽

Jori Hardin

Keyword(s):

Monoclonal Antibody ◽

Wound Healing ◽

Pyoderma Gangrenosum ◽

Healthcare Providers ◽

Interleukin 12 ◽

Systemic Immunosuppression ◽

Topical Treatments ◽

Interleukin 23 ◽

High Degree

Pyoderma gangrenosum is an ulcerating disease associated with a high degree of morbidity and mortality. Currently, little is known about the pathophysiology of pyoderma gangrenosum, though it has been linked to increased levels of inflammatory cytokines including interleukin-23. As pyoderma gangrenosum is a rare disease, evidence for pyoderma gangrenosum treatment is dependent on reporting of cases with successful therapies. Here, we describe a case of pyoderma gangrenosum developing on the lateral leg of a medically complex 47-year-old male already on chronic immunosuppressive therapy, who achieved successful wound healing with the use of ustekinumab, a monoclonal antibody targeting inhibition of interleukin-12 and interleukin-23. This case lends further evidence for the role of interleukin-23 in the pathogenesis of recalcitrant pyoderma gangrenosum and also suggests that healthcare providers may consider a trial of ustekinumab in pyoderma gangrenosum that has failed previous topical treatments or systemic immunosuppression.

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Recombinant human epidermal growth factor enhances wound healing of pyoderma gangrenosum in a patient with ulcerative colitis

Inflammatory Bowel Diseases ◽

10.1002/ibd.20327 ◽

2008 ◽

Vol 14 (5) ◽

pp. 725-727 ◽

Cited By ~ 5

Author(s):

Tae Yeob Kim ◽

Dong Soo Han ◽

Chang Soo Eun ◽

Yong Woo Chung

Keyword(s):

Ulcerative Colitis ◽

Wound Healing ◽

Growth Factor ◽

Epidermal Growth Factor ◽

Pyoderma Gangrenosum ◽

Human Epidermal Growth Factor ◽

Epidermal Growth

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ultrastructural process of intestinal wound healing

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100141494 ◽

1995 ◽

Vol 53 ◽

pp. 1024-1025

Author(s):

Rick L. Vaughn ◽

Shailendra K. Saxena ◽

John G. Sharp

Keyword(s):

Wound Healing ◽

Epithelial Cells ◽

Smooth Muscles ◽

Microscopic Level ◽

Light Microscopic Level ◽

Ileal Mucosa ◽

Wound Model ◽

Serosal Surface ◽

Complex Process ◽

Orderly Fashion

We have developed an intestinal wound model that includes surgical construction of an ileo-cecal patch to study the complex process of intestinal wound healing. This allows approximation of ileal mucosa to the cecal serosa and facilitates regeneration of ileal mucosa onto the serosal surface of the cecum. The regeneration of ileal mucosa can then be evaluated at different times. The wound model also allows us to determine the rate of intestinal regeneration for a known size of intestinal wound and can be compared in different situations (e.g. with and without EGF and Peyer’s patches).At the light microscopic level it appeared that epithelial cells involved in regeneration of ileal mucosa originated from the enlarged crypts adjacent to the intestinal wound and migrated in an orderly fashion onto the serosal surface of the cecum. The migrating epithelial cells later formed crypts and villi by the process of invagination and evagination respectively. There were also signs of proliferation of smooth muscles underneath the migratory epithelial cells.

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Healing gone wrong: convergence of hemostatic pathways and liver fibrosis?

Clinical Science ◽

10.1042/cs20191102 ◽

2020 ◽

Vol 134 (16) ◽

pp. 2189-2201

Author(s):

Jessica P.E. Davis ◽

Stephen H. Caldwell

Keyword(s):

Wound Healing ◽

Liver Disease ◽

Hepatic Fibrosis ◽

Cell Activation ◽

Stellate Cell ◽

Factor Xa ◽

Clinical Trial Data ◽

Chronic Liver ◽

Healing Response ◽

Wound Healing Response

Abstract Fibrosis results from a disordered wound healing response within the liver with activated hepatic stellate cells laying down dense, collagen-rich extracellular matrix that eventually restricts liver hepatic synthetic function and causes increased sinusoidal resistance. The end result of progressive fibrosis, cirrhosis, is associated with significant morbidity and mortality as well as tremendous economic burden. Fibrosis can be conceptualized as an aberrant wound healing response analogous to a chronic ankle sprain that is driven by chronic liver injury commonly over decades. Two unique aspects of hepatic fibrosis – the chronic nature of insult required and the liver’s unique ability to regenerate – give an opportunity for pharmacologic intervention to stop or slow the pace of fibrosis in patients early in the course of their liver disease. Two potential biologic mechanisms link together hemostasis and fibrosis: focal parenchymal extinction and direct stellate cell activation by thrombin and Factor Xa. Available translational research further supports the role of thrombosis in fibrosis. In this review, we will summarize what is known about the convergence of hemostatic changes and hepatic fibrosis in chronic liver disease and present current preclinical and clinical data exploring the relationship between the two. We will also present clinical trial data that underscores the potential use of anticoagulant therapy as an antifibrotic factor in liver disease.

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