Exploring Dermatological Manifestations in Gastroparesis and the Associated Link Between Delayed Gastric Emptying and Nutrient Deficiencies

INTRODUCTION Gastroparesis, a condition defined by delayed gastric emptying in the absence of mechanical obstruction, profoundly impacts the body’s ability to process and absorb nutrients. Gastroparesis has a largely idiopathic etiology, but is frequently associated with diabetes and surgery [1]. In diabetic patients, uncontrolled blood glucose can, over time, damage the vagus nerve, which is responsible for gastric and intestinal motility [1]. Post-surgical gastroparesis can occur due to surgical damage to the vagus nerve or other factors affecting gastric motility. This greatly delays the rate at which the stomach empties its contents, thereby causing early satiety, abdominal distension, bloating, diarrhea, and postprandial fullness. Notably, such malabsorption can also have deleterious consequences on the skin barrier, the body’s largest organ with a high nutrient demand [2]. Gastroparesis disrupts the breakdown and assimilation of essential vitamins and minerals that are critical for maintaining overall health. The production of antioxidants, melanin, and tissue regeneration becomes compromised and hinders normal wound healing. Dermatological manifestations can range from xerosis (dry skin) to more severe conditions such as acrodermatitis enteropathica-like lesions and angular cheilitis [3]. This breach of cutaneous integrity also poses a systemic threat: increased susceptibility to viral and bacterial infections. Upon damage to the epidermis, key effectors of the innate immune system become activated along with epidermal keratinocytes, which release bactericidal antimicrobial proteins (AMPs). Their ability to then detect pathogen-associated molecular patterns (PAMPs) instigates the release of inflammatory cytokines, toll-like-receptors (TLRs), nucleotide-binding oligomerization domain-like receptors, and c-type lectin receptors (CLrs) [4]. These proteins are directly involved in defense against Staphylococcus aureus, herpesvirus, papillomaviruses, and Candida albicans [4]. The term “gut-brain axis” is used in clinical academia to underscore the relationship between gastrointestinal and cutaneous health. Histopathologic findings and clinical presentation are key in diagnosing mineral and nutrient dermatoses and may demonstrate spongiosis, hyperkeratosis, parakeratosis, vacuolization, epidermal pallor, ballooning degeneration, and necrolysis [5]. Essential micronutrients such as zinc, copper, iron, and selenium are involved in skin morphogenesis, maintenance, repair, and gene expression. Their deficiencies illustrate their importance in maintaining cutaneous health. For example, deficiencies in zinc present with eczematous plaques and can progress to pustular, annular erosions in skin folds. Advanced cases may present with angular cheilitis and growth delay [6]. Deficiencies in copper, which functions as a cofactor for lysyl oxidase and is involved in crosslinking collagen and elastin, present with hypopigmented, brittle hairs, as well as poor wound healing and seborrheic dermatitis. Low levels of fat-soluble vitamins (A, D, E, and K) and B12 are also commonly seen in patients with gastroparesis, with manifestations ranging from phrynoderma to oral ulcers and coagulopathies [7]. Because these vitamins are involved in the expression of inflammatory cytokines and elimination of reactive oxygen species, patients are left susceptible to respiratory infections and certain forms of breast cancer [7]. These nutritional deficiencies highlight the systemic ramifications of malabsorption and rightfully demand our clinical attention. This paper explores the complex interplay between gastroparesis, nutrient malabsorption, and dermatological health, while examining current therapeutic approaches and the need for integrated care.