|Year : 2020 | Volume
| Issue : 2 | Page : 69-75
Diet in dermatology: a review
Rita V Vora MBBS, MD Dermatology , Modasia H Khushboo, Aishni J Shah, Dhruv R Patel, Trisha B Patel
Department of Dermatology, Shree Krishna Hospital, Pramukhswami Medical College, Karamsad, Gujarat, India
|Date of Submission||10-Sep-2019|
|Date of Acceptance||01-Mar-2020|
|Date of Web Publication||09-Jun-2020|
Dr. Rita V Vora
Department of Dermatology, Shree Krishna Hospital, Pramukhswami Medical College, Karamsad 388325
Source of Support: None, Conflict of Interest: None
Diet plays a very important role in various dermatological conditions. Many conditions occur due to deficiency or excess of a particular nutrient, while some conditions are related to abnormal metabolism of a particular nutrient. In this review, important dermatological conditions have been highlighted in which diet has a definite role and dietary change helps to control or prevent that particular condition. In diseases like dermatitis herpetiformis, dietary restrictions play a major role in their treatment. Dietary habits also play some role in diseases such as atopic dermatitis, acne vulgaris, psoriasis vulgaris, pemphigus, and urticaria. Genetic and metabolic disorders such as phenylketonuria, tyrosinemia, homocystinuria, galactosemia, Refsum’s disease, glucose-6-phosphate dehydrogenase deficiency, xanthomas, gout, and porphyria also require dietary modifications. Imbalanced diet leads to nutritional deficiency disorders such as kwashiorkar, marasmus, phrynoderma, pellagra, scurvy, acrodermatitis enteropathica, carotenemia, and lycopenemia
Keywords: dermatology, diet, metabolism, nutrient
|How to cite this article:|
Vora RV, Khushboo MH, Shah AJ, Patel DR, Patel TB. Diet in dermatology: a review. Egypt J Dermatol Venerol 2020;40:69-75
| Introduction|| |
There are various myths and facts about diet in the layman population which needs proper guidance. Diet can play a miraculous role in a better quality of life if proper information about diet is highlighted. ‘Diet’ originates from the word ‘diaeta’ which translates to ‘a prescribed way of life’ or ‘way of life, regimen, dwelling’ . Diet is related to the body and mind of an individual. Patients usually need dietary advice from the dermatologist, as many of the health problems are linked to the diet they consume, including dermatological diseases. Dermatologists often face difficulty to clear the misbelief of the patients regarding their diet and dermatological disease. Certain specific factors also play a role in the etiopathogenesis of many dermatological as well as genetic and metabolic conditions.
Dermatological disorders in which diet has a definite role
Diet modification is the cornerstone in the treatment of dermatitis herpetiformis (DH). The rash of DH is gluten-dependent, and gluten-free diet (GFD) reduces the need for medications, resolution in enteropathy, and protection from lymphoma . Patients with DH often have malabsorption. Absorption of essential nutrients prevents alimentary deficiencies of iron and vitamin B12 and folate is improved by GFD . The increased risk of developing lymphoma in the gastrointestinal tract can be due to polyclonal stimulation of lymphocytes by gluten, giving rise to malignant transformation. Foods containing gluten are wheat, rye, oats, and barley. Rice, corn, and potatoes are safe for consumption. Iodides worsen DH by local chemotaxis and by stimulating neutrophil migration . Thus, iodine-containing foods (fish, kelp, iodized salt, and vitamin) may be avoided in patients who do not respond to a GFD. Patients not responding to GFD should restrict iodide and milk in their diet. Elemental diet (in which antigenic proteins are replaced by amino acid) decreases immunoglobulin A production and improves skin lesions.
Dermatological disorders in which diet has a probable role in etiopathogenesis
By the first year of life around 60% of children develop atopic dermatitis (AD) with food allergens .
The mechanisms of aggravation of AD due to food are:
- In children aged between 15 days and 6 years especially atopic patients with primarily altered antigen transfer, there is an increased binding of antigen to immature gut microvillis, along with increased intestinal permeability, which can prompt immune responses .
- The role of pathogenic bacteria in the gut may be similar to the role of Staphylococcus aureus in the skin of AD patients, both as an infectious agent as well as a superantigen . In food-allergic patients with AD, ingestion of the food item can provoke a whole spectrum of immunoglobulin E-mediated symptoms from oral allergy syndrome to severe anaphylaxis . Food allergy is commonly caused by foods such as wheat, milk, soy, fish, eggs, and peanuts, and thus should be avoided ,. Avoidance of food with proven food allergens can be beneficial in improvising moderate to severe AD, only food elimination is not recommended .
Chronic consumption of high-glycemic load carbohydrates such as potatoes, chocolates, white rice, and white bread may contribute to acne by elevating serum insulin concentrations, which influence circulating concentrations of free insulin-like growth factor-1 and insulin-like growth factor-binding protein-3, which in turn directly regulate keratinocyte proliferation and apoptosis and may initiate an endocrine cascade that affects the sebaceous gland and follicular keratinization involving insulin-like growth factor, insulin-like growth factor-binding protein-3, androgens, and retinoid signaling pathways. High insulin levels suppress sex hormone-binding globulin (SHBG) concentrations, and raise androgen concentrations. On the contrary, low-glycemic-index foods increased SHBG and reduced androgen levels; this is important since higher SHBG levels were associated with lower acne severity . Thus, a low-glycemic load diet has been shown to be beneficial in patients with acne vulgaris. The formulae for calculating glycemic load is: glycemic index for food item×its carbohydrate content in grams/100 . Androgens can increase growth and productivity of sebaceous glands, which aggravates acne. Animal foods and saturated fats tend to promote androgen release in the body and hence should be avoided in acne. Lower fat, higher fiber diets can increase the levels of sex hormone-binding proteins, thus lowering free levels of circulating androgens, and is helpful in controlling acne .
While the tendency to develop to psoriasis is inherited, the disease is influenced by environmental factors such as infections and stress, and possibly diet. Diet plays an important role in psoriasis as given below.
Energy intake in psoriasis also has a positive correlation with BMI, which means more severely affected patients with psoriasis are more likely to be obese; hence, weight reduction is recommended in obese psoriatic patients. The pathophysiology of both psoriasis and obesity shows many shared cytokines, which lead to a state of systemic inflammation known as metabolic syndrome. Metabolic syndrome is characterized by hypertension, dyslipidemia, and insulin resistance and may thereby aggravate skin lesions . There is an adverse effect of alcohol consumption on psoriasis. It acts by multiple mechanisms, such as increased susceptibility to infections, lymphocyte and keratinocyte proliferation stimulation, and production of proinflammatory cytokines. Alcohol misuse can predispose to a greater risk of liver disease and thus potential drug interactions . Alcohol stimulates histamine release, increase in the intake of fatty foods, and reduced consumption of fresh vegetables and fruits. Hence, alcohol intake should be restricted in psoriasis. The consumption of fresh fruits and vegetables, such as carrots, tomatoes, broccoli, orange, and sweet pepper may be beneficial in psoriasis because of their high content of carotenoids, flavonoids, and vitamin C . A sufficient status of antioxidants (e.g. vitamin C, vitamin E, β-carotene, and selenium) may be helpful to prevent an imbalance of oxidative stress and antioxidant defense in psoriasis . A diet containing good sources of folic acid (fresh green leafy vegetables, fruits, organ meats, dried nutritional yeast) and vitamin B12 (yeast, liver, beef, eggs, kidney) is recommended. The intake of folic acid is also important in patients on methotrexate therapy ([Table 1] and [Table 2]). In a study of 1206 psoriasis patients with compared age-matched and sex-matched controls, psoriasis patients consumed significantly less sugar, whole grain fiber, dairy, and calcium (P<0.001), while consuming more fruits, vegetables, and legumes (P<0.01). Dietary modification showed improvement in 86% of the study population. Subjects showing skin improvement was greatest after reducing alcohol (53.8%), gluten (53.4%), nightshades (52.1%), and after adding fish oil/omega-3 (44.6%), vegetables (42.5%), and oral vitamin D (41%). Pagano (72.2%), vegan (70%), and Paleolithic (68.9%) were special diets with which majority of subjects showed improvement . Rucevic et al.  in a study of 82 patients with a history of psoriasis from 10 years concluded that after 4 weeks participants on low energy diet showed a statistically significant decrease in serum lipids in relation to the control group as well as a significant decrease in clinical skin disorders. Naldi et al.  in their study with 316 psoriatic patients a significant inverse relationship with psoriasis was observed for the intake of carrots [χ2(1) trend 4.8, P<0.05], tomatoes [χ2(1) trend 26.3, P<0.01], fresh fruit [χ2(1) trend 11.7, P<0.01] and index of β-carotene intake [χ2(1) trend 9.1, P<0.01].
Omega-3 fatty acids
Eicosapentaenoic acid and docosahexaenoic acid are abundant in fish such as salmon, mackerel, herring, tuna, trout, sardines, and pilchards. Eicosapentaenoic acid and docosahexaenoic acid together with α-linolenic acid have been shown to reduce inflammation by reducing the synthesis of leukotrienes that are thought to play a role in psoriasis.
General nutritional status
Extensive psoriasis is known to result in nutritional deficiencies through the loss of proteins and other nutrients in the scales, resulting in hypoproteinemia and macrocytic anemia . Patients with poor nutritional status should not be given methotrexate as it reduces appetite and is contraindicated. The administration of cyclosporine along with grape fruit juice increases its oral bioavailability. This is because grapefruit juice is an inhibitor of cyclosporin drug metabolism interfering at the intestinal level; hence increasing the serum levels and decreasing the elimination. This was noticed with cyclosporin A formulation but not with cyclosporin microemulsion .
Various substances like thiols, thiocyanates, phenols, and tannins can precipitate the pemphigus in a genetically predisposed individual . Food containing such substances are  the ones given below:
- Vegetables: garlic, onion, mustard, turnip, broccoli, radish, cabbage, cauliflower, potato, leek, shallots, chives, tomatoes, ginger.
- Fruits and nuts: mango, raspberry, pistachio, avocado, cherry, cashew, banana, cranberry, guarana, pear, blackberry, walnut, peach.
- Masticatories and stimulants: coffee, tea, betel nut leaf, katha, cassava.
- Beverages: beer, wine, soft drinks.
- Miscellaneous: ice cream, candy, baked foods, spices (red chilies), aspartame, sodium benzoate, tartrazine, coloring agents, nutritional supplements.
- Water: high tannin content in Brazil river water may be the reason for endemicity of fogo selvagem. Tannins can be removed by chlorination, which would explain why the incidence of fogo selvagem has decreased with urbanization.
Mechanism of induction of pemphigus is given in [Table 3].
|Table 3 Chemical compounds and their mechanism in induction of pemphigus|
Click here to view
Food is the most commonly discussed cause of urticaria. Both allergic and pseudoallergic reactions have frequently been discussed as possible eliciting factors in different types of urticaria. Aromatic volatile ingredients in food are agents eliciting pseudoallergic reactions in chronic urticaria as has been demonstrated by a recent study, where reactions also frequently occurred in response to natural ingredients in tomatoes, white wine, and herbs .
Decrease in dietary protein intake has been found to reduce the symptoms of uremic pruritus, apart from reducing the complications of chronic renal disease, such as albuminuria . Cholestatic pruritus is benefited by supplementation of dietary polyunsaturated fatty acids .
Allergic contact dermatitis
Approximately 30–50% of individuals who are allergic to natural rubber latex show an associated hypersensitivity to some plant-derived foods, especially freshly consumed fruits . The latex–fruit syndrome is explained as an association of latex allergy and allergy to plant-derived foods. An increasing number of plant sources, such as avocado, banana, chestnut, kiwi, peach, tomato, potato and bell pepper and, recently, turnip, zucchini, and cassava have been associated with this syndrome.
In nickel-sensitive individuals oral intake of nickel can induce systemic contact dermatitis . Most common clinical manifestation of systemic nickel contact dermatitis is flare up of a recurrent vesicular hand eczema . Cocoa, chocolate, soybeans, oatmeal, nuts and almonds, and fresh and dried legumes are high in nickel .
Balsam of Peru is used as flavoring in wine, candy, chocolate, cinnamon, curry, citrus fruit, tomatoes, and flavorings are the most common food causing aggravation of dermatitis as mentioned by the patients.
Pityriasis rubra pilaris
The condition is controlled by vitamin-A-rich food items like green leafy vegetables, carrots, tomatoes, and eggs .
Dermatologic disorders in which specific factors in the diet are directly implicated in the etiopathogenesis of the disorder
Fish odor syndrome (trimethylaminuria)
Trimethylaminuria or ‘fish odor syndrome’ is due to excessive excretion into body fluids and breath of trimethylamine derived from the enterobacterial metabolism of dietary precursors such as trimethylamine N-oxide, choline, lecithin and possibly carnitine and other betaines . It occurs due to autosomal recessively inherited impairment of hepatic trimethylamine oxidation because of deficiency of flavin monooxygenase 3. Marine (seawater or saltwater) fish (including cephalopods and crustaceans) should especially be avoided, particularly deep sea fish, in which the trimethylamine N-oxide content is very high. Restriction should be kept on foods with a relatively high content of choline, including eggs, liver, kidney and other offal, and peas, beans, peanuts, soy products, and other legumes .
Fixed drug eruption
Occasionally, classic fixed drug eruptions can be caused by artificial flavors, colors, and preservatives in foods and dyes .
Genetic and metabolic disorders wherein either an elimination diet is mandatory or dietary supplementation of specific factors is beneficial
Phenylketonuria and tyrosinemia
The dietary restriction of phenylalanine and tyrosine is the key to management of the two conditions. Protein should be restricted to 2 g/kg/day in infants and 1 g/kg/day later in the childhood. Protein intake is altered according to plasma tyrosine levels .
Reduced intake of methionine diet is compulsory. Milk and milk products, meat and fish, wheat, maize, rice, pulses, legumes, nuts, and dried fruits are to be avoided. Fruits and vegetables can be taken in small quantities. Foods like sago, arrowroot, corn flour, custard, sugars, fats, tea, and coffee can be taken freehand .
Throughout childhood galactose and lactose should be avoided. A nutritionally adequate galactose/lactose-free milk should be used during infancy. In later childhood, occasional lactose-free milk and calcium and vitamin supplements may suffice .
Phytanic acid is almost exclusively of exogenous origin and thus, dietary restriction reduces plasma and tissue levels. Fish, beef, lamb, and dairy products should be avoided. The average daily intake of phytanic acid is 50–100 mg/day, which should ideally be reduced to 10–20 mg/day. Decrease in phytanic acid levels can reverse neurological, cardiac, and dermatological sequelae, but there is less response to visual and hearing impairments .
Glucose-6-phosphate dehydrogenase deficiency
Fava beans, green beans, and chick peas can induce hemolytic anemia in patients with glucose 6 phosphate dehydrogenase deficiency .
High-cholesterol containing food including dairy products and nonvegetarian foods should be avoided .
Episodes of gout is exacerbated by a high-purine diet. Meat, seafood, and green leafy vegetables are rich sources of purine, while wine, ascorbic acid, and low-fat dairy products are protective against gout .
Carrots and green leafy vegetables that are rich in carotene are beneficial in porphyria .
Disorders related to deficiency or excess of specific nutrients
Protein energy malnutrition results in diseases like kwashiorkar and marasmus. Phrynoderma is caused by deficiency of vitamin A, pellagra by niacin, and scurvy by vitamin C deficiency. Inherited zinc deficiency causes acrodermatitis enteropathica, a disease characterized by periorificial and acral dermatitis, alopecia and diarrhea. High intake of carrot causes carotenemia and tomato causes lycopenemia .
Miscellaneous disorders with an uncertain relationship to diet
Flushing in rosacea increases by intake of tea, coffee, hot beverages, tobacco, alcohol, and spicy food .
The widely held belief in India is that foods that are excessively sour should be avoided by vitiligo patients. These foods include citrus fruits, sour yoghurt, sour pickles, etc. Simultaneous consumption of milk and fish is also discouraged. Childhood vitiligo has been related to malnutrition and intake of junk food. Oral supplementation with antioxidants containing α-lipoic acid and vitamin B12 before and during NB-UVB broadband UVB significantly improves the clinical effectiveness of phototherapy .
Although the cause of oral aphthous ulcers is unknown, there is a well-established association with celiac disease. Recurrent aphthous ulceration may, in some cases, be due to gluten sensitivity in the absence of coeliac disease. Every patient with recurrent aphthous stomatitis should be asked about any history of gastrointestinal complaints and screened for markers of coeliac disease because recurrent aphthous stomatitis may, in some cases (particularly those with antiendomysial antibodies or intestinal histologic changes), respond to a GFD .
Food additives such as dyes and preservatives may lead to leukocytoclastic vasculitis .
Iron and protein deficiency seems to be associated with hair loss. Therefore foods rich in iron and protein are recommended in telogen effluvium. Nuts, seeds, legumes, bean products, raisins, green leafy vegetables, whole grains, and meat are beneficial. Starvation and eating disorders are also associated with hair loss. Zinc and biotin have a role in hair growth .
Diet in leprosy
Iodine has an aggravating effect in leprosy and hence a low-iodine diet should be advised. So, leprosy patients should consume raw noniodized salt. They should avoid seafood, spinach, cabbage, asparagus, carrots, garlic, onion, strawberries, tomatoes, and whole rice.
- B-carotene: papaya, carrot, pumpkin, mango, sweet potato.
- Glutathione: spinach and other leafy vegetables.
- Quercetin: white onion.
- Allicin: garlic, onion, onion leek.
- Capsaicin: chili, pepper.
- Ellagic acid: apple, cherry, orange, strawberries.
- Lycopene: tomato, pink guava, watermelon, red papaya, palm oil.
Licorice − Botanical name of licorice is Glycyrrhiza glabra. Glabridin is the hydrophobic fraction while glycyrrhizin and glycyrrhetinic acid are the hydrophilic fraction.
Mechanism of action: Glabridin inhibits melanogenesis and superoxide anion formation while liquiritin (flavonoids) acts as antioxidants.
Licorice extract is available as 0.1% and topical liquiritin is as 2% flavanoidal extract which is present in certain cosmetic formulation.
Soy: Soy is rich in flavanoids like isoflavone genistein.
Mechanism of action: flavanoid is an antioxidant, anticancer, and photoprotective agent. Some soy proteins like soybean trypsin inhibitors and Bowman Birk inhibitor inhibits melanin production. Soy also has some estrogen-type effects which can worsen melasma. Soy protein Lecithin and phytosterols are believed to improve barrier functions.
Alpha lipoic acid
Alpha lipoic acid is a biological and universal antioxidant which has skin penetration.
Mechanism of action: it chelates metals, scavenges O2 radicals, repairs oxidative damage, and inhibits cross-linking of proteins. It is soluble in both water and lipids and hence called a universal antioxidant. It is available as 1–7% in cosmetic preparations. It is less irritating than tretinoin and hydroxyl acids. It is used for superficial peeling especially around the eyes. Sometimes, it can cause skin inflammation.
Green tea is obtained by steaming and drying of the fresh leaves of the tea plant camellia sinensis.
Mechanism of action: catechin which is present in green tea has antioxidant, photoprotective, anti-inflammatory, and anticancer properties.
It is available as green tea oil, which is a popular antioxidant ingredient of moisturizers, cleansers, shower gels, toothpastes, depilatories, shampoo, and perfumes.
Dehydroepiandrosterone is derived from dioscorea plants.
Mechanism of action: it has antioxidant, photoprotective, immunomodulatory, and anticancer properties.
It is a natural antioxidant in skin.
Mechanism of action: it combats free radicals.
It is a bioflavonoid which is an extract of milk thistle plant.
Mechanism of action: It is an antioxidant and tumor-protective agent.
| Conclusion|| |
Dietary interventions have been underappreciated as a dermatological therapy in the past. Recent research, however, has found a significant association between diet and some dermatological diseases. Dermatologists must be well −educated and should apply their knowledge related to diet in counselling the patients appropriately.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Garioch JJ, Lewis HM, Sargent SA, Leonard JN, Fry L. Twenty five years’ experience of a gluten-free diet in the treatment of dermatitis herpetiformis. Br J Dermatol 1994; 131:541–545.
Turchin I, Barankin B. Dermatitis herpetiformis and glutenfree diet. Dermatol Online J 2005; 11:6.
Rottmann LH. Details of the gluten-free diet for the patient with dermatitis herpetiformis. Clin Dermatol 1992; 9:409–414.
Dhar S, Srinivas SM. Food allergy in atopic dermatitis. Indian J Dermatol 2016; 61:645–648.
] [Full text]
Thestrup-Pedersen K, Ring J. Atopic dermatitis: summary of the1st Georg Rajka Symposium 1998 and a literature review. Acta Derm Venereol 1999; 79:257–264.
Wüthrich B. Food-induced cutaneous adverse reactions. Allergy 1998; 53:131–135.
Oranje AP, de Waard-van der Spek FB. Atopic dermatitis anddiet. J Eur Acad Dermatol Venereol 2000; 14:437–438.
Bath-Hextall F, Delamere FM, Williams HC. Dietary exclusionsfor established atopic eczema. Cochrane Database Syst Rev 2008; 1:CD005203.
Devlin J, David TJ, Stanton RH. Elemental diet for refractoryatopic eczema. Arch Dis Child 1991; 66:93–99.
Smith RN, Mann NJ, Braue A, Mäkeläinen H, Varigos GA. Alow glycemic load diet improves symptoms in acne vulgarispatients: a randomized controlled trial. Am J ClinNutr 2007; 86:107–115.
Wolters M. Diet and psoriasis: experimental data and clinicalevidence. Br J Dermatol 2005; 153:706–714.
Smith RN, Braue A, Varigos GA, Mann NJ. The effect of a low glycemic load diet on acne vulgaris and the fatty acid composition of skin surface triglycerides. J Dermatol Sci 2008; 50:41–52s.
Collier PM, Ursell A, Zaremba K, Payne CM, Staughton RC, Sanders T. Effect of regular consumption of oily fish comparedwith white fish on chronic plaque psoriasis. Eur J ClinNutr 1993; 47:251–254.
Cassano N, Vestita M, Apruzzi D, Vena GA. Alcohol, psoriasis, liver disease, and anti-psoriasis drugs. Int J Dermatol 2011; 50:1323–1331.
Marfatia YS, Asmi P. Diet in dermatology. Indian J Dermatol Venereol Leprol 2002; 68:313.
] [Full text]
Afifi L, Danesh MJ, Lee KM, Beroukhim K, Farahnik B, Ahn RS et al.
Dietary behaviors in psoriasis: patient-reported outcomes from a US national survey. Dermatol Ther (Heidelb) 2017; 7:227–242.
Rucevic I, Perl A, Barisic-Drusko V, Adam-Perl M. The role of the low energy diet in psoriasis vulgaris treatment. Coll Antropol 2003; 27(Suppl. 1):41–48.
Naldi L, Parazzini F, Peli L, Chatenoud L, Cainelli T. Dietary factors and the risk of psoriasis. Results of an Italian case–control study. Br J Dermatol 1996; 134:101–106.
Zuberbier T. The role of allergens and pseudoallergens inurticaria. J Investig Dermatol Symp Proc 2001; 6:132–134.
Simopoulos AP. Omega-3 fatty acids in inflammation andautoimmune diseases. J Am Coll Nutr 2002; 21:495–505.
Brunner LJ, Pai KS, Munar MY, Lande MB, Olyaei AJ, Mowry JA. Effect of grapefruit juice on cyclosporin A pharmaco-kinetics in pediatric renal transplant patients. Pediatr Transplant 2000; 4:313–321.
Feliciani C, Ruocco E, Zampetti A, Toto P, Amerio P, Tulli A et al.
Tannic acid induces in vitro acantholysis of keratinocytesvia IL-1alpha and TNF-alpha. Int J Immunopathol Pharmacol 2007; 20:289–299.
Cabré E, Gassull MA. Polyunsaturated fatty acid deficiency inliver diseases: pathophysiological and clinical significance. Nutrition 1996; 12:542–548.
Wagner S, Breiteneder H. The latex-fruit syndrome. Biochem Soc Trans 2002; 30:935–940.
Pereira C, Tavares B, Loureiro G, Lundberg M, Chieira C. Turnipand zucchini: new foods in the latex-fruit syndrome. Allergy 2007; 62:452–453.
Chalmers RA, Bain MD, Michelakakis H, Zschocke J, Iles RA. Diagnosis and management of trimethylaminuria (FMO3deficiency) in children. J Inherit Metab Dis 2006; 29:162–172.
Posada de la Paz M, Philen RM, Borda AI. Toxic oil syndrome:the perspective after 20 years. Epidemiol Rev 2001; 23:231–247.
Giffiths WAD. Pityriasis rubra pilaris. Cli Exp Dermatol 1980; 5:105.
Brandt O, Rieger A, Geusau A, Stingl G. Peas, beans, and the Pythagorean theorem − the relevance of glucose-6-phosphate dehydrogenase deficiency in dermatology. J Dtsch Dermatol Ges 2008; 6:534–539.
Ashorn M, Pitkänen S, Salo MK, Heikinheimo M. Current Strategies for the treatment of hereditary tyrosinemia type I. Pediatr Drugs 2006; 8:47–54.
Kabra M. Dietary management of inborn errors of metabolism. Indian J Pediatr 2002; 69:421–426.
Wills AJ, Manning NJ, Reilly MM. Refsum’s disease. QJM 2001; 94:403–406.
Sarkany RPE, Breathnach SM, Seymour CA, Weismann K, Burns DA. Metabolic and nutritional disorders. In: Burns T, Breathnach S, Cox N, Griffiths C, editors. Rook’s Textbook of Dermatology. 7th ed. Massachusetts: Blackwell Science; 2004. 57. 1–124.
Lee SJ, Terkeltaub RA, Kavanaugh A. Recent developments in diet and gout. Curr Opin Rheumatol 2006; 18:193–198.
Dabrowska E, Jaboñska-Kaszewska I, Falkiewicz B. Effect of high fiber vegetable-fruit diet on the activity of liver damage and serum iron level in porphyria cutanea tarda (PCT). Med Sci Monit 2001; 7:282–286.
Pelle MT. Rosacea. In: Wolff K, Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ, editors. Fitzpatrick’s Dermatology in General Medicine. 7th ed. New York, NY: McGraw Hill 2008. 703–708
Dell′Anna ML, Mastrofrancesco A, Sala R, Venturini M, Ottaviani M, Vidolin AP et al.
Antioxidants and narrow band-UVB in the treatment of vitiligo: a double-blind placebo controlled trial. Clin Exp Dermatol 2007; 32:631–636.
Olszewska M, Sulej J, Kotowski B. Frequency and prognostic value of IgA and IgG endomysial antibodies in recurrent aphthous stomatitis. Acta Derm Venereol 2006; 86:332–334.
Lowry MD, Hudson CF, Callen JP. Leukocytoclastic vasculitis caused by drug additives. J Am Acad Dermatol 1994; 30:854–855.
Kaimal S, Thappa DM. Diet in dermatology: revisited. Indian J Dermatol Venereol Leprol 2010; 76:103–115.
[Table 1], [Table 2], [Table 3]