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