A Clinical Trial of Oral Hyposensitization in Systemic Allergy to Nickel

Schiavino, Domenico; Nucera, Eleonora; Alonzi, Cristiana; Buonomo, Alessandro; Pollastrini, Emanuela; Roncallo, Chiara; Pasquale, Tiziana De; Lombardo, Carla; Torre, G La; Sabato, Vito; Pecora, Valentina; Patriarca, Giampiero

doi:10.1177/039463200601900315

Cited by 36 publications

(32 citation statements)

References 34 publications

(48 reference statements)

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“…The most common gastrointestinal symptoms include nausea, gastric pyrosis, meteorism, abdominal pain, diarrhea. This condition is known as Systemic Nickel Allergy Syndrome (SNAS) (1)(2). It has been demonstrated that Nickel assumption in SNAS patients is associated to an infiltrate of lymphocytes and plasma cells with edema and vasodilatation of the lamina propria at gastrointestinal mucosal level (2).…”

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confidence: 99%

Lactose Intolerance in Systemic Nickel Allergy Syndrome

Cazzato

Vadrucci²,

Cammarota

et al. 2011

Int J Immunopathol Pharmacol

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Some patients affected by nickel-contact allergy present digestive symptoms in addition to systemic cutaneous manifestations, falling under the condition known as Systemic Nickel Allergy Syndrome (SNAS). A nickel-related pro-inOammatory status has been documented at intestinal mucosal level. The aim of the present study is to evaluate the prevalence of lactose intolerance in patients affected by SNAS compared to a healthy population. Consecutive patients affected by SNAS referring to our departments were enrolled. The control population consisted of healthy subjects without gastrointestinal symptoms. All subjects enrolled underwent lactose breath test under standard conditions. One hundred and seventyeight SNAS patients and 60 healthy controls were enrolled. Positivity of lactose breath test occurred in 74.7% of the SNAS group compared to 6.6% ofthe control group. Lactose intolerance is highly prevalent in our series of patients affected by SNAS. Based on our preliminary results, we can hypothesize that in SNAS patients, the Nickel-induced pro-inOammatory status could temporarily impair the brush border enzymatic functions, resulting in hypolactasia. Further trials evaluating the effect of a nickel-low diet regimen on lactase activity, histological features and immunological pattern are needed.Nineteen percent of patients with nickel contact allergy, present digestive symptoms in addition to systemic cutaneous manifestations after ingestion of nickel-rich foods and experience symptom reduction with a low-nickel diet. The most common gastrointestinal symptoms include nausea, gastric pyrosis, meteorism, abdominal pain, diarrhea. This condition is known as Systemic Nickel Allergy Syndrome (SNAS) (1-2). It has been demonstrated that Nickel assumption in SNAS patients is associated to an infiltrate of lymphocytes and plasma cells with edema and vasodilatation of the lamina propria at gastrointestinal mucosal level (2). Moreover, an apoptotic decrease of epithelial CD8+ cells and an infiltration of CD4+ cells have been detected after oral challenge with the metal as well as a significant increase ofplasmatic ICAM-l, IL13, IL5 and eosinophilic cation protein (3-4).Lactose, a disaccharide composed of glucose and galactose bound in a B-glycosidic linkage, is the primary carbohydrate found exclusively in the mammalian milk. Absorption of lactose requires lactase-phlorizin hydrolase (LPH) activity in the small intestinal brush border to break the linkage between the two monosaccharides, a step preceding the transport of glucose and/or galactose across the brush border membrane.. Primary adult-type hypolactasia, an autosomal recessive condition resulting from the physiological decline of LPH enzyme activity in the intestinal cells, occurs in

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confidence: 99%

Lactose Intolerance in Systemic Nickel Allergy Syndrome

Cazzato

Vadrucci²,

Cammarota

et al. 2011

Int J Immunopathol Pharmacol

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“…The last definition, proposed by one of us (MDG), seems more adherent to the clinical picture of the disease. In a wide clinical survey performed in Italy on 1086 patients with Ni-contact allergy, 209 (19.2%) resulted affected not only by systemic cutaneous manifestations (urticaria, edema, eczema, erythema) but also by respiratory and digestive symptoms (nausea, gastric pyrosis, meteorism, abdominal pain, diarrhea and constipation) (13)(14)(15). Intestinal biopsies from SNAS patients show, compared to normal histological findings in ACD and healthy subjects, an inflammatory infiltrate of lymphocytes and plasma cells with edema and vasodilatation of the lamina propria (14), furthermore it has been detected an apoptotic decrease of epithelial CD8+ cells and an infiltration of CD4+ cells after an oral challenge with the metal (12).…”

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confidence: 99%

Oral Hyposensitization to Nickel Induces Clinical Improvement and a Decrease in TH1 and TH2 Cytokines in Patients with Systemic Nickel Allergy Syndrome

Minelli¹,

Schiavino

Musca³

et al. 2010

Int J Immunopathol Pharmacol

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Some patients with nickel (Ni) allergic contact dermatitis suffer from systemic (intestinal or cutaneous) symptoms after ingestion of Ni-rich foods and experience symptoms reduction with low-Ni diet, a condition termed "systemic Ni allergy syndrome" (SNAS). We aimed at evaluating whether oral administration of low nickel doses improved clinical conditions and modulated immunological aspects of SNAS, without significant side effects. Thirty-six SNAS patients were enrolled. Treatment started after L-month of lowNi diet and consisted in an incremental oral NiOH dose phase (O.3ng to 1.5 ug/week) followed by a 12-months maintenance phase (1.5 ug/week). Randomly, twenty-four patients added Ni therapy to low-Ni diet and 12 remained with diet alone. All patients were allowed rescue medications (antihistamines and topical steroids). After 4 months, Ni-rich foods were gradually reintroduced. In vitro allergen-driven IL13, IL5 and IFNy release by peripheral blood mononuclear cells was evaluated before and after treatment. Twenty-three patients receiving NiOH and the 12 control patients completed the study. Evaluation of SNAS clinical severity (by VAS and drug consumption) showed a significant difference in favor of NiOHtreated patients compared to controls. Twenty of 23 patients in the NiOH group and none in the control group tolerated Ni-rich food reintroduction. Release of all studied cytokines in culture supernatants was significantly lower after NiOH treatment. In conclusion NiOH is effective in reducing symptoms and drug consumption in SNAS and is able to modulate inflammatory parameters.Nickel (Ni), a ubiquitous metal, is the commonest cause of allergic contact dermatitis (ACD), with a prevalence of about 10% in the adult population (1-4). Ni allergy can cause dermatological lesions not only in skin regions in contact with the metal, but also in other regions, as demonstrated by cases of generalized eczema and urticaria in patients with Nicontaining dental (5-7) or orthopedic (8) prostheses.

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“…The trypcanocidal activity of L929 cells was dependent on endogenous nitric oxide synthase activity, which is largely induced by IFN-γ produced by NK cells. Moreover, studies in mice revealed an enhanced cytolytic activity of NK cells as early as 24 hours into T. cruzi infection (9)(10)(11)(12)(13)(14) and direct NK-mediated destruction of the extracellular epimastigote and trypomastigote forms of T. cruzi and T. lewisi in vitro (15)(16)(17).…”

Section: Nk Cells and Parasitesmentioning

confidence: 99%