Blisters

Blisters: A Comprehensive Reference in the Context of Nutrition and Natural Health

1. Definition and Overview

A blister is a specialized physiological defense mechanism where the body creates a fluid-filled pocket between skin layers to protect underlying tissue from mechanical or thermal damage. In a broader clinical sense, blistering of the skin occurs as a primary event and is associated with tissue injury and fluid accumulation within a specific layer of the skin: intraepidermal, dermal-epidermal junction, or subepidermal.

The pathophysiology of blistering diseases illustrates how impairments in epithelial adhesion lead to disorders characterized by substantial morbidity and/or mortality. Blistering diseases can be inherited or acquired. Blister formation in this latter group of diseases is due to either genetic mutation or an autoimmune response. Genodermatoses associated with blisters are typically manifested in the neonate, whereas the autoimmune blistering disorders are acquired and usually expressed later in life.

The fluid contained within a common friction blister is largely interstitial in origin. Blisters form when shear forces cause the epidermis to detach from the dermis, creating a void that fills with sterile interstitial fluid. When the epidermal layer detaches, the nerve endings in the dermis become sensitized. This is why a filled blister is often less painful than a "de-roofed" or popped blister, as the fluid acts as a protective barrier.

2. Classification and Presentation

Blisters are broadly categorized by their cause and by the depth at which they form within the skin:

• Friction (mechanical) blisters: A friction blister results from mechanical fatigue within the stratum spinosum layer of the epidermis. Friction blisters are formed as a result of abrasion caused by the frictional forces applied directly to the skin's top layer of the epidermis, the stratum corneum. The frictional force applied to the stratum corneum is transmitted through the stratum granulosum into the stratum spinosum of the epidermis, causing micro-tearing between skin layers.
• Thermal (burn) blisters: Superficial second-degree burns involve both the epidermis and part of the dermis. Deep second-degree burns penetrate the dermis and may present with intact blisters.
• Autoimmune blistering diseases: Most acquired blistering diseases are autoimmune in nature and are characterized by autoantibodies that target adhesion junctions promoting either cell-cell or cell-matrix adhesion in skin.
• Nutritional deficiency blisters: As discussed further below, certain vitamin and mineral deficiencies — most notably niacin — can produce vesicular or bullous skin eruptions.

The inflammatory response within a blister is a dynamic process. Accumulation of the complement fragment C5a and leukotriene B4 are detectable within 3 hours; IL-6, IL-8, IL-1 beta, tumor necrosis factor-alpha, and granulocyte-macrophage colony-stimulating factor become markedly elevated by 24 hours. The sequential appearance of mediators at an inflammatory focus suggests that a carefully regulated dynamic system is responsible for controlling the evolution of the inflammatory response.

3. Body Systems Involved

The integumentary system is the primary site of blister formation. Recent advances have uncovered the relevance of the keratinocyte cytoskeleton, the desmosome, the hemidesmosome, and extracellular matrix proteins in blister formation.

The immune system plays a central role in both the formation and resolution of blistering. In patients with bullous pemphigoid (BP), IgG autoantibodies bind to the skin basement membrane. This binding activates complement and inflammatory mediators. Activation of the complement system is thought to play a critical role in attracting inflammatory cells to the basement membrane. These inflammatory cells are postulated to release proteases, which degrade hemidesmosomal proteins and lead to blister formation.

In autoimmune blistering disease, the immune system targets specific structural proteins. Intraepidermal blistering found in pemphigus disorders is caused by autoantibodies targeting cadherin proteins in desmosomes; subtypes pemphigus vulgaris and pemphigus foliaceus are associated with antibodies against desmoglein (dsg)-3 and -1, respectively. In bullous pemphigoid, autoantibodies target two hemidesmosome components BP180 and BP230; and in epidermolysis bullosa acquisita patients have autoantibodies targeting type VII collagen anchoring fibrils.

The musculoskeletal system is relevant to the biomechanics of friction blistering. Foot friction blisters are caused by repetitive shear deformation. The three fundamental elements of blister-inducing shear deformation are (1) motion of bone, (2) high friction force, and (3) repetition of the resulting shear events. The movement force or shear force that generates blister formation originates from the bones moving relative to the soft tissues within the foot.

The gastrointestinal and metabolic systems are implicated in nutritional deficiency-associated blistering. Deficiencies of specific nutrients (discussed below) that arise from dietary inadequacy, malabsorption, or systemic disease can manifest as cutaneous blistering.

4. Contributing and Associated Factors

4.1 Mechanical and Environmental Factors

Identified risk factors for friction blistering include excess moisture, temperature, heavy load-bearing, activity duration, inappropriate footwear and socks, as well as inadequate adaptation and conditioning to the undertaken route.

Friction blisters are more frequent in hotter environmental conditions. Furthermore, an increase in skin temperature precedes blister formation, and a prolonged increase in temperature is present after a blister forms. However, histologic studies have shown that friction blisters are not a thermal injury. Moisture from perspiration is also relevant to blister formation because it increases friction force.

Even mild to moderate hydration levels of the feet are known to increase skin friction and the likelihood of blisters. Naylor recognized the protective effect of dried skin against blister formation, confirming that moisture reduced the number of shear applications the skin could withstand before blister damage.

Exacerbating factors include heat — blisters are particularly prevalent in tropical climates. Prolonged or vigorous exercise is common in athletes (especially marathon runners) and soldiers; one third of 872 American soldiers surveyed when in Iraq had blisters. Carrying a heavy load increases the risk of blisters. Excessive sweating (hyperhidrosis) softens the skin so the skin splits more easily. Tight, uncomfortable, or new shoes that repetitively rub on one or two areas of skin are also a key factor.

4.2 Nutritional Deficiency as a Cause of Blistering

Certain nutritional deficiencies are directly associated with blister or vesicle formation in the skin. This represents an important nutritional-health dimension that is distinct from the mechanical or autoimmune pathways.

Niacin (Vitamin B3) Deficiency — Pellagra

Chronic vitamin B3 (niacin) deficiency results in pellagra, the features of which are often quoted as the four Ds: dermatitis, diarrhea, dementia, and (if left untreated) death. The characteristic dermatitis is a photosensitive eruption. Initially, there is erythema and edema after sun exposure, which may be painful, burning, or pruritic and may resemble a sunburn. If severe, vesicles or bullae may be seen, sometimes termed wet pellagra.

Niacin is a part of nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP) and is crucial for energy production, metabolic processes, DNA repair, and antioxidant function. Tissues with high turn-over rates, such as the skin and the bowel, or with high energy consumption, such as the brain, are the most affected by niacin deficiency. Niacin deficiency is commonly associated with deficiency of other nutrients, including protein, riboflavin, pyridoxine, thiamine, folic acid, vitamin A, magnesium, potassium, iron, and zinc, which can further complicate the clinical assessment of pellagra.

Zinc Deficiency

Skin contains a relatively high (about 5% of body content) zinc content, primarily associated within the epidermis (50–70 μg/g dry weight). Mild zinc deficiency is noted to lead to roughened skin and impaired wound healing. In more severe cases, zinc deficiency produces overt blistering skin lesions. Affected individuals develop a classical triad of dermatitis, depression, and diarrhea. The eruption is symmetrically distributed over the extensor surfaces of the major joints, the fingertips, and perioroficially (around eyes, nose, mouth, and perineum), characterized by erythematous erosions and blisters.

Severe zinc deficiency was found to be related to acrodermatitis enteropathica (AE), a potentially fatal genetic disorder in which individuals are unable to absorb sufficient dietary zinc as a result of mutations in the SLC39A4 gene, which encodes hZIP4. Zinc deficiency associated with AE leads to dermatitis, diarrhea, secondary bacterial/fungal infections, and often mortality in untreated infants.

5. Nutrients, Herbs, and Natural Ingredients: Traditional Use and Scientific Evidence

5.1 Vitamin C (Ascorbic Acid)

Traditional Use

Vitamin C-rich plant foods — including citrus fruits, rosehips, and sea buckthorn — have been used for centuries in many traditional healing traditions to support wound closure and skin integrity, though these uses were not formally distinguished from other constituents of these foods in pre-scientific literature.

Scientific Evidence

Vitamin C (ascorbic acid), a cofactor for collagen synthesis and a primary antioxidant, is rapidly consumed post-wounding. From the inflammatory phase — by acting as a free radical scavenger to reduce oxidative stress — to the proliferative phase in which the synthesis, maturation, and secretion of collagen takes place, to the maturation phase during which collagen production occurs throughout, vitamin C's role in wound healing is inextricably linked to improved wound recovery.

Along with its role in collagen synthesis, there is also evidence that vitamin C increases the proliferation of dermal fibroblasts, a function important for wound healing. Vitamin C is consumed in these processes, so there is likely to be increased turnover at wound sites, suggesting that supplementation may be beneficial in healing. In addition, inflammation probably hastens the degradation and consumption of vitamin C, which is normally present to at least a small degree in all wounds.

A 2022 systematic review (18 studies, databases including PubMed, Embase, and the Cochrane Library) found that overall, vitamin C supplementation improved healing outcomes in certain pathologies, predominantly pressure ulcers. However, many of the studies had small sample sizes, combined nutritional treatments, and did not test baseline vitamin C.

Intervention studies show that an energy and protein-rich oral nutritional supplement providing high doses of vitamin C and zinc in combination with arginine may prevent the development of pressure ulcers. This measure seems to improve the healing of pressure ulcers, which is questionable for vitamin C alone. Much of the data surrounding the use of vitamin C and zinc in wound healing is a result of multiple, concomitant nutritional interventions in patients with noted existing nutritional deficiencies. No studies were found that examined vitamin C alone.

Evidence strength: Mechanistic evidence for vitamin C in collagen synthesis and wound repair is well established. Clinical trial evidence for supplementation specifically in blister healing is indirect; most human RCT data derive from pressure ulcer studies and are confounded by multi-nutrient protocols. Vitamin C deficiency (scurvy) produces impaired healing as a direct documented consequence. Supplementation in already-replete individuals is not clearly supported by high-quality RCT evidence.

5.2 Zinc

Traditional Use

Zinc-containing preparations — including calamine (a zinc carbonate/oxide mineral pigment) and zinc sulfate solutions — have been used topically for centuries across multiple traditions for their astringent, drying, and skin-protective properties on ulcers, wounds, and blistered skin.

Scientific Evidence

Zinc functions to aid in the wound healing process by supporting collagen and protein synthesis, membrane stability, and clot formation. Zinc deficiency results in lowered populations of both precursor and mature B-cells and can reduce antibody production. Diminishing B-cell populations and, consequently, circulating antibodies would negatively affect phagocytosis, causing hindered wound clearance and chronic wounds.

A 2023 systematic review and meta-analysis (five clinical trials meeting inclusion criteria) found that zinc treatment may be associated with improvements in ulcers healing at the final endpoint (MD: 1.41; 95% CI 1.04–1.92; p = 0.03). Given the limitations of the included studies, a GRADE assessment indicated a moderate quality of evidence.

A randomized, double-blind, placebo-controlled trial assessed topical zinc oxide (1.1%) in an oil-in-water emulsion; zinc oxide is commonly applied to inflamed and injured skin due to the anti-phlogistic effects of bioactive Zn²⁺. Pretreatment of normal human epidermal keratinocytes with Zn²⁺ reduced secretion of the proinflammatory cytokine interleukin (IL)-1α. Furthermore, topical administration of zinc oxide to murine skin increases keratinocyte mitosis, which is beneficial in wound healing.

A review of the literature found that there is insufficient evidence to support the routine use of supplemental zinc and/or vitamin C in individuals with adequate nutrition. Prolonged intake of high-dose zinc supplementation (40 mg/day) could inhibit the absorption and ultimately the bioavailability of copper, causing zinc-induced copper deficiency, which is known to cause further clinical issues including anemia and neutropenia.

Evidence strength: Zinc's biochemical necessity for skin integrity and wound healing is well established; clinical benefits from supplementation are moderate in quality for ulcer healing and most clearly demonstrated in zinc-deficient individuals. Topical zinc formulations have a long empirical and some clinical basis for skin use.

5.3 Vitamin A

Traditional Use

Vitamin A-rich foods such as liver, cod liver oil, and leafy greens have been used in traditional nutritional practice to maintain skin and mucosal integrity, though no single-ingredient traditional blister remedy specific to vitamin A is documented in major pharmacopeias.

Scientific Evidence

Vitamins A, C, and E, as well as minerals such as zinc, selenium, and iron, are essential for cell proliferation and the formation of new tissues. Vitamin A is considered necessary for epithelial cell turnover and immune competence; a healing-supportive diet should include adequate protein (for tissue rebuilding), vitamin A (for skin integrity and immune function), zinc, and sufficient calories to fuel the metabolic demands of repair.

Evidence strength: Evidence for vitamin A in skin wound healing is largely derived from animal models and observational data in deficiency states. Specific RCT evidence for vitamin A supplementation in blister healing is lacking.

5.4 Aloe Vera (Aloe barbadensis miller)

Traditional Use

Aloe vera is a medicinal plant, traditionally used to improve skin integrity. Aloe vera is known for its anti-inflammatory, skin protection, antibacterial, antiviral, antiseptic, and wound healing properties. Its use for burns and skin injuries is documented across ancient Egyptian, Greek, and Ayurvedic traditions, where the gel from freshly cut leaves was applied directly to the affected area.

Scientific Evidence

Aloe vera has been traditionally used for burn healing, but clinical evidence remains unclear. A systematic review identified four controlled trials with 371 patients; there is some evidence to suggest that aloe vera may be effective as an intervention in healing first- and second-degree burns.

A 2012 Cochrane Review assessed aloe vera across five trials in people with acute wounds (burns, haemorrhoidectomy patients, and skin biopsies). Aloe vera mucilage did not increase burn healing compared with silver sulfadiazine (risk ratio 1.41, 95% CI 0.70 to 2.85). The Cochrane review concluded that there is currently an absence of high-quality clinical trial evidence to support the use of aloe vera topical agents or aloe vera dressings as treatments for acute and chronic wounds.

A broader systematic review of 23 trials (PMC, 2019) found that aloe vera has been used to prevent skin ulcers and to treat burn wounds, postoperative wounds, cracked nipples, genital herpes, psoriasis, and chronic wounds including pressure ulcers. Considering the properties of aloe vera and its compounds, it can be used to retain skin moisture and integrity and to prevent ulcers. Animal studies have suggested that aloe vera may help accelerate the wound healing process.

Evidence strength: Preliminary and mixed. Animal and in vitro data support anti-inflammatory and wound-healing properties. Human clinical trial evidence is heterogeneous, methodologically limited, and does not yet establish superiority over standard care for burns or blistered skin. The Cochrane conclusion (2012) remains that high-quality evidence is absent.

5.5 Calendula (Calendula officinalis)

Traditional Use

Calendula officinalis has been historically used to treat minor wounds, skin irritation, and minor burns. In European herbal medicine, preparations made from the dried flower heads — typically as infused oils, ointments, or poultices — have been applied to wounds, blisters, and inflamed skin for centuries. The German Commission E has recognized calendula flower for use in wounds and burns.

Scientific Evidence

A 2019 systematic review (14 studies: 7 animal experiments and 7 clinical trials; searched across PubMed, EMBASE, Cochrane, CINAHL, and Scopus to April 2018) found that findings on acute wound healing showed faster resolution of the inflammation phase with increased production of granulation tissue in test groups treated with calendula extract. These findings were consistent in five animal studies and one randomized clinical trial. Chronic wound healing studies were varied. Two clinical control studies on venous ulcers demonstrated decreased ulcer surface area compared to controls. Another randomized clinical trial demonstrated no improvement for the calendula group in diabetic leg ulcer healing. Burn healing similarly showed mixed results.

The review's overall conclusion was that there is some evidence for the beneficial effects of C. officinalis extract for wound healing, consistent with its role in traditional medicine. There is a need for larger, well-designed randomized control trials to assess the effect of calendula on wound healing including complications.

Evidence strength: Preliminary. Some signal in animal experiments and a small number of clinical trials for wound-healing promotion, but sample sizes are small, study designs vary considerably, and evidence specific to blisters is not available. Data from large comparative trials are not yet sufficient to support routine clinical recommendation.

5.6 Honey (Medical-Grade)

Traditional Use

Honey has been used as a wound dressing across ancient Egyptian, Greek, Ayurvedic, and Islamic medical traditions. Historical preparations involved applying raw honey directly to burns, blisters, and open wounds, often combined with other botanical ingredients.

Scientific Evidence

Honey has antioxidant, antibacterial, and anti-inflammatory properties. It can be used as a wound dressing to promote rapid and improved healing. These effects are due to honey's antibacterial action, secondary to its high acidity, osmotic effect, antioxidant content, and hydrogen peroxide content.

The use of honey leads to improved wound healing in acute cases, pain relief in burn patients, and decreased inflammatory response in such patients. However, it has proven to be ineffective in chronic leg ulcers. Honey has almost equal or slightly superior effects when compared with conventional treatments for acute wounds and superficial partial thickness burns. More randomized controlled trials with significant statistical power comparing different kinds of honey are required in order to create a strong body of evidence.

Evidence strength: Moderate for acute wounds and superficial burns (including burn blisters): several RCTs support comparable or slightly better outcomes versus standard care in these specific wound types. Evidence for friction blisters specifically is not available. Methodological quality varies across studies, and honey formulations differ significantly.

5.7 Protein, Amino Acids, and Overall Caloric Adequacy

Traditional Use

Diets rich in protein — from animal foods, legumes, and whole grains — have been recognized across all major traditional medicine systems as important supports for recovery from skin injury and illness.

Scientific Evidence

Evidence suggests that bioactive compounds found in functional foods and dietary supplements can help prevent chronic conditions and promote wellness beyond basic nutrition. Protein is necessary for the synthesis of collagen, growth factors, and immune proteins involved in all phases of wound healing. Multiple comorbid disease states or malnutrition place individuals at risk for poor wound healing. Vitamin C is an essential cofactor for collagen and protein synthesis of bones, skin, capillary walls, and connective tissue, as well as providing enhanced neutrophil function and angiogenesis, which aid in wound healing functions.

Evidence strength: Indirect but well established. The relationship between overall nutritional adequacy, protein status, and wound healing is supported by extensive observational and clinical data. Isolated blister-specific RCTs for protein interventions are not available in the literature.

6. Dietary and Lifestyle Factors

6.1 Skin Hydration and Moisture Management

Higher skin hydration was found in the blister group (61.6%) compared to the control group (38.4%). A significant relationship between hydration and blisters was observed in the left foot (p = 0.032) in a case-control study of 86 hikers. Increased cutaneous surface hydration enhances the rate of skin temperature change and the risk of blister formation. This does not mean that systemic dehydration reduces risk; rather, excess surface moisture (primarily from sweat) acts as a mechanical risk factor.

6.2 Physical Conditioning and Activity Level

Friction blisters on the feet commonly occur when individuals engage in active pursuits such as running, hiking, and military training. The high prevalence of blisters in active individuals underscores the fact that the pathomechanics of this condition are not fully understood. Blisters are known to occur primarily in endurance activities. Gradual conditioning of the skin through progressive activity is widely cited as a protective strategy, as the skin adapts structurally to repeated shear stress.

6.3 Footwear, Socks, and Friction Reduction

Socks can potentially prevent blisters by reducing moisture content on the surface of the foot, thereby reducing the coefficient of friction. Sock-fiber properties and construction that may affect friction blister rates include moisture regain, swelling properties, water transport, heat transfer, and the coefficient of friction.

Minimizing any of the three causative factors — motion of bone, high friction force, and repetition — will reduce the risk of friction blisters.

6.4 Nutritional Status and Overall Diet Quality

The nutritional context for blistering is most clearly relevant in two areas: (a) deficiency diseases that directly cause blistering eruptions (notably niacin deficiency, as discussed above), and (b) nutritional support for blister healing and skin barrier maintenance.

The recent reemergence of forgotten nutritional deficiencies, such as scurvy and pellagra, in the context of predisposing risk factors makes this topic timely. Populations at elevated risk for nutritional blistering include those with highly restrictive dietary patterns, food insecurity, malabsorption syndromes, alcohol use disorder, and post-bariatric-surgery patients.

For healing, a diet supplying adequate amounts of the key nutrients involved in skin repair — vitamin C, zinc, vitamin A, protein, and sufficient energy — is broadly supported by the nutritional wound healing literature. Considerable evidence suggests that supplementation of vitamin C together with zinc by an oral nutritional supplement rich in energy, protein, and arginine may be an efficient tool for pressure ulcer healing. However, most of the studies on the role of vitamins and trace metals in wound healing were done in animal models, in patients with hereditary deficiencies, or in those with documented acquired deficiencies.

6.5 Alcohol Consumption

Chronic alcohol use impairs the absorption and utilization of multiple B vitamins (including niacin, thiamine, and riboflavin) and zinc. Although pellagra has become less prevalent in developed countries due to improved nutrition and the fortification of foods with niacin, isolated cases continue to emerge among vulnerable groups — including those with alcohol use disorder. Because people with niacin deficiency often have other nutritional deficiencies, eating a balanced diet is important.

6.6 Hyperhidrosis (Excessive Sweating)

Excessive sweating (hyperhidrosis) softens the skin so the skin splits more easily. Managing hyperhidrosis — through measures that reduce surface moisture — is considered a practical friction blister prevention strategy, particularly in athletes and military personnel.

7. Summary of Evidence Quality by Intervention

• Niacin repletion in pellagra: Strong. The association between niacin deficiency and blistering eruptions is well established and clinically validated; correction with nicotinamide resolves the blistering dermatitis.
• Zinc repletion in deficiency states: Strong in deficiency. Moderate evidence for supplementation in suboptimal zinc status; evidence is weaker in replete individuals.
• Vitamin C: Mechanistically strong; human RCT evidence for supplementation in wound healing is mostly in pressure ulcers and multi-nutrient protocols. Evidence specifically for blister healing is indirect.
• Honey (topical, acute wounds/burns): Moderate; several RCTs suggest comparable or marginally superior outcomes to standard care for superficial burns and acute wounds. No specific data for friction blisters.
• Aloe vera (topical): Preliminary and mixed. High-quality trial evidence is absent per Cochrane assessment.
• Calendula (topical): Preliminary. Some animal and limited clinical trial evidence for acute wound healing; mixed results for burns; no blister-specific data.
• Overall diet quality (protein, micronutrient adequacy): Well supported as a modifier of wound healing capacity, but blister-specific dietary intervention RCTs are not available.

References

• PMC: Dynamics of the cellular and humoral components of the inflammatory response elicited in skin blisters in humans
• PMC / JCI: The pathophysiology of autoimmune blistering diseases (Yancey, 2005)
• PMC: Skin Barrier and Autoimmunity — Mechanisms and Novel Therapeutic Approaches for Autoimmune Blistering Diseases of the Skin
• PubMed: End of the century overview of skin blisters
• PMC: Friction Blisters of the Feet: A New Paradigm to Explain Causation
• PMC: Friction Blisters of the Feet: A Critical Assessment of Current Prevention Strategies
• PMC: Influence of skin hydration level on the occurrence of blisters on the foot during hiking
• PMC: Cutaneous signs of nutritional disorders
• PMC: Hidden Hunger: A Pellagra Case Report
• PMC: Pellagra: A Non-Eradicated Old Disease
• PMC: Steroid-Resistant Rash With Neuropsychiatric Deterioration and Weight Loss: A Modern-Day Case of Pellagra
• WHO/CDC: Pellagra and its prevention and control in major emergencies (WHO/NHD/00.10)
• PMC: Zinc in Wound Healing Modulation
• PMC: Systematic review and meta-analysis of the effect of zinc on wound healing
• PMC: Wound problems due to zinc deficiency
• PMC: Topical Zinc Oxide Assessed in Two Human Wound-healing Models
• PMC: Vitamin C promotes wound healing through novel pleiotropic mechanisms
• PMC: A Systematic Review on the Role of Vitamin C in Tissue Healing
• PubMed: Efficacy of vitamin supplementation in situations with wound healing disorders: results from clinical intervention studies
• IHS/NPTC: Nutritional Supplements in Wound Healing (Formulary Brief)
• PMC: The Roles of Micronutrition and Nutraceuticals in Enhancing Wound Healing and Tissue Regeneration: A Systematic Review
• PMC / Cochrane: Aloe vera for treating acute and chronic wounds (Cochrane Review)
• PubMed: The efficacy of aloe vera used for burn wound healing: a systematic review
• PMC: The Effect of Aloe Vera Clinical Trials on Prevention and Healing of Skin Wound: A Systematic Review
• Wound Repair and Regeneration: A systematic review of Calendula officinalis extract for wound healing (Givol et al., 2019)
• PMC: Evidence for Clinical Use of Honey in Wound Healing as an Anti-bacterial, Anti-inflammatory Anti-oxidant and Anti-viral Agent: A Review
• DermNet NZ: Friction blisters