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&Clinicalofaltology Rmaesermeperi ntal DExISSN: 2155-9554Journal of Clinical & ExperimentalDermatology ResearchBergman et al., J Clin Exp Dermatol Res 2016, 7:3DOI: 10.4172/2155-9554.1000355rcheaJournShort CommunicationOpen AccessLow Nickel Diet: A Patient-Centered ReviewBergman D1, Goldenberg A1, Rundle C1 and Sharon Eyes Jacob2*1Schoolof Medicine, Loma Linda University, California, USA2Departmentof Dermatology, Loma Linda University, California, USA*Correspondingauthor: Jacob SE, Department of Dermatology, Loma Linda University, USA, Tel: 1-909-558-2890; E-mail: [email protected] date: March 21, 2016; Accepted date: May 17, 2016; Published date: May 24, 2016Copyright: 2016 Bergman D, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricteduse, distribution, and reproduction in any medium, provided the original author and source are credited.AbstractNickel allergic contact dermatitis (ACD) has become a more widely recognized disease process over the lastthree decades in the United States. A subpopulation of ACD patients will manifest with systemic contact dermatitis(SCD). Specifically, those cases of widespread recalcitrant nickel ACD with only partial clinical relief after strict nickelavoidance, suggest SCD. Evidence indicates that application of the low nickel diet has the highest efficacy inpatients with SCD, and that a targeted, points-based approach is most meaningful. Furthermore, as the immunologicpathways of how oral nickel provokes cutaneous dermatitis are complex, involving interplay between the Th2 andTh1 response, more specific investigative work in this area is much needed.Keywords: Systemic Contact Dermatitis (SCD); Systemic NickelAllergy Syndrome (SNAS); Nickel allergy; Low nickel dietIntroductionPrevalence of nickel contact dermatitis is estimated to be 19.5% inadults and 25.6% in children patch tested within the US [1,2]. Theexact prevalence within the general, non-patch tested, US population islargely unknown, as the last study to evaluate healthy US volunteerstook place over 30 years ago [3]. At that time, Prystowsky et al. showedthat 5.7% of an asymptomatic study population had been(unknowingly) sensitized to nickel [3]. The reported rates of nickelsensitization are on the rise, suggesting a large proportion of the USpopulation continues to be exposed and sensitized to nickel [4].The relationship between allergic contact dermatitis (ACD) andnickel is undisputed and widely confirmed in literature. Systemicallyinduced contact dermatitis (SCD) is a cutaneous manifestationsecondary to allergen exposure via the oral, per rectum, intravesical,transcutaneous, intravenous, or inhalation routes [5]. While SCD isoften considered a cutaneous form of systemic nickel allergy syndrome(SNAS), it is important to recognize that SNAS is a broader syndrome.In addition to cutaneous symptoms, SNAS often presents with a host ofsystemic symptoms including heartburn, abdominal pain, nausea,vomiting, constipation, abdominal distension rhinitis, asthma,headache, chronic fatigue syndrome, arthralgia, fibromyalgia, andfever [6,7]. SCD may also be a misleading term, because skin contactwith nickel is not a requirement for disease elicitation thoughreactivation of previous nickel contact sites may be seen, clinicalpresentation also includes generalized skin manifestations, such asurticaria and eczema [6,7]. Fabbro et al. remark that the typical clinicalpresentation of SNAS may be a severe recurring ACD despite propertreatment and avoidance [8]. The most common clinical presentationof SNAS is often refractory vesicular hand dermatitis, with possiblepruritic papules on the elbows [8].The prevalence of SCD in the population of patients with ACD islargely unknown. In one recent study, SNAS alone was identified in upto 6% of patients presenting to allergy clinics in Europe, implying thatSCD may be under-identified in the dermatitis population [9].Additionally, Jensen demonstrated that up to 10% of nickel sensitizedpatients exhibit SCD due to the amount of nickel found in a normaldiet [10]. SCD to nickel is one of the most commonly reported anddescribed forms of dietary SCD, consistent with the fact that nickel isone of the most common contact allergens ingested due to itsubiquitous nature [8,11].Food Sourcemg/kgNickel content (μg)Serving Size (g)Mussels1.0331541 cup (150)Spirulina2.71511 cup (56)Canned Refried Beans0.5411311 cup (242)Oatmeal0.354831 cup (234)White beans0.329821 cup (250)Wheat germ0.713821 cup (115)Oat ring cereal2.124591 cup (28)J Clin Exp Dermatol ResISSN:2155-9554 JCEDR an open access journalVolume 7 Issue 3 1000355

Citation:Bergman D, Goldenberg A, Rundle C, Jacob SE (2016) Low Nickel Diet: A Patient-Centered Review . J Clin Exp Dermatol Res 7: 355.doi:10.4172/2155-9554.1000355Page 2 of 5Pinto beans0.578461/2 cup (80)Lima beans0.062451/2 cup (72)Avocado0.315431 avocado (136)Granola with raisins0.946411 bar (43)Milk chocolate0.921411 bar (44)Lasagna with meat0.129381 serving (297)Chocolate cake0.521371 piece (71)Prune juice0.136358 Oz (256)Peanuts0.494351/2 cup (70)Chocolate milkshake0.142358 Oz (244)Pineapple juice, from concentrate0.128328 Oz (250)Tomato salsa0.13321 cup (245)Green beans0.077281 cup (240)Iceberg lettuce0.118281 cup (240)Spaghetti with meat sauce0.09251 cup (283)Pork sausage0.111251 sausage (227)French Fries0.196231 medium serving (117)Canned tomato soup0.086221 cup (250)Clam chowder0.084211 cup (245)Canned Pineapple0.082211 cup (250)Sweet potatoes0.089211 large potato (200)Tomato sauce0.096201 cup (212)Peas0.203201/2 cup (98)Chocolate milk0.0792201 cup (244)Tomato juice0.078208 Oz (250)Canned fruit cocktail0.065171 cup (253)Potato0.058151 large potato (250)Peanut butter0.481152 tbsp (32)Catfish0.105151 fillet (143)Brownie0.622151 brownie (24)Cocoa powder0.98153 tbsp (15)Doughnut0.244151 doughnut (60)Asparagus0.112151 cup (134)Pumpkin pie0.102141 piece (133)Taco/tostada with beef and cheese0.13131 taco (99)Cantaloupe0.071131 cup (177)J Clin Exp Dermatol ResISSN:2155-9554 JCEDR an open access journalVolume 7 Issue 3 1000355

Citation:Bergman D, Goldenberg A, Rundle C, Jacob SE (2016) Low Nickel Diet: A Patient-Centered Review . J Clin Exp Dermatol Res 7: 355.doi:10.4172/2155-9554.1000355Page 3 of 5Peach0.078121 cup (154)Corn/tortilla chips0.195121 cup (63)Canned chicken noodle soup0.045111 cup (250)Raisins0.068111 cup (165)Presweetened cereal0.397111 cup (28)Fast-food quarterpound cheeseburger0.056101 cheeseburger (186)Pizza, cheese and pepperoni0.084101 slice (120)Winter squash (Hubbard/acorn)0.087101 cup (113)Chicken nuggets0.131105 pieces (75)Table 1: Nickel Content by Food Source Following a point based diet 10 μg 1 point. Daily goal is less than 15 points [20]. Amounts of dietarynickel were gathered from literature review [17,20,22].The specific non-cutaneous dose of nickel required to evoke ahypersensitivity reaction has been in question due to variance of thenickel dose reported in oral challenge tests. A meta review by Jensenspecifically assessed elicitation of SCD due to nickel ingestion, andfound that 1% of those sensitized to nickel react to the nickel contentof a “normal” diet, defined as 0.22 mg, 0.35 mg, or 0.53 mg [12].Furthermore, a dose-response relationship was revealed showing 10%of nickel sensitized patients responding to exposures between 0.55 mgand 0.89 mg. Such low exposures can be easily attained by consumingfoods high in nickel content (see Table 1, Figure 2 and Figure 3) [12].Figure 1: Nickel Survey QR Code: link to take the survey. t-dermatitis-survey.However, many patients sensitized to nickel are unaware thatdietary exposure may play a role in their morbidity. Recent data fromthe first self-reporting nickel allergy patient registry study showed thatwithin 280 participants endorsing a self-reported history of nickelallergy, only 37% recognized nickel could be found in foods (LomaLinda University, Nickel Allergy Alliance, and Dermatitis AcademyTM)(Figure 1).J Clin Exp Dermatol ResISSN:2155-9554 JCEDR an open access journalFigure 2: Points Based Low Nickel Diet Food Pyramid: Schematic oflower nickel foods with points in superscript. Suggested for nickelsensitized patients with recalcitrant ACD due to nickel, despitestandard nickel avoidance measures.Thus, further patient and provider education regarding noncutaneous nickel exposures, specifically in diet, are necessary.Underlying ImmunologyThe immunologic response to oral provocation of nickel allergy iscomplex and diverse. The cytokine profile of SNAS involves both a Th1and Th2 response. The delayed cytotoxic cellular immunity shared bySNAS and ACD is mediated through a predominant Th1 reaction,evident by elevations of IFN-γ, IL-2, and TNF-α [13]. An observedrapid cutaneous response following oral nickel provocation, suggests acomplex interplay within SNAS between Type IV (cellular) and III(humoral) hypersensitivity reactions [13,14]. Jensen et al.demonstrated a statistically significant rise in IL-5, a Th2 response,within 24 hours after oral challenge, highlighting the role of the Th2response in the initial elicitation phase of SNAS [13]. Of interest, theVolume 7 Issue 3 1000355

Citation:Bergman D, Goldenberg A, Rundle C, Jacob SE (2016) Low Nickel Diet: A Patient-Centered Review . J Clin Exp Dermatol Res 7: 355.doi:10.4172/2155-9554.1000355Page 4 of 5Th2 response that is shared with atopic dermatitis and asthma, offers aplausible explanation for the cutaneous and extra cutaneousmanifestations of SNAS [15]. The immunological complexities extendto include underlying cross-facilitating pathways, demonstrated byRicciardi et al. where 16 out of the 98 SNAS patients (16.3%, p 0.001)presented with an IgE-mediated food allergy [9]. Ultimately, SNASexhibits Th1 and Th2 responses with clinical presentation dictated bythe predominating immune response.modification [19]. The case study outlined four children with knownnickel allergy who had a 60%-80% improvement of their dermatitisfollowing avoidance strategies and a low nickel diet. However, allchildren developed acute generalized dermatitis exacerbations afteringestion of chocolate—a nickel-rich food. After educating the patientsand parents regarding foods to avoid, the patients’ symptoms ofgeneralized dermatitis resolved by the next follow-up appointment.A retrospective case series by Antico and Soana showed that lownickel diets dramatically improved dermatitis symptoms in nickelsensitive patients [14]. The study analyzed 339 patients sensitized tonickel via patch testing. Simple avoidance of nickel contact resulted ina 15% recovery rate. However, 80% of the patients who combined a lownickel diet with avoidance of nickel contact had a complete or nearlycomplete resolution of skin symptoms. A double-blind placebocontrolled oral nickel challenge was then conducted on the improvedpatients, with an 89% recurrence or worsening of symptoms, whichaccounted for 10% of the total patient population.Nutraceuticals and functional food ingredients (such as the plantbased Mediterranean meal plan) have been highly used as alternativecare treatments, especially in reducing cardiovascular risk in patientsthat cannot tolerate statin therapy to decreased morbidity andmortality [20]. Notably, many of these diets contain high nickel foodssuch as legumes and grains. As a result, subpopulations of patientswith nickel sensitization using nutraceuticals and functional foodingredients may be at increased risk of SNAS or SCD.Figure 3: Points Based High Nickel Diet Food Pyramid: Schematicof higher nickel foods with points in superscript. Suggested foods toavoid in nickel sensitized persons, especially with recalcitrant nickelACD patients. *Note: Nickel can accumulate in tap water, and pipesshould be flushed for 5 minutes before drinking.All oral nickel exposure does not result in SCD, and in fact ifrepeated oral exposure occurs prior to topical prolonged contact,immunologic tolerance may be conferred. In a study from Denmark,adolescent girls with dental braces before ear piercings exhibited alower prevalence of nickel allergy compared to those girls with earpiercings before dental braces [16]. A more recent study by DiGioacchino et al. showed that nickel oral hyposensitization alsoresulted in immune tolerance [17]. Nickel oral hyposensitization is amechanism of immune tolerance, in a nickel-sensitized patient,through the ingestion of low dose nickel. When comparing nickel oralhyposensitization to placebo in patients with SNAS, those patientsexposed to oral low dose nickel for one year exhibited dose-dependentimprovement in gastrointestinal symptoms and cutaneous visualanalog scores [17]. Those taking the highest dose of 1.5 μg Ni/weekdemonstrated increased tolerance as seen by the higher challenge doseof oral allergen needed to elicit cutaneous symptoms. Additionally, astatistically significant number of hyposensitized patients had anegative patch test when retested at the conclusion of the study. Thehypothesized mechanism is an active cellular suppression through aTh2 response regulating nickel-specific T lymphocytes [17,18].Low Nickel Diet—does it work?In the recent literature there have been many documented cases ofSCD linked to diet. Jacob et al. reported dramatic improvement incutaneous symptoms of four pediatric patients with refractory nickelACD after following strict avoidance measures including dietJ Clin Exp Dermatol ResISSN:2155-9554 JCEDR an open access journalThe literature continues to expand the understanding of nickelallergy, specifically the complexities related to oral exposure. Patientcentered education is key when explaining these complexpathophysiological processes and applying them to pragmaticguidelines. Table 1 provides a streamlined reference for practitionersoffering information regarding food groups and nickel content i