Introduction

Skin changes can be signs of underlying nutritional deficiencies. Recognition of these cutaneous findings can aid with diagnosis and treatment of underlying disease, reverse cutaneous signs, and prevent irreversible systemic complications [1]. Elderly populations are at higher risk of developing nutritional deficiencies due to low dietary intake, impaired absorption of nutrients, or failure to convert nutrients to their active forms [2]. “Anorexia of aging” describes the reduction in appetite and food intake with aging, consequently resulting in an inadequate consumption of nutrients [3], and is estimated to affect up to 20–30% of elderly individuals [4]. Physiologic factors that affect the process of anorexia include changes in the gastrointestinal tract and oral health (e.g. impaired chewing ability, reduced function of salivary glands, decreased esophageal motility, reduced gastric secretion), hormones (e.g. impaired response to cholecystokinin, low ghrelin plasma levels, impaired central feeding drive), and sensory impairment (e.g. reduced sense of smell and taste) [2, 4]. Additionally, psychological and social factors such as depression, apathy, and social isolation can affect food intake in the elderly. [5]

There are many complications associated with nutritional deficiencies in elderly individuals. Malnutrition, which includes undernutrition and micronutrient deficiencies, plays a key role in causing frailty and increased morbidity and mortality in geriatric patients [2, 6]. Malnutrition in older patients can lead to a greater risk of infection, longer hospital stays, increased potential of hospital readmission, slowed wound healing, and mortality [6]. Vitamin deficiencies highly associated with frailty include Vitamins B9, C, and D. Certain nutritional deficiencies increase the risk for cognitive impairment (e.g. vitamin B-complex, vitamin C, calcium, magnesium, and zinc); early identification of these deficiencies can help mitigate risk of irreversible neurologic effects [6, 7]. In this review article, we aim to highlight key cutaneous findings associated with nutritional deficiencies in the geriatric population.

Zinc Deficiency

Zinc is an important micronutrient that plays a critical role in wound repair, immune function, and reproduction [8]. This nutrient can be found in many foods including fish, meat, legumes, and nuts [8].

Plasma zinc levels under 65 ug/dL (postprandial) and 70 ug/dL (fasting) are suggestive of zinc deficiency [9]. According to survey data from the Third National Health and Nutrition Examination Survey, 57.5% of those 71 years and older had inadequate zinc intake, defined as less than 77% of the 1989 recommended dietary allowance (RDA) [10]. Older individuals are at greater risk for zinc deficiency because of inadequate dietary intake. Additional risk factors include malnutrition and malabsorption, which can be affected by chronic conditions such as hepatic, gastrointestinal, and renal disease, sickle cell disease, and alcohol abuse [8, 11].

Zinc functions to suppress tumor necrosis in keratinocytes and is important for normal cell proliferation and decreasing inflammation [8]. Acquired acrodermatitis enteropathica (AE) from zinc deficiency is characterized by acral and periorificial dermatitis, diarrhea, and alopecia [8]. Cutaneous manifestations of zinc deficiency can progress within days, particularly in the periorificial region, and angular cheilitis is commonly seen early in the disease (Table 1, Fig. 1). An image of angular cheilitis can be found in Fig. 2 in another article of this series by McAlpine et al. [12] Advanced deficiency can lead to generalized alopecia and widespread psoriasiform dermatitis, which is characterized by eczematous scaly plaques, annular psoriasiform plaques, and sometimes vesicles, bullae, or pustules [8, 9]. Zinc deficiency can also cause vitiligo-like skin lesions as well as nail and scalp changes, such as paronychia and thin or brittle hair [8, 13]. Some non-cutaneous symptoms of zinc deficiency include hypogonadism, diarrhea, and central nervous system effects such as mental disturbance, impaired taste, and emotional lability [8].

Table 1 Cutaneous manifestations of nutritional deficiencies
Full size table
Fig. 1
figure 1

Key skin findings of nutritional deficiencies and select differential diagnoses. Abbreviations: Vit, vitamin; EFA, essential fatty acid; Cu, copper; Fe, iron; Zn, zinc. Created with BioRender.com

Full size image
Fig. 2
figure 2

Perifollicular hemorrhage in a patient with scurvy (Photo credit: Brandon Adler, MD)

Full size image

The RDA of zinc for the elderly is 11 mg/day in men and 8 mg/day in women with an upper limit of 25–40 mg/day. Treatment of acquired AE is elemental zinc 0.5–1 mg/kg/day with dosage adjusted based on plasma zinc levels drawn every 4 to 6 months [9]. Zinc supplementation and sufficient dietary intake commonly resolve diarrhea within 24 h and skin lesions within one to two weeks [8].

Iron Deficiency

Iron is an essential element involved in a wide variety of metabolic processes, including oxygen transport, deoxyribonucleic acid (DNA) synthesis, and electron transport. Iron is recycled and conserved by the body [14], and can be found mainly in the hemoglobin of erythrocytes and also in circulation through bones and liver [15]. Sources of dietary iron include heme–iron in animal meat and non-heme–iron in plants [15].

Iron deficiency is the most common nutrient deficiency worldwide. Studies in the U.S. and Europe have reported a prevalence of anemia in older adults to range from 8–25% [2]. Iron deficiency is particularly common in the elderly population due to decreased food intake, GI malabsorption, and occult bleeding. Comorbidities such as rheumatoid arthritis, chronic kidney disease, and irritable bowel disease can increase the risk of iron deficiency [15].

Serum ferritin level is the most effective way to diagnose iron deficiency anemia since serum iron levels vary during the day and are influenced by diet [16]; serum ferritin levels lower than 30 ng/mL in the absence of inflammation are indicative of absolute iron deficiency [15]. If symptomatic, patients can present with decreased exercise capacity, fatigue, generalized weakness, irritability, and headaches [1]. Cutaneous findings may include koilonychia, brittle nails, dry skin, hair loss, atrophic glossitis, and cheilosis [1, 15].

The RDA of iron is 8 mg/day for both sexes with an upper tolerable limit of 45 mg/day [2]. Mild iron deficiency can be corrected by a diet adequate in iron. However, for severe iron deficiency, oral or IV iron therapy may be warranted [15]. For older adults, typical doses of iron repletion of 50 to 60 mg can be challenging due to side effects such as constipation, diarrhea, and abdominal cramping. Low-dose iron formulations should be considered in patients who cannot tolerate iron > 50 mg [17]. One study on iron-deficiency anemia in patients over 80 years of age found an equivalent response in hemoglobin with fewer adverse effects in the group managed with 15 mg compared with 50 mg or 150 mg of iron daily [18].

Protein Deficiency

Inadequate protein intake, reduced ability to use available protein (e.g. insulin resistance, immobility, etc.), and greater need for protein (e.g. inflammatory disease) with aging results in a high risk of protein deficiency in the elderly population [19]. Lower protein levels are associated with chronic muscle wasting, functional loss, and frailty, and more than 30% of individuals 60 years and older and more than 50% of individuals 80 years and older are estimated to be sarcopenic [2].

Diagnosing protein deficiency often depends on clinical symptoms and interpretation of multiple tests, which can include decreased levels of serum albumin, prealbumin, total protein levels, and other levels of visceral proteins [20,21,22].

Protein deficiency can cause two different clinical presentations: kwashiorkor and marasmus. Kwashiorkor is associated with inadequate protein intake in the setting of adequate caloric intake, resulting in a characteristic edema. Marasmus occurs with chronic inadequate protein intake in the setting of total caloric deficit [1].

Cutaneous findings associated with Kwashiorkor include dermatitis with hypopigmented to erythematous-violaceous patches in intertriginous areas that can be misdiagnosed as atopic dermatitis. Cutaneous findings of marasmus include wrinkled skin due to loss of subcutaneous fat, excess lanugo-like hair, thin hair, and fissured nails [1].

Traditional dietary guidelines of protein intake of 0.8 g/kg/day for all adults, regardless of age or sex, are inadequate in the elderly population [19]. Multiple studies recommend a range of 1 to 1.73 g/kg/day of protein intake in the elderly population for positive protein status and improved health status [2].

Fat-soluble vitamin deficiencies

Fat-soluble vitamins are absorbed by the small intestine along with dietary fat and are stored in the body. There is a higher risk of toxicity than with water-soluble vitamins due to potential for excessive accumulation and storage in fat [23].

Vitamin A deficiency

The term “Vitamin A” includes a group of chemically related fat-soluble compounds such as retinol, retinyl palmitate, and beta-carotene. Common sources of beta-carotenoid (provitamin A) include yellow and orange-pigmented fruits and vegetables, such as carrots, red peppers, mangos, and apricots. Common sources of retinol and retinyl ester (preformed vitamin A) include animal sources such as milk, dairy products, meat, eggs, and fish [24, 25].

Serum retinol concentration levels < 0.35 μmol/L and < 0.70 μmol/L indicate severe and subclinical vitamin A deficiency, respectively [26]. Inadequate dietary intake is the most common cause of deficiency. Additional risk factors include chronic malabsorptive disorders, such as inflammatory bowel disease (IBD) and cirrhosis [6, 24].

Early signs of xerophthalmia include diminished ability of the eye to adjust to darkness and night blindness, and can resolve with adequate supplementation [25]. Later signs include corneal and conjunctival xerosis, retinopathy, and ophthalmic ulceration, which can lead to scarring and permanent vision loss despite treatment [1, 24]. Chronic vitamin A deficiency can also predispose individuals to increased frequency of gastrointestinal, pulmonary, and urinary infections [24].

Vitamin A plays an important role in the innate immune system and its deficiency can increase risk of skin infection and inflammatory skin conditions [27]. Cutaneous findings associated with vitamin A deficiency can be characterized by keratinization of the skin and a dry epidermis [25]. Phrynoderma appears as “toad skin”-like, with hyperkeratotic, spiny, follicular-based papules primarily on extensor surfaces of extremities with a symmetric distribution. As the condition progresses, lesions may extend to the trunk and face [9]. Phrynoderma is distinctive from other follicular papules such as keratosis pilaris [1]. A visual representation of phrynoderma could be found in Box 1 of Verheyden et al. [28].

The RDA of vitamin A in healthy adults is 700 ug/day and 900 ug/day for women and men, respectively. A balanced diet often provides sufficient levels of vitamin A for physiological needs, but if not available, vitamin supplementation is necessary [25]. Suggestive regimens for treatment of phrynoderma include 50,000 IU daily or 2000 ug IV daily for 2–3 days [9].

Vitamin D Deficiency

Vitamin D is obtained mainly through its synthesis in the skin under sunlight and dietary intake to a smaller extent. Under UVB irradiation from sunlight, Vitamin D3 (cholecalciferol) is synthesized in the skin and absorbed into circulation. Common dietary sources of vitamin D include egg yolks, milk, cheese, fatty and oily fish, red meat, liver, and mushrooms [6, 29].

Serum vitamin D levels below 30 nmol/L are considered deficient and between 30–50 nmol/L are considered inadequate [6]. The prevalence of vitamin D deficiency in community-dwelling older adults has been reported to be between 17–56% and up to 80–90% in nursing homes [6]. High rates of vitamin D deficiency are seen in the elderly due to reduced dietary intake, ability of the skin to synthesize vitamin D3, sun exposure, and gut absorption [29, 30]. Additionally, increased fat composition, common in the older population, makes accessing the biologically active form of vitamin D more difficult [6].

Vitamin D plays an important role in cutaneous innate and adaptive immunity. A diminished innate immune system due to vitamin D deficiency has been shown to increase the risk of cutaneous infections [13]. Other cutaneous conditions associated with vitamin D deficiency include atopic dermatitis, psoriasis, acne, skin cancer, and autoimmune skin diseases [13, 31, 32]. Thus, a new diagnosis or worsening of pre-existing atopic dermatitis and psoriasis should prompt consideration of an underlying nutritional deficiency such as vitamin D.

Vitamin D deficiency also has musculoskeletal health implications, especially in the elderly population. Osteomalacia, presenting as bone and muscle pain, marked proximal muscle weakness, and a ‘waddling’ gait, may be seen in older people; it is curative with vitamin D treatment [29]. Poor vitamin D repletion is also associated with an increased risk of osteoporosis, and supplementation has been shown to reduce rates of bone loss over time [33]. Recent studies have also shown a connection between vitamin D deficiency and depression, cancer, diabetes, cardiovascular diseases, and autoimmune diseases [34].

The estimated average requirement of vitamin D is 800 IU/day in older adults with appropriate sun exposure, but in older adults with limited sun exposure and obesity, a higher dose of 2000 IU/day is recommended [2]. Vitamin D3 supplementation has been found more effective than vitamin D2. If vitamin D3 and D2 supplementation are inadequate, calcitriol can be used; however, calcium levels should be closely monitored to avoid hypercalcemia [34, 35].

Vitamin K Deficiency

Vitamin K, another fat-soluble vitamin, is critical for cardiovascular health, blood clotting, and bone metabolism [36]. Vitamin K is found in foods such as leafy greens and fermented foods and can be synthesized by certain gut microbiota [36]. Gastrointestinal flora can synthesize up to 50% of the body’s daily vitamin K needs [13].

Vitamin K levels are challenging to assess due to its relatively low endogenous concentration. The most frequently used marker is serum phylloquinone (K1) concentration, with < 0.15 ug/L indicating deficiency in non-fasting subjects [37].

Insufficient dietary intake of vitamin K is the most common cause of deficiency. Other risk factors include conditions that affect fat absorption, such as IBD and celiac disease, and prolonged antibiotic use [36]. Vitamin K deficiency may initially manifest as bleeding after minor trauma or at venipuncture locations [36]. Cutaneous manifestations include petechiae, ecchymoses, and hematomas [13]. Nodular purpura has been seen in adults with vitamin K deficiency [38]. The RDA for vitamin K in healthy adults is 90 ug/day and 120 ug/day for women and men, respectively [36].

Water-soluble Vitamin Deficiencies

Compared to fat-soluble vitamins, water-soluble vitamins are not as easily stored and have fewer concerns for toxicity with over-supplementation [39, 40].

Vitamin B-complex

The water-soluble B vitamins are closely linked to aging processes such as oxidative stress, inflammation, and immune pathways that contribute to the onset of frailty [6]. Among the elderly, Vitamin B6, B9, and B12 deficiencies are known to affect cognitive functioning and depressive symptoms. Vitamin B deficiencies have shared cutaneous findings such as glossitis, angular cheilitis, and mucosal erosions [41].

Vitamin B1 Deficiency

Vitamin B1, also known as thiamine, is solely obtained via dietary intake and is not physiologically produced. Common food sources of thiamine include bread, whole grains, nuts, and meat [42].

Low thiamine concentration has been found in many older age populations in different countries [43]. Risk factors for thiamine deficiency include a vitamin B-deficient diet, malabsorption, impaired metabolism, and a diet high in thiaminases or thiamine antagonists [42]. Thiamine levels can be evaluated by assessing the degree of thiamine diphosphate (ThDP) saturation of a thiamine-dependent enzyme (erythrocyte transketolase assay) or by measuring thiamine metabolites in accessible tissues. Though there is no universally accepted cutoff value for thiamine deficiency, the expected concentration of ThDP in whole blood is approximately 70–180 nmol/L for healthy individuals [44].

Thiamine plays a significant role in oxidative metabolism that results in ATP production; a lack of ATP causes lactic acidosis and a decrease in important neurotransmitters [42]. Initial symptoms of thiamine deficiency include short-term memory impairment, anorexia, and irritability. Prolonged deficiency can lead to more serious neurologic and cardiovascular symptoms [45, 46]. Severe thiamine deficiency can lead to Korsakoff’s syndrome, beriberi, and Wernicke’s encephalopathy, which is characterized by the triad of loss in muscle coordination, irregular eye movement, and cognitive impairments [42].

In addition to cutaneous findings shared with B-complex vitamin deficiency, dermatologic changes such as skin atrophy, hair loss, and skin glossiness can occur due to a decrease in autonomic nerve fiber production [45]. Patients with vitamin B1 deficiency have also been found to present with facial seborrheic dermatitis [38].

The RDA of vitamin B1 for adults 51 years old and greater is 1.1 mg/day and 1.2 mg/day for women and men, respectively [47]. Supplementing the diet with foods higher in Vitamin B1 is often sufficient for physiological needs. Treatment for thiamine deficiency due to alcohol abuse must be administered intravenously because alcohol abuse depletes gastrointestinal absorption [42].

Vitamin B2 Deficiency

Vitamin B2, also known as riboflavin, is an important enzymatic cofactor in oxidation–reduction reactions that are critical in biosynthetic processes [42]. Vitamin B2 uptake comes solely from the diet due to inability of endogenous synthesis [42]. Food sources that supplement riboflavin are mainly milk and dairy products but also include eggs, meats, nuts, legumes, and some vegetables and grains. Risk factors for deficiency include elderly age, alcohol abuse, and vegetarian diet due to insufficient dietary intake [1]. Riboflavin levels can be measured in the urine and blood, however, the erythrocyte glutathione reductase assay is a more effective biomarker of riboflavin insufficiency, with an activity coefficient > 1.4 indicating riboflavin insufficiency.

Chronic vitamin B2 deficiency can present with cheilitis, conjunctivitis, and glossitis [1]. Oculo-orogenital syndrome from vitamin B2 deficiency is characterized by these ocular and mucosal findings as well as dermatitis involving the genital region [48, 49]. Other cutaneous findings of deficiency include hair loss, edema of mucous membranes, and facial seborrheic dermatitis [1, 42].

The RDA of riboflavin for adults is 1.1 mg/day and 1.3 mg/day for women and men, respectively. In some countries, foods fortified with riboflavin assist in supplying sufficient dietary levels [42].

Vitamin B3 Deficiency

Vitamin B3, also known as niacin, is sourced exogenously through diet. Common food sources of niacin include meat, dairy, wheat, peanuts, yeast, mushrooms, and fish [42]. Risk factors include alcohol abuse, malabsorption, and lack of access to fortified foods (e.g. certain developing countries) [42]. Laboratory testing includes testing for tryptophan, NAD, NADP, and niacin levels [50]. Urinary excretion rate of N1-methylnicotinamide < 5.8 umol/day is suggestive of niacin deficiency [51].

Pellagra, meaning “rough skin”, can result from niacin deficiency. The “3-D’s” of pellagra refer to dermatitis, diarrhea, and dementia, and more chronic cases could result in a fourth “D”, death [42]. Classic findings include a photosensitive eruption in sun-exposed areas that progress to leathery, hyperpigmented plaques. When this hyperpigmentation occurs around the neck and on the anterior chest in a collar-shaped band, this is known as Casal’s necklace [52]. With further progression of disease, “wet pellagra” may develop with bullae or vesicles [1]. Some non-cutaneous symptoms include muscle weakness, tremors, hallucinations, and mood changes [52].

The RDA for adults is measured in niacin equivalents (NE) and is 14 mg NE/day and 16 mg NE/day for women and men, respectively [50]. Treatment for this deficiency includes average daily supplementation of 10–300 mg of vitamin B3, and up to 1000 mg for more severe cases [42].

Vitamin B6 Deficiency

Vitamin B6, also known as pyridoxine, is an important cofactor in many metabolic processes and a strong antioxidant that plays a critical role in neutralizing reactive oxygen species that contribute to aging [6]. Food sources of vitamin B6 include meat, fish, and many fruits and vegetables [53].

Serum levels < 20 nmol/l indicate B6 deficiency [54]. Risk factors of vitamin B6 deficiency include the elderly, irritable bowel syndrome, alcoholism, pregnancy, obesity, celiac disease, HIV, renal and hepatic disease, and certain vitamin B6-inactivating medications such as isoniazid [6]. B6 deficiency is associated with lower immune function and makes geriatric patients more susceptible to infection [6, 54].

The most common cutaneous manifestation of vitamin B6 deficiency is seborrheic dermatitis, which may be found on the scalp, face, neck, shoulders, and buttocks [1]. Early onset symptoms include dermatitis, impaired mental status, and sensory neuropathy [55]. With progression of disease, oral ulcers, glossitis, and cheilitis may develop [13]. In severe cases, pellagra (due to vitamin B6 requirement for niacin production) and neurologic symptoms such as confusion, drowsiness, and peripheral neuropathy can develop [13].

The RDA of vitamin B6 for adults older than 50 years are 1.5 mg/day and 1.7 mg/day in women and men, respectively [56]. To treat vitamin B6 deficiency, 100 mg of vitamin B6 daily is recommended [13], and in severe cases, a higher dose or intravenous administration may be required [55].

Vitamin B7 Deficiency

Vitamin B7, commonly known as biotin, is an essential coenzyme for five carboxylases that catalyze pathways involved in fatty acid biosynthesis, gluconeogenesis, the tricarboxylic acid cycle and other metabolic processes [57]. Dietary intake is the main source of vitamin B7, however, some enteric bacteria can synthesize biotin. Food sources with high B7 levels include egg yolk, nuts, grains, and milk [53].

Risk factors include elderly age, pregnancy, alcohol abuse, smoking, medications such as phenobarbital and carbamazepine, and prolonged use of antibiotics [58, 59]. Low urinary excretion of biotin of < 18 nmol/day is an indicator of biotin deficiency [57, 60].

Biotin deficiency initially presents as gradual hair loss and dry skin. Cutaneous manifestations of biotin deficiency are mainly due to decreased fatty acid metabolism and present as alopecia, periorificial dermatitis, and skin infections [58]. Periorificial dermatitis, also common in zinc deficiency, is characterized by red, scaly plaques around the nose, mouth, and eyes [58]. Biotin deficiency may also cause neurological and gastrointestinal symptoms such as seizures, tingling of extremities, depression, lethargy, nausea, vomiting, and anorexia [58].

The RDA of biotin for adults 19 years and older is 30 ug biotin daily [60]. Biotin deficiency can be supplemented through dietary intake of foods rich in vitamin B7 [58].

Vitamin B9 Deficiency

Vitamin B9, also known as folate, functions as a coenzyme in nucleic acid synthesis and amino acid metabolism. Common dietary sources of folate include leafy greens, yeast, internal organs of animals, mushrooms, and grasses [53]. Some vitamin B9 comes from the human intestinal flora [53].

Folate absorption occurs in the proximal small intestine [61]. Intestinal diseases, alcoholism, and insufficient dietary intake increase the risk of vitamin B9 deficiency in the elderly [6]. Certain drugs such as methotrexate and trimethoprim act as folate antagonists and can cause folate deficiency by inhibiting the enzyme dihydrofolate reductase, which converts unreduced dietary folates to the biologically active tetrahydrofolates [62]. Diets poor in folate can lead to deficiency in just a few weeks or months [63]. Generally, a serum folate level < 2 ng/mL is considered deficient.

Vitamin B9 deficiency can cause several disorders such as megaloblastic anemia and neuropathy [6]. Low folate levels are associated with mild cognitive impairment, Alzheimer’s disease, and depression [64, 65]. Additionally, folic acid supplementation has been shown to lower risk of stroke and overall cardiovascular diseases [66]. Cutaneous findings include glossitis, cheilitis, and mucocutaneous hyper/hypo-pigmentation [13]. Studies have shown that patients with psoriasis have lower levels of folate compared to normal controls [67].

The RDA of folate for adults 19 years and older is 400 ug daily [68]. A diet rich in fruits and vegetables will help reverse folic acid deficiency [63]. Oral supplementation with 1 to 5 mg daily of folic acid is used to treat folate deficiency [69]. Patients who cannot handle oral intake can be supplemented intravenously [63].

Vitamin B12 Deficiency

Vitamin B12, also called cobalamin, is derived from animal products; dietary sources include red meats, cheeses, milk, eggs, and animal livers [53].

The prevalence of vitamin B12 deficiency among geriatric populations worldwide is 10–19% [7]. Risk factors for developing vitamin B12 deficiency include malabsorption, pernicious anemia, and a history of ileocecal resection [53]. Gastric atrophy found commonly in the elderly contributes to malabsorption of vitamin B12. Additionally, certain medications like metformin can lead to gastric atrophy in geriatric patients [6].

Serum B12 levels less than 200 pg/mL are suggestive of B12 deficiency [69]. Early signs of vitamin B12 deficiency include atrophic linear lesions on the tongue and hard palate. Chronic complications can lead to neurologic disorders such as neuropathy and dementia.

Cutaneous manifestations of vitamin B12 deficiency include hyperpigmentation, typically on the face, palmar creases, and flexural areas, pigmentation of the nails, as well as vitiligo and depigmentation of the hair. Oral changes such as glossitis, stomatitis, and oral ulcers may be present [1]. Vitamin B12 has been found to be helpful for re-pigmentation in vitiligo patients, but optimal dosage for this response still needs to be identified [70].

The RDA for adults 19 years and older is 2.4 ug daily [71]. Vitamin B12 supplementation has been shown to reverse symptoms and pathologic consequences [7]. Treatment includes intramuscular injection of hydroxocobalamin daily for five days [7].

Vitamin C Deficiency

Vitamin C is a water-soluble vitamin and an important antioxidant that supports the growth of skin, cartilage, bone, and teeth [72]. Dietary intake is the only source of vitamin C. Common dietary sources include fresh fruits and vegetables such as spinach, broccoli, and red peppers [73].

Insufficient dietary intake, which is common in the elderly, is the most common risk factor for vitamin C deficiency [72]. Alcohol abuse, restrictive diet, psychiatric disease, malabsorptive disorders, bariatric surgeries, food allergies, smoking, and Type 1 diabetes are all additional risk factors [72]. Increased inflammation and oxidative stress seen in individuals with diabetes and obesity have been linked to vitamin C depletion despite dietary uptake [74].

Scurvy can develop within 4 to 12 weeks of insufficient dietary intake of vitamin C [72]. Plasma vitamin C levels < 11 umol/L indicate vitamin C deficiency [75]. Symptoms of scurvy initially include lethargy, fatigue, anorexia, and malaise, and later progress to bone and joint aches, diminished wound healing, bleeding gums, and skin rash. Further progression can manifest as ocular diseases, seizures, and organ failure [76].

Vitamin C plays an important role in collagen production. Cutaneous findings include fragile skin, impaired wound healing, petechiae, gingivitis with bleeding, corkscrew hairs, alopecia, and bruising [76]. Evidence of dermal disruption resulting from vitamin C deficiency includes perifollicular hemorrhage, dilated hair follicles, and follicular hyperkeratosis (Fig. 2) [72].

The RDA of vitamin C for adults 19 years and older is 75 mg/day and 90 mg/day in women and men, respectively [77]. Treatment of scurvy includes 500 to 1000 mg/d of vitamin C until symptoms or signs resolve, and then adequate dietary intake of Vitamin C [72].

Role of Multivitamin

Currently, no prospective randomized data support a beneficial effect of multivitamins on morbidity or mortality. Observational studies have not demonstrated a decrease in risk of cancer [78]. However, one randomized clinical trial did show a statistically significant improvement in memory recall for the intervention group assigned to multivitamin supplementation compared to the placebo group at both 1 and 3 years [79]. Multivitamin supplementation may benefit older individuals with nutritional deficiencies or difficulties absorbing vitamins from their diet. However, supplement usage should be carefully monitored to minimize the risk of toxicity [2].

Conclusions

Considering underlying nutritional deficiencies is important when evaluating cutaneous findings in the elderly population, especially in the context of increased risk factors for nutritional deficiencies, such as malnutrition, with aging. Early recognition of dermatologic manifestations associated with nutritional deficiencies can lead to appropriate supplementation and help prevent sequelae of both cutaneous and systemic complications.

Key References

  • Wong CY, Chu DH. Cutaneous signs of nutritional disorders. Int J Womens Dermatol. 2021;7(5Part A):647-652. doi:10.1016/j.ijwd.2021.09.003.

    • Highlights distinctive cutaneous signs to help distinguish a nutrient deficiency from other common dermatologic conditions

  • Gana W, De Luca A, Debacq C, et al. Analysis of the Impact of Selected Vitamins Deficiencies on the Risk of Disability in Older People. Nutrients. 2021;13(9):3163. doi:10.3390/nu13093163.

    • Reviews high-risk nutritional deficiencies in the elderly population in high-income countries with a particular focus on Vitamins B, C, and D

  • Nosewicz J, Spaccarelli N, Roberts KM, et al. The epidemiology, impact, and diagnosis of micronutrient nutritional dermatoses part 1: Zinc, selenium, copper, vitamin A, and vitamin C. Journal of the American Academy of Dermatology. 2022;86(2):267-278. doi:10.1016/j.jaad.2021.07.079.

    • Reviews the importance of considering nutritional dermatoses in the United States in the setting of increasing longevity of patients with chronic conditions and high prevalence of obesity, restrictive diets, and alcohol and substance use