Ramin Zargham

Bio: Ramin Zargham is an academic researcher from McGill University Health Centre. The author has contributed to research in topics: Atrophoderma & Linear atrophoderma of Moulin. The author has an hindex of 2, co-authored 2 publications receiving 47 citations.

Insights into the Pathophysiology of Hypertrophic Scars and Keloids: How Do They Differ?

Abstract: GENERAL PURPOSE:To provide information about the clinical presentation of hypertrophic scars and keloids based on their varied structural components.TARGET AUDIENCE:This continuing education activity is intended for physicians, physician assistants, nurse practitioners, and nurses with an interest i

Linear atrophoderma of Moulin: an underrecognized entity

Abstract: Linear atrophoderma of Moulin (LAM) is an acquired skin condition that manifests in early childhood and adolescence. It likely represents a form of cutaneous mosaicism that presents with linear, hyperpigmented and atrophic lesions appearing on the trunk and limbs. Its clinical appearance varies and may closely resemble that of atrophoderma of Pasini and Pierini (APP) and linear scleroderma. LAM usually follows a benign course and no effective treatment options exist. We present a case of a young and healthy patient that developed such lesions on her upper and lower extremities over 5 years. The initial clinical impression of linear scleroderma was reviewed in favor of LAM following histological examination of the lesions which revealed no significant inflammatory changes. LAM remains a rare and possibly under recognized entity with reports confined only to the dermatologic literature. This case highlights the importance of recognizing LAM and distinguishing it from linear scleroderma given the significant differences in management and prognosis.

Cutaneous Manifestations of Scleroderma and Scleroderma-Like Disorders: a Comprehensive Review

Abstract: Scleroderma refers to an autoimmune connective tissue fibrosing disease, including three different subsets: localized scleroderma, limited cutaneous systemic sclerosis, and diffuse cutaneous systemic sclerosis with divergent patterns of organ involvement, autoantibody profiles, management, and prognostic implications. Although systemic sclerosis is considered the disease prototype that causes cutaneous sclerosis, there are many other conditions that can mimic and be confused with SSc. They can be classified into immune-mediated/inflammatory, immune-mediated/inflammatory with abnormal deposit (mucinoses), genetic, drug-induced and toxic, metabolic, panniculitis/vascular, and (para)neoplastic disorders according to clinico-pathological and pathogenetic correlations. This article reviews the clinical presentation with emphasis on cutaneous disease, etiopathogenesis, diagnosis, and treatment options available for the different forms of scleroderma firstly and for scleroderma-like disorders, including scleromyxedema, scleredema, nephrogenic systemic fibrosis, eosinophilic fasciitis, chronic graft-versus-host disease, porphyria cutanea tarda, diabetic stiff-hand syndrome (diabetic cheiroartropathy), and other minor forms. This latter group of conditions, termed also scleroderma mimics, sclerodermiform diseases, or pseudosclerodermas, shares the common thread of skin thickening but presents with distinct cutaneous manifestations, skin histology, and systemic implications or disease associations, differentiating each entity from the others and from scleroderma. The lack of Raynaud's phenomenon, capillaroscopic abnormalities, or scleroderma-specific autoantibodies is also important diagnostic clues. As cutaneous involvement is the earliest, most frequent and characteristic manifestation of scleroderma and sclerodermoid disorders, dermatologists are often the first-line doctors who must be able to promptly recognize skin symptoms to provide the affected patient a correct diagnosis and appropriate management.

Toward understanding scarless skin wound healing and pathological scarring.

Abstract: The efficient healing of skin wounds is crucial for securing the vital barrier function of the skin, but pathological wound healing and scar formation are major medical problems causing both physiological and psychological challenges for patients. A number of tightly coordinated regenerative responses, including haemostasis, the migration of various cell types into the wound, inflammation, angiogenesis, and the formation of the extracellular matrix, are involved in the healing process. In this article, we summarise the central mechanisms and processes in excessive scarring and acute wound healing, which can lead to the formation of keloids or hypertrophic scars, the two types of fibrotic scars caused by burns or other traumas resulting in significant functional or aesthetic disadvantages. In addition, we discuss recent developments related to the functions of activated fibroblasts, the extracellular matrix and mechanical forces in the wound environment as well as the mechanisms of scarless wound healing. Understanding the different mechanisms of wound healing is pivotal for developing new therapies to prevent the fibrotic scarring of large skin wounds.

Keloids: a review of therapeutic management

Abstract: Keloid scar formation arises from a disorganized fibroproliferative collagen response that extends beyond the original wound margins because of excessive production of extracellular matrix (ECM). Despite treatment options for keloid scars including medical and surgical therapies, such as intralesional steroid injection and surgical excision, the recurrence rate remains high. Herein we consolidate recently published narrative reviews, systematic reviews, and meta-analyses to provide an overview of updated treatment recommendations for keloidal scar formation. PubMed search engine was used to access the MEDLINE database to investigate updates regarding keloid incidence and treatment. More than 100 articles were reviewed. Keloid management remains a multimodal approach. There continues to be no gold standard of treatment that provides a consistently low recurrence rate; however, the increasing number of available treatments and synergistic combinations of these treatments (i.e., laser-based devices in combination with intralesional steroids, or 5-fluorouracil (5-FU) in combination with steroid therapy) is showing favorable results. Future studies could target the efficacy of novel treatment modalities (i.e., autologous fat grafting or stem cell-based therapies) for keloid management. This review article provides updated treatment guidelines for keloids and discusses insight into management to assist patient-focused, evidence-based clinical decision making.

Keloids: A Review of Etiology, Prevention, and Treatment.

Abstract: Keloids are abnormal scars that cause significant emotional and physical distress in patients when inadequately treated. Keloid formation is theorized to occur as a result of an imbalance between an increased synthesis of collagen and extracellular matrix and decreased degradation of these products. Inflammatory mediators- namely, transforming growth factor beta-have been proposed to influence the dysregulation of collagen remodeling in the scar healing process. Though limited, current knowledge of keloid pathophysiology has guided clinicians to explore novel therapies for keloid prevention and treatment. In addition to conducting research refining the use of common therapies, such as steroids and radiation, clinicians have evaluated the potential of anti-inflammatory and chemotherapeutic molecules to suppress keloid recurrence. Procedural focused therapies, such as cryotherapy and lasers, have also found a role in reducing keloid symptomatology. The purpose of this report is to examine the current literature and review the mechanisms of action, efficacy, and side effects of different keloid therapies. Despite the growing literature investigating reliable methods for keloid management, there are no standardized guidelines or treatment protocols supported by academic governing bodies. Stronger evidence with high-fidelity randomized clinical trials will be needed to determine the optimal therapy regimens for keloids.

Hypertrophic scars and keloids: Overview of the evidence and practical guide for differentiating between these abnormal scars.

Abstract: Although hypertrophic scars and keloids both generate excessive scar tissue, keloids are characterized by their extensive growth beyond the borders of the original wound, which is not observed in hypertrophic scars. Whether or not hypertrophic scars and keloids are two sides of the same coin or in fact distinct entities remains a topic of much debate. However, proper comparison between the two ideally occurs within the same study, but this is the exception rather than the rule. For this reason, the goal of this review was to summarize and evaluate all publications in which both hypertrophic scars and keloids were studied and compared to one another within the same study. The presence of horizontal growth is the mainstay of the keloid diagnosis and remains the strongest argument in support of keloids and hypertrophic scars being distinct entities, and the histopathological distinction is less straightforward. Keloidal collagen remains the strongest keloid parameter, but dermal nodules and α-SMA immunoreactivity are not limited to hypertrophic scars alone. Ultimately, the current hypertrophic scars-keloid differences are mostly quantitative in nature rather than qualitative, and many similar abnormalities exist in both lesions. Nonetheless, the presence of similarities does not equate the absence of fundamental differences, some of which may not yet have been uncovered given how much we still have to learn about the processes involved in normal wound healing. It therefore seems pertinent to continue treating hypertrophic scars and keloids as separate entities, until such a time as new findings more decisively convinces us otherwise.