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Systemic nickel allergy syndrome. Biological monitoring of dietary nickel intake and induction of immunotolerance

Abstract

Nickel sensitized patients may suffer of contact dermatitis,but also of urticaria-like, pruritus-erythema and cutaneous rush,sometimes associated with intestinal symptoms.The role of Nickel absorption due to food is still debated, but a clinical framework of Systemic Nickel Allergy Syndrome (SNAS) may be proposed, while a possible induction of oral tolerance deserves to be investigated. In the same Allergy Unit 152 subjects (126 F,26 M) were diagnosed as allergic by positive patch test to Nickel sulphate (class 2-3). All underwent Urinary Nickel determinations (NiU), by AAS with Zeman corrector and results standardized to creatinine concentration. According to single diagnosis patients were selected. Group A (65 pt) with only contact dermatitis. Group B (87 pt) with skin troubles of SNAS. At the first determinationt NiU values in Group B (mean 2,25 mcg/g creatinine) were significantly higher when compared to Group A (mean 0,87 mcg/g creatinine), with p<0,0001. Abnormal values measured at free diet exceeded the fixed limit of attention of 1,7 in 55% of Group B (48/87 cases) and only 20% in Group A (13/65). The 48 subjects of Group B received a Nickel-scanty diet that observed for six months; end-NiU resulted below the adopted limit for all patients. In spite of this dietary restriction 30 of them claimed again episodic cutaneous urticaria-like symptoms and frequent itching. 12 subjects were included in an experimental oral treatment (Lofarma Laboratories, Milan) based on subsequent microdoses of Nickel sulphate,from 0,1 to 1000 nanograms (1 mcg), aimed to induce an immunotolerance. Treatments were monitored by NiU. All these cases reported improvement; absence of symptoms was documented after 8 months of maintenance with the highest dose. SNAS is statistically related to an increased Nickel intake from dietary habit. NiU seems to be a reliable indicator in biological monitoring. A "Nickel-scanty"diet may reduce the incidence of SNAS, according to a decrease of NiU. A surveilled oral treatment by microdoses of Nickel sulphate seems to induce a specific immunotolerance and clinically to realise reduction or suppression of symptoms.
P O STER P RESENTATION Open Access
Systemic nickel allergy syndrome. Biological
monitoring of dietary nickel intake and induction
of immunotolerance
Cirla Angelo Mario
From Food Allergy and Anaphylaxis Meeting 2011
Venice, Italy. 17-19 February 2011
Nickel sensitized patients may suffer of contact dermati-
tis,but also of urticaria-like, pruritus-erythema and cuta-
neous rush,sometimes associated with intestinal
symptoms.The role of Nickel absorption due to food is
still debated, but a clinical framework of Systemic Nickel
Allergy S yndrome (SNAS) may be proposed, while a
possible induction of oral tolerance deserves to be
investigated.
In the same Allergy Unit 152 subjects (126 F,26 M)
were diagnosed as allergic by positive patch test to
Nickel sulphate (class 2-3). All underwent Urinary
Nickel determinations (NiU), by AAS with Zeman cor-
rector and results standardized to creatinine concentra-
tion. According to single diagnosis patients were
selected. Group A (65 pt) with only contact dermatitis.
Group B (87 pt) with skin troubles of SNAS.
At the first determinationt NiU values in Group B
(mean 2,25 mcg/g creatinine) were significantly higher
when compared to Group A (mean 0,87 mcg/g creati-
nine), with p<0,0001. Abno rmal values measured at free
diet exceeded the fixed limit of attention of 1,7 in 55%
of Group B (48/87 cases) and only 20% in Group A (13/
65). The 48 subjects of Group B received a Nickel-
scanty diet that observed for six months; end-NiU
resulted below the adopted limit for all patients. In spite
of this dietary restriction 30 of them claimed again epi-
sodic cutaneous urticaria-like symptoms and frequent
itching. 12 subjects were included in an experimental
oral treatment (Lofarma Laboratories, Milan) based o n
subsequent microdoses of Nickel sulphate,from 0,1 to
1000 nanograms (1 mcg), aimed to induce an immuno-
tolerance. Treatments were monitored by NiU. All these
cases reported improvement; absence of s ymptoms was
documented after 8 months of maintenance with the
highest dose.
SNAS is statistic ally related to an increased Nickel
intake from dietary habit. NiU seems to be a reliable
indicator in biological monitoring. A Nickel-scanty"diet
may reduce the incidence of SNAS, according to a
decrease of NiU. A surveilled oral treatment by micro-
doses of Nickel sulphate see ms to induc e a specific
immunotolerance and clinically to realise reduction or
suppression of symptoms.
Published: 12 August 2011
doi:10.1186/2045-7022-1-S1-P108
Cite this article as: Angelo Mario: Systemic nickel allergy syndrome.
Biological monitoring of dietary nickel intake and induction of
immunotolerance. Clinical and Translational Allergy 2011 1(Suppl 1):P108.
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Centro Italiano Medicina Ambiente Lavoro, Section of Allergy, Cremona, Italy
Angelo Mario Clinical and Translational Allergy 2011, 1(Suppl 1):P108
http://www.ctajournal.com/content/1/S1/P108
© 2011 Angelo Mario; licensee BioMed Central Ltd. This is an open ac cess article distributed under the terms of the Creative Commons
Attribution License (http://creativecommons.org/licenses/by/2.0), which permits u nrestricted use, distribution, and reproduction in
any med ium, provided the or iginal work is properly cited.
Article
Systemic contact dermatitis (SCD), a cutaneous reaction that is a direct manifestation of systemic exposure to a known allergen in a sensitized individual, has been increasingly recognized as a cause of persistent cutaneous contact dermatitis that is refractory to conventional therapies. While SCD in response to drugs has been described well in the literature, SCD to allergens in common foodstuffs is a less well-articulated phenomenon. Several foods that are universally consumed throughout the world contain potent allergens including nickel, balsam of Peru, trace metals, urushiol, and sesquiterpene lactones as well as a host of others that may cause a distinctive clinical picture. In this review article, the authors review the typical presentation and prevalence of SCD to foods, pathophysiology, the most common offensive ingestible food allergens, several appropriate diets, and effectiveness of dietary avoidance for situations in which SCD is suspected.
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