Nickel Abstracts 1


Helicobacter pylori


Nickel free-diet enhances the Helicobacter pylori eradication rate: a pilot study.
            (Campanale et al., 2014) Download
BACKGROUND:  The Helicobacter pylori eradication rate with standard triple therapy is very low. H. pylori is known to require the nickel-containing metalloenzymes urease and NiFe-hydrogenase to survive at the low pH environment in the stomach. AIM:  To compare the H. pylori eradication rate of a nickel free-diet associated with standard triple therapy and standard triple therapy alone as the first-line regimen. METHODS:  Fifty-two sex- and age-matched patients at the first diagnosis of H. pylori infection were randomized 1:1 into two different therapeutic schemes: (1) standard LCA (26 patients): lansoprazole 15 mg bid, clarithromycin 500 mg bid and amoxicillin 1,000 mg bid for 7 days with a common diet; (2) standard LCA plus a nickel free-diet (NFD-LCA) (26 patients). Patients followed 30 days of a nickel-free diet plus a week of lansoprazole 15 mg bid, clarithromycin 500 mg bid and amoxicillin 1,000 mg bid starting from day 15 of the diet. RESULTS:  All patients completed the study. A significantly higher eradication rate was observed in the NFD-LCA group (22/26) versus LCA group (12/26) (p < 0.01). Only a few patients (9 of 52) reported the occurrence of mild therapy-related side effects, without any significant differences between the two groups. CONCLUSIONS:  The addition of a nickel-free diet to standard triple therapy significantly increases the H. pylori eradication rate. The reduction of H. pylori urease activity due to the nickel-free diet could expose the bacterium to gastric acid and increase H. pylori's susceptibility to amoxicillin. Further studies are necessary to confirm this preliminary result.
Due to its ubiquitous nature, it is not possible to completely avoid oral intake of nickel. Nevertheless, all foods with a high nickel content, such as apricots, figs, pears, plums, raisins, pineapples, peanuts, cocoa, almonds, walnuts, hazelnuts, lobster, mussels, oysters, mussels, plaice, asparagus, cauliflower, carrots, cabbage, onions, beans, lentils, potatoes, peas, tomatoes, spinach, margarine and corn, were strictly prohibited for 4 weeks. Furthermore, patients were asked to avoid the use of stainless-steel utensils to reduce nickel contamination during cooking.


Common themes and unique proteins for the uptake and trafficking of nickel, a metal essential for the virulence of Helicobacter pylori.
            (de Reuse et al., 2013) Download
Nickel is a virulence determinant for the human gastric pathogen Helicobacter pylori. Indeed, H. pylori possesses two nickel-enzymes that are essential for in vivo colonization, [NiFe] hydrogenase and urease, an abundant virulence factor that contains 24 nickel ions per active complex. Because of these two enzymes, survival of H. pylori relies on an important supply of nickel, implying a tight control of its distribution and storage. In this review, we will present the pathways of activation of the nickel enzymes as well as original mechanisms found in H. pylori for the uptake, trafficking and distribution of nickel between the two enzymes. These include (i) an outer-membrane nickel uptake system, the FrpB4 TonB-dependent transporter, (ii) overlapping protein complexes and interaction networks involved in nickel trafficking and distribution between urease and hydrogenase and, (iii) Helicobacter specific nickel-binding proteins that are involved in nickel storage and can play the role of metallo-chaperones. Finally, we will discuss the implication of the nickel trafficking partners in virulence and propose them as novel therapeutic targets for treatments against H. pylori infection.

Comprehensive mapping of the Helicobacter pylori NikR regulon provides new insights in bacterial nickel responses.
            (Vannini et al., 2017) Download
Nickel homeostasis is important for pathogenic and ureolytic bacteria, which use this metal ion as enzymatic cofactor. For example, in the human pathogen Helicobacter pylori an optimal balance between nickel uptake and incorporation in metallo-enzymes is fundamental for colonization of the host. Nickel is also used as cofactor to modulate DNA binding of the NikR regulator, which controls transcription of genes involved in nickel trafficking or infection in many bacteria. Accordingly, there is much interest in a systematic characterization of NikR regulation. Herein we use H. pylori as a model to integrate RNA-seq and ChIP-seq data demonstrating that NikR not only regulates metal-ion transporters but also virulence factors, non-coding RNAs, as well as toxin-antitoxin systems in response to nickel stimulation. Altogether, results provide new insights into the pathobiology of H. pylori and contribute to understand the responses to nickel in other bacteria.



Elevated serum nickel concentration in psoriasis vulgaris.
            (Smith et al., 1994) Download
BACKGROUND:  Psoriasis vulgaris is a common skin disease afflicting 1-3% of the American population. Its pathogenesis remains unknown despite concerted research efforts. Our purpose was to study baseline serum nickel concentrations in psoriasis vulgaris subjects and in healthy control subjects. METHODS:  Sixteen psoriasis vulgaris subjects with active disease (in 14 of moderate to marked severity), and 11 age- and sex-matched healthy control subjects were studied. Serum nickel determinations were performed using electrothermal atomic absorption spectrophotometry (ETAAS). RESULTS:  Despite the relatively small sample size, significant elevation of mean serum nickel concentration was found in the psoriasis group compared to the control group (P = 0.019). CONCLUSIONS:  Recognition of abnormal nickel homeostasis could point the way to greater understanding of the primary biochemical defect in the psoriatic process. Alternatively, this finding may mark an association without pathogenic significance. Further investigation is needed.

Improvement of psoriasis vulgaris with oral nickel dibromide.
            (Smith et al., 1997) Download
A possible connection between nickel and the pathogenesis of psoriasis is indicated in at least 2 diverse studies. Bromide absorption has been proposed as a beneficial factor in treatment in psoriasis treatment at the Dead Sea, and bromide salts were found to have an antiproliferative effect on cell growth in cultures. A pilot study was designed to evaluate the effect of oral nickel and bromide therapy on psoriasis vulgaris.

Clinical Spectroscopy: The Quantitative Retention of Nickel in Psoriasis; Observations on Forty-Six Cases
            (Gaul and Staud, 1934) Download
This report includes the various sources for nickel in human tissue, the incidence of nickel in apparently normal dermal biopsy specimens and the quantity of nickel found in psoriatic biopsy specimens.



Contact Dermatitis Due to Nickel Allergy in Patients Suffering from Non-Celiac Wheat Sensitivity.
            (D'Alcamo et al., 2017) Download
BACKGROUND: Non-celiac wheat sensitivity (NCWS) is a new clinical entity in the world of gluten-related diseases. Nickel, the most frequent cause of contact allergy, can be found in wheat and results in systemic nickel allergy syndrome and mimics irritable bowel syndrome (IBS). Objective: To evaluate the frequency of contact dermatitis due to nickel allergy in NCWS patients diagnosed by a double-blind placebo-controlled (DBPC) challenge, and to identify the characteristics of NCWS patients with nickel allergy. Methods: We performed a prospective study of 60 patients (54 females, 6 males; mean age 34.1 ± 8.1 years) diagnosed with NCWS from December 2014 to November 2016; 80 age- and sex-matched subjects with functional gastrointestina l symptoms served as controls. Patients reporting contact dermatitis related to nickel-containing objects underwent nickel patch test ( registration number: NCT02750735). RESULTS: Six out of sixty patients (10%) with NCWS suffered from contact dermatitis and nickel allergy and this frequency was statistically higher (p = 0.04)than observed in the control group(5%. The main clinical characteristic of NCWS patients with nickel allergy was a higher frequency of cutaneous symptoms after wheat ingestion compared to NCWS patients who did not suffer from nickel allergy (p < 0.0001. CONCLUSIONS: Contact dermatitis and nickel allergy are more frequent in NCWS patients than in subjects with functional gastrointestinal disorders; furthermore, these patients had a very high frequency of cutaneous manifestations after wheat ingestion. Nickel allergy should be evaluated in NCWS patients who have cutaneous manifestations after wheat ingestion.

Are nickel, vanadium, silicon, fluorine, and tin essential for man? A review.
            (Nielsen and Sandstead, 1974) Download
“Nickel is so ubiquitous, it will never be of concern to the human nutritionist.” Three new elements (nickel, vanadium, and silicon) have been found essential and two (fluorine and tin) possibly essential for animals. To date, these elements have not been shown essential for man. However, from animal data, it seems probable that they have an essential function in human nutrition and metabolism.


Nutritional requirements for boron, silicon, vanadium, nickel, and arsenic: current knowledge and speculation.
            (Nielsen, 1991) Download
Definition of specific biochemical functions in higher animals (including humans) for the ultratrace elements boron, silicon, vanadium, nickel, and arsenic still has not been achieved although all of these elements have been described as being essential nutrients. Recently, many new findings from studies using molecular biology techniques, sophisticated equipment, unusual organisms, and newly defined enzymes have revealed possible sites of essential action for these five elements. Based on these findings and the response of animals and/or humans to low intakes of these elements, the following speculations have been presented: 1) Boron has a role that affects cell membrane characteristics and transmembrane signaling. 2) Silicon is necessary for the association between cells and one or more macromolecules such as osteonectin, which affects cartilage composition and ultimately cartilage calcification. 3) Vanadium reacts with hydrogen peroxide to form a pervanadate that is required to catalyze the oxidation of halide ions and/or stimulate the phosphorylation of receptor proteins. 4) Nickel is needed for the CO2-fixation to propionyl-CoA to form D-methylmalonyl-CoA. 5) Arsenic has an important role in the conversion of methionine to its metabolites taurine, labile methyl, and the polyamines. If any of these speculations are found to be true, the element involved will be firmly established as having a nutritional requirement because the body obviously cannot synthesize it. Based on animal findings, the dietary requirement is likely to be small; that is, expressed in micrograms per day.

Low nickel diet in dermatology.
            (Sharma, 2013) Download
Nickel is a ubiquitous trace element and the commonest cause of metal allergy among the people. Nickel allergy is a chronic, recurring problem; females are affected more commonly than males. Nickel allergy may develop at any age. Once developed, it tends to persist life-long. Nickel is present in most of the dietary items and food is considered to be a major source of nickel exposure for the general population. Nickel in the diet of a nickel-sensitive person can provoke dermatitis. Careful selection of food with relatively low nickel concentration can bring a reduction in the total dietary intake of nickel per day. This can influence the outcome of the disease and can benefit the nickel sensitive patient.



Nickel sensitization and dietary nickel are a substantial cause of symptoms provocation in patients with chronic allergic-like dermatitis syndromes.
            (Antico and Soana, 2015) Download
Data in literature seem to show that, in patients with contact allergic dermatitis, dietary nickel might be a cause of systemic dermatitis, but little information exists in literature about the role of nickel sensitization and dietary nickel in patients with allergic-like chronic dermatitis syndromes. The prevalence of nickel sensitization in patients with chronic allergic-like, non-IgE-mediated skin diseases, and the possible impact of dietary nickel on symptom provocation and persistence has been assessed in the present retrospective study on a case series of 1726 patients referred to our allergy unit for chronic allergic-like skin diseases. IgE-mediated pathogenesis and other differential diagnoses excluded, patients were patch tested. Nickel-positive patients underwent an elimination diet and double-blind placebo-controlled nickel challenge (DBPCNC) test. A total of 339 (20%) tested nickel-positive. Fifty-two patients (15%) recovered by avoiding sources of nickel contact and 29 (10%) dropped out. Out of the remaining nickel-sensitized patients, 277 (80%) achieved complete or near complete recovery with low-nickel content diet, and 185 of them (89%) were positive to DBPCNC. We conclude that nickel sensitization and dietary nickel seem to be the chief trigger for provocation and persistence of symptoms in an important part (∼11%) of patients with chronic allergic-like dermatitis syndromes.

Mobile Phones: Potential Sources of Nickel and Cobalt Exposure for Metal Allergic Patients.
            (Aquino et al., 2013) Download
The use of cellular phones has risen exponentially with over 300 million subscribers. Nickel has been detected in cell phones and reports of contact dermatitis attributable to metals are present in the literature. We determined nickel and cobalt content in popular cell phones in the United States. Adults (>18 years) who owned a flip phone, Blackberry(®), or iPhone(®) were eligible. Seventy-two cell phones were tested using SmartPractice's(®) commercially available nickel and cobalt spot tests. Test areas included buttons, keypad, speakers, camera, and metal panels. Of the 72 cell phones tested, no iPhones or Droids(®) tested positive for nickel or cobalt. About 29.4% of Blackberrys [95% confidence interval (CI), 13%-53%] tested positive for nickel; none were positive for cobalt. About 90.5% of flip phones (95% CI, 70%-99%) tested positive for nickel and 52.4% of flip phones (95% CI, 32%-72%) tested positive for cobalt. Our study indicates that nickel and cobalt are present in popular cell phones. Patients with known nickel or cobalt allergy may consider their cellular phones as a potential source of exposure. Further studies are needed to examine whether there is a direct association with metal content in cell phones and the manifestation of metal allergy.


Nickel and cobalt activate complement factor C3 faster than magnesium.
            (Acevedo and Vesterberg, 2003) Download
We have found that incubation of heparin plasma with Ni(2+) or Co(2+) at concentrations below 100 microM can stimulate the conversion of complement factor C3 to C3b faster than magnesium, which is the natural cofactor in the alternative complement activation. This conversion was monitored by light absorbance measurement after separation by isotachophoresis, immunofixation and protein staining. The generation of C3b stimulated by these metals (<0.5 mM) proceeds up to about four times faster than the stimulation by Mg(2+). Half of total C3 in the incubation media was converted by Ni(2+) or Co(2+) at 0.5 mM after 20 min at 37 degrees C. Increasing Ni(2+) concentrations over 0.5 mM decreased the C3 conversion rate. Activation of C3 stimulated by Ni(2+), Co(2+) and Mg(2+) was concomitant with the conversion of complement factor B to Bb, but complement factor C4 was not affected by the activation. The conversion of B to Bb was monitored after separation by isotachophoresis and immunoblotting. Other divalent metal ions tested, namely Ca(2+), Ba(2+), Cu(2+) and Zn(2+), did not stimulate the complement cascade. We postulate that the increased rate of C3-fragment production induced by nickel or cobalt ions is central for the immunotoxicity of these metals.

Nickel, chromium and cobalt in consumer products: revisiting safe levels in the new millennium.
            (Basketter et al., 2003) Download
The transition metals nickel (Ni), chromium (Cr) and cobalt (Co) are common causes of allergic contact dermatitis (ACD). Given the high frequency with which these allergens can be associated with hand eczema in those responsible for domestic work, it has been suggested that contamination of household consumer products with these metals may be of relevance to the causation/chronicity of hand dermatitis. Dose-response studies using 48 h occlusive patch test conditions in sensitized individuals show that >/=90% of sensitized patients fail to react below 1 p.p.m., even on irritated skin. Assessment under more realistic exposure conditions has shown that in the presence of irritants and/or following repeated exposures, such individuals rarely react to levels below 10 p.p.m. On the basis of this information, it was recommended a decade ago that household (and other consumer) products should not contain more than 5 p.p.m. of each of Ni, Cr or Co and that, for an even greater degree of protection, the ultimate target level should be 1 p.p.m. The data generated since the original recommendations were made serve to reinforce the validity of these recommendations. Indeed, it is our view that typically the level of each of these transition metals should not normally exceed 1 p.p.m. Then, where consumer products meet this guideline fully, modern quantitative risk assessment shows clearly that elicitation of ACD is highly improbable, and the chance of the induction of sensitization is even lower.

Respiratory manifestations due to nickel.
            (Brera and Nicolini, 2005) Download
Nickel sulphate more frequently determines allergic dermatitis due to contact (contact eczema); less known are nasal inflammation (rhinitis) and bronchial asthma caused by nickel sulphate. Sporadic cases, often related to patients' work have been reported in the literature. The research described herein refers to 20 patients presenting clear nickel allergy with rhinitis (associated in 11 cases with asthma). The patients, all females, revealed positivity to this kind of allergy: patch test, prick tests with nickel sulphate, nasal provocation test by nickel sulphate, computed tomography of paranasal sinuses, spirometry and bronchial provocation test with metacholine, oral provocation test with nickel sulphate were employed. A strict long-term diet with food with low nickel content (2-4 months at least) led to a progressive reduction of nasal symptoms (rhinorrea, sneezing, nasal obstruction) and an improvement in bronchial symptoms and functional parameters.

Is systemic nickel important
            (Burrows, 1992) Download
Whenever dermatologists with an interest in contact dermatitis meet, the discussion often turns to the role of systemic nickel in nickel dermatitis and rejection of metal prostheses. The reason is twofold. A high percentage of women are allergic to nickel, possibly 15% to 20%, with an even higher percentage in those seen in a dermatology department. If nickel ingestion is an important factor in keeping the dermatitis active, then it would be important to know this and to take measures to reduce dietary intake of nickel.

Nickel, its adverse health effects & oxidative stress.
            (Das et al., 2008) Download
Nickel-induced toxicity and carcinogenicity, with an emphasis on the generation and role of reactive oxygen species is reviewed. Nickel is a known haematotoxic, immunotoxic, neurotoxic, genotoxic, reproductive toxic, pulmonary toxic, nephrotoxic , hepatotoxic and carcinogenic agent. This article presents a selective review on nickel and effect of its acute, subchronic and chronic doses on certain metabolically active tissues in human as well as animals. Nickel exposure causes formation of free radicals in various tissues in both human and animals which lead to various modifications to DNA bases, enhanced lipid peroxidation, and altered calcium and sulphydryl homeostasis. The primary route for nickel toxicity is depletion of glutathione and bonding to sulphydryl groups of proteins. Nickel homeostasis, nickel-induced activation of signaling pathways and the protective role of enzymatic and non-enzymatic antioxidants against nickel toxicity and carcinogenicity are also discussed.

Assessment of indirect human exposure to environmental sources of nickel: oral exposure and risk characterization for systemic effects.
            (De Brouwere et al., 2012) Download
This paper describes the indirect human exposure to Ni via the oral route for the regional scale in the EU, together with a method to assess additional local exposure from industrial emissions. The approach fills a gap in the generic REACH guidance which is inadequate for assessing indirect environmental exposure of metals. Estimates of regional scale Ni dietary intake were derived from Ni dietary studies performed in the EU. Typical and Reasonable Worst Case dietary Ni intakes for the general population in the EU were below the oral Derived No Effect Level (DNEL) of Ni sulfate for systemic effects. Estimates for the Ni dietary intake at the local scale take into account the influence of aerial Ni deposition and transfer from soil to crops grown near industrial plants emitting Ni. The additional dietary exposure via this local contribution was small. Despite the use of conservative parameters for these processes, this method may underestimate dietary exposure around older industrial sites because REACH guidance does not account for historical soil contamination. Nevertheless, the method developed here can also be used as a screening tool for community-based risk assessment, as it accounts for historical soil pollution. Nickel exposure via drinking water was derived from databases on Ni tap water quality. A small proportion of the EU population (<5%) is likely to be exposed to tap water exceeding the EU standard (20 μg Ni/l). Taking into account the relative gastrointestinal absorption of Ni from water (30%) versus from solid matrices (5%), water intake constitutes, after dietary intake, the second most important pathway for oral Ni intake. Incidental ingestion of Ni from soil/dust at the regional scale, and also at the local scale, was low in comparison with dietary intake.

Stainless steel leaches nickel and chromium into foods during cooking.
            (Kamerud et al., 2013) Download
Toxicological studies show that oral doses of nickel and chromium can cause cutaneous adverse reactions such as dermatitis. Additional dietary sources, such as leaching from stainless steel cookware during food preparation, are not well characterized. This study examined stainless steel grades, cooking time, repetitive cooking cycles, and multiple types of tomato sauces for their effects on nickel and chromium leaching. Trials included three types of stainless steels and a stainless steel saucepan, cooking times of 2-20 h, 10 consecutive cooking cycles, and four commercial tomato sauces. After a simulated cooking process, samples were analyzed by ICP-MS for Ni and Cr. After 6 h of cooking, Ni and Cr concentrations in tomato sauce increased up to 26- and 7-fold, respectively, depending on the grade of stainless steel. Longer cooking durations resulted in additional increases in metal leaching, where Ni concentrations increased 34-fold and Cr increased approximately 35-fold from sauces cooked without stainless steel. Cooking with new stainless steel resulted in the largest increases. Metal leaching decreases with sequential cooking cycles and stabilized after the sixth cooking cycle, although significant metal contributions to foods were still observed. The tenth cooking cycle resulted in an average of 88 μg of Ni and 86 μg of Cr leached per 126 g serving of tomato sauce. Stainless steel cookware can be an overlooked source of nickel and chromium, where the contribution is dependent on stainless steel grade, cooking time, and cookware usage.

Yes, systemic nickel is probably important
            (Möller, 1993) Download
To the Editor: Professor Desmond Burrows argues for a no to his question: Is systemic nickel important for exacerbating or maintaining chronic palmar eczema in a patient  with nickel allergy?  His attitude and conclusions are surprising because the bulk of his (and others')  evidence speaks for a yes.

Nickel and cobalt allergy before and after nickel regulation--evaluation of a public health intervention.
            (Thyssen, 2011) Download
Over the 20th century, the frequent use of nickel in consumer products resulted in an increasing prevalence of nickel allergy. Risk items included suspenders in the 1950s-1960s; buttons, zippers and rivets in the 1970s; and ear-piercing jewellery in the 1980s. When subjects allergic to nickel were exposed to nickel in high concentrations, it often resulted in allergic nickel contact dermatitis and hand eczema. In 1990, the Danish government began to regulate consumer nickel exposure as a response to the increasing nickel allergy problem. In 1994, the EU Nickel Directive was passed, a regulation that was based on the Danish and Swedish nickel regulations. These major public health interventions were expected to change the epidemiology of nickel allergy and dermatitis in Europe. Furthermore, it was debated whether nickel would be replaced by cobalt in inexpensive jewellery and result in higher prevalence of cobalt allergy. An evaluation of the possible effects of the European nickel regulations is of importance to ensure protection of consumers and dermatitis patients. This doctoral thesis aimed to evaluate the effects of regulatory interventions on nickel exposure by investigating the development of nickel allergy and dermatitis before and after nickel regulation. Furthermore, a change in the association between nickel allergy and hand eczema was evaluated. The nickel spot test was validated to determine its value when used for screening purposes. Possible explanations for the persistence of nickel allergy were explored including genetic predisposition and consumer nickel exposure from jewellery and accessories. A cobalt spot test was developed and validated. Finally, it was evaluated whether a cobalt allergy epidemic had replaced the nickel allergy epidemic after nickel regulation in terms of increasing cobalt sensitization and cobalt exposure. The thesis showed that the prevalence of nickel allergy decreased significantly after nickel regulation in young Danish women from the general population (18-35 years) and in young Danish female dermatitis patients from a university patch test clinic (0-30 years). Stratification by ear-piercing status revealed that women ear pierced before 1990 had a significantly higher prevalence of nickel allergy and dermatitis than women ear pierced after 1990. Furthermore, the association between hand eczema and nickel allergy decreased in young women aged 18-35 years when a comparison was made between women who were patch tested and questioned in, respectively, 1990 and 2006. Despite the decreasing prevalence of nickel allergy, this condition remains prevalent in young Danish women, as about 10% are nickel allergic. Genetic predisposition to nickel allergy was evaluated by investigating the possible association between filaggrin null mutation status and nickel allergy. A positive association was found but it was also concluded that environmental nickel exposure is of much greater importance. Thus, of 354 consumer items purchased from 36 different stores in Copenhagen, 22% released nickel in concentrations that may result in nickel dermatitis in sensitized subjects. Therefore excessive consumer nickel exposure remains common in Denmark and may be an important explanation for the persistence of nickel allergy. Excessive nickel release was also frequent when samples of earrings purchased in Warsaw and London were examined with the nickel spot test, in particular earrings purchased from street markets and shops with independent ownership. Only very weak indications of an emerging cobalt allergy epidemic were found, as the prevalence of cobalt allergy has not yet increased in young people and only four of 354 consumer items purchased in Copenhagen released cobalt in concentrations that may result in cobalt dermatitis in sensitized individuals. The specificity of the nickel spot test was 98% and the sensitivity 59%. Also, a cobalt spot test was developed and validated and seemed to be a useful diagnostic tool. In conclusion, the Danish nickel regulation and the EU Nickel Directive have changed the epidemiology of nickel allergy in Denmark. However, the Nickel Directive and its reference methods need to be revised to better protect consumers and dermatitis patients.




Acevedo, F and O Vesterberg (2003), ‘Nickel and cobalt activate complement factor C3 faster than magnesium.’, Toxicology, 185 (1-2), 9-16. PubMed: 12505440
Antico, A and R Soana (2015), ‘Nickel sensitization and dietary nickel are a substantial cause of symptoms provocation in patients with chronic allergic-like dermatitis syndromes.’, Allergy Rhinol (Providence), 6 (1), 56-63. PubMed: 25747857
Aquino, M, et al. (2013), ‘Mobile Phones: Potential Sources of Nickel and Cobalt Exposure for Metal Allergic Patients.’, Pediatr Allergy Immunol Pulmonol, 26 (4), 181-86. PubMed: 24380018
Basketter, DA, et al. (2003), ‘Nickel, chromium and cobalt in consumer products: revisiting safe levels in the new millennium.’, Contact Dermatitis, 49 (1), 1-7. PubMed: 14641113
Brera, S and A Nicolini (2005), ‘Respiratory manifestations due to nickel.’, Acta Otorhinolaryngol Ital, 25 (2), 113-15. PubMed: 16116834
Burrows, D (1992), ‘Is systemic nickel important’, J Am Acad Dermatol, 26 (4), 632-35. PubMed: 1597551
Campanale, M, et al. (2014), ‘Nickel free-diet enhances the Helicobacter pylori eradication rate: a pilot study.’, Dig Dis Sci, 59 (8), 1851-55. PubMed: 24595654
D’Alcamo, A, et al. (2017), ‘Contact Dermatitis Due to Nickel Allergy in Patients Suffering from Non-Celiac Wheat Sensitivity.’, Nutrients, 9 (2), PubMed: 28157173
Das, KK, SN Das, and SA Dhundasi (2008), ‘Nickel, its adverse health effects & oxidative stress.’, Indian J Med Res, 128 (4), 412-25. PubMed: 19106437
De Brouwere, K, et al. (2012), ‘Assessment of indirect human exposure to environmental sources of nickel: oral exposure and risk characterization for systemic effects.’, Sci Total Environ, 419 25-36. PubMed: 22285091
de Reuse, H, D Vinella, and C Cavazza (2013), ‘Common themes and unique proteins for the uptake and trafficking of nickel, a metal essential for the virulence of Helicobacter pylori.’, Front Cell Infect Microbiol, 3 94. PubMed: 24367767
Gaul, LE and AH Staud (1934), ‘Clinical Spectroscopy: The Quantitative Retention of Nickel in Psoriasis; Observations on Forty-Six Cases’, Arch Derm Syphil, 30 (5), 697-703. PubMed:
Kamerud, KL, KA Hobbie, and KA Anderson (2013), ‘Stainless steel leaches nickel and chromium into foods during cooking.’, J Agric Food Chem, 61 (39), 9495-501. PubMed: 23984718
Möller, H (1993), ‘Yes, systemic nickel is probably important’, J Am Acad Dermatol, 28 (3), 511-13. PubMed: 8445078
Nielsen, FH and HH Sandstead (1974), ‘Are nickel, vanadium, silicon, fluorine, and tin essential for man? A review.’, Am J Clin Nutr, 27 (5), 515-20. PubMed: 4596029
Nielsen, FH (1991), ‘Nutritional requirements for boron, silicon, vanadium, nickel, and arsenic: current knowledge and speculation.’, FASEB J, 5 (12), 2661-67. PubMed: 1916090
Sharma, AD (2013), ‘Low nickel diet in dermatology.’, Indian J Dermatol, 58 (3), 240. PubMed: 23723488
Smith, SA, F Aamir, and MP Otis (1994), ‘Elevated serum nickel concentration in psoriasis vulgaris.’, Int J Dermatol, 33 (11), 783-85. PubMed: 7822082
Smith, SA, et al. (1997), ‘Improvement of psoriasis vulgaris with oral nickel dibromide.’, Arch Dermatol, 133 (5), 661-63. PubMed: 9158427
Thyssen, JP (2011), ‘Nickel and cobalt allergy before and after nickel regulation--evaluation of a public health intervention.’, Contact Dermatitis, 65 Suppl 1 1-68. PubMed: 21777241
Vannini, A, et al. (2017), ‘Comprehensive mapping of the Helicobacter pylori NikR regulon provides new insights in bacterial nickel responses.’, Sci Rep, 7 45458. PubMed: 28393877