Nikel-free Cooking: Tips and recipes for people with nickel allergies Read online

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  The following is an example of a standard series that is commonly used for allergy evaluation:

  SolfaNikel sulfate

  Paraphenylenediamine Mercaptobenzothiazole Tetramethylthiuramdisulfid Balsam of Peru

  Formalin

  Turpentine

  Sodium bisulfite Benzocaine

  Perfumes mix

  Phenylcyclohexylparaphen

  Ylenediamine

  Difenilparaendiamina Lattice Clorochinaldolo Colofonia

  Acido benzoico Lanolina

  Bicromato di potassio Cloruro di cobalto Disperso giallo Disperso rosso Disperso blu

  The correlation between celiac disease and nickel allergies

  Many professionals have noticied a correlation between celiac disease and nickel allergies. To understand how the two phenomena can be associated, it is necessary to consider the pathogenesis of celiac disease, autoimmune pathology, and the fundamental role of the intestinal barrier.

  Celiac disease is a systemic autoimmune disease that can affect all organs and systems. The cornerstone of the pathogenesis is the production of autoantibodies (anti-transglutaminases and anti-endomysium) that activate gastrointestinal immune response. This then leads the destruction of the mucous membrane (villous atrophy) in genetically predisposed subjects (presence of HLA alleles DQ2 and / or DQ8).

  Exposure to gluten triggers autoimmune response. Currently, other environmental factors that determine the development of the disease are unknown. Gluten, contained especially in wheat, barley, rye, spelt, and many other cereals are composed of two proteins: gliadin and glutenin. In genetically predisposed subjects, ingested gliadin is activated by an enzyme (tissue transglutaminase). This transformation then activates the T lymphocytes, which regulates the production of numerous pro-inflammatory cytokines including interleukin-2, interleukin-4, interferon gamma, TNF (tumor necrosis factor) alpha. The consumption of these toxic substances causes damage characterized by the flattening of intestinal villi and hyperplasia of intestinal crypts.

  The intestinal barrier is a structure that acts as a filter and prevents the absorption of large molecules, such as proteins, in the intestine. The barrier is also able to recognize the difference between “self” and “non-self” molecules. This is thanks to the presence of "localized" antibodies between the intestinal cells which allows the recognition of viruses and bacteria, preventing their internalization.

  This mechanism allows the body to block the movement of pathogens. Likewise, even macromolecules, such as proteins with high molecular weights, cannot pass through the barrier and remain in the intestinal lumen.

  Therefore, it can be concluded that in the absence of the intestinal barrier the mucous membrane would absorb all proteins consumed in a diet. This would lead to serious changes of the individual's homeostasis.

  Now, let's dive into why the celiac subject is more likely to suffer from nickel allergies. This can happen for two reason. First, celiac disease, as we have seen, creates damage to the mucous membrane of the intestinal wall in conditions of complete restitutio ad integrum failure. This can cause an altered passage of substances through the same lesions in the intestinal barrier.

  Furthermore, the only treatment that has been found to be effective for celiac disease is a gluten-free diet which is when the celiac subject eats foods that naturally contain larger quantities of nuts, such as corn and vegetables.

  Contact reactions to foods

  Contact dermatitis (DAC), widely discussed in another chapter of this book, can manifest itself through contact with the "oleoresins" present in some vegetables and fruits. The main allergen is the "sequiretene", which can be found in high quantities in many vegetables (broccoli, turnips, cabbage) and in some fruits (lemons, oranges) (1), (2), (3).

  Irritative contact dermatitis (DIC) is an acute dermatitis that occurs when a person encounters certain foods and is not immune mediated. Instead, it is the result of a simple irritation and, unlike the DAC, it is not delayed but instead, is immediate. A histological examination of the lesions does not show the presence of cells typical to the immune allergic reaction. The substances that most commonly cause inactive dermatitis are lemons, garlic, pineapples, radishes.

  Allergic urticaria is an immediate immunological reaction that is characterized by the involvement of IgE. Therefore, it can affect potentially allergic subjects. The allergic patient is sensitive to specific foods and to the subsequent contact when an allergic reaction occurs. This is usually characterized by intense itching and the appearance of wheals (4), (5), (6).

  Non-allergic contact urticaria is like DIC but is distinguished by the appearance of the lesions. This reaction, unlike that of DIC, is characterized by numerous wheals and the involvement of chemical inflammation mediators, such as histamine and citochiine. (7), (8).

  Systemic contact dermatitis to foods: nickel, BOP, and more. Fabbro S.K., Zirwas M.J.

  Curr Allergy Asthma Rep. 2014 Oct; 14(10):463.

  Cutaneous Manifestation of Food Allergy. Tam J.S.

  Immunol Allergy Clin North Am. 2017 Feb; 37(1):217–231.

  Contact allergy to food. Brancaccio RR, Alvarez MS. Dermatol Ther. 2004; 17(4):302–13.

  When should the diagnosis ‘contact urticaria’ be used? Aalto-Korte K.

  Contact Dermatitis. 2017 Nov; 77(5):323-324. doi: 10.1111/cod.12884. Epub 2017 Sep 21.

  A Case of Anaphylaxis Induced by Contact with Young Radish (Raphanus sativus L). Lee Y.H., Lee J.H., Kang H.R., Ha J.H., Lee B.H., Kim S.H.

  Allergy Asthma Immunol Res. 2015 Jan; 7(1):95–7. Immunologic contact urticaria.

  McFadden J.

  Immunol Allergy Clin North Am. 2014 Feb; 34(1):157-67.

  Contact reactions to food. Killig C., Werfel T.

  Curr Allergy Asthma Rep. 2008 May ;8(3):209–14.

  Garlic (Allium sativum L.): adverse effects and drug interactions in humans. Borrelli F,. Capasso R., Izzo A.A.

  Mol Nutr Food Res. 2007 Nov; 51(11):1386-97.

  Occupational contact urticaria and protein contact dermatitis. Doutre M.S.

  Eur J Dermatol. 2005 Nov–Dec; 15(6):419–24.

  Food intolerances: fake news or reality?

  We often see deceptive advertising on television that has the power to influence our decision making. I wonder why there is not a government organization that censors “scam” advertising. The issue becomes even more serious when this type of marketing influences our health. In Italy, each year three hundred million euros is spent on useless “pseudo”-studies that focus on discovering non-existent food intolerances.

  Let's take stock of the situation. First we need to distinguish the difference between allergic reactions and food intolerances. Allergic reactions are those reactions mediated by IgE-type antibodies that are not dose-dependent, manifest with skin rashes, itching, edemas, and begin immediately after taking the substance (10-30minutes). These reactions affect genetically predisposed individuals and can be studied with appropriate scientific analyses.

  Food intolerances have been defined as "non-allergic allergies" (Kaplan 1991), reactions in the organism not mediated by IgE. Two, and only two types, are scientifically proven, lactose and gluten intolerances.

  There are numerous tests on the market that can uncover all intolerances the patient has. These tests, however, have never been tested on a valid sample size of people to ascertain their validity. To be considered reliable, a test must include two essential elements: sensitivity and specificity.

  Let's try to understand the meaning of these two terms. A test has valid sensitivity when it can identify all patients who are clinically ill. This means that 100% of sick subjects must show positive results when given the test. Therefore, the patient who tests negative is certainly a negative patient also from the clinical point of view.

  The specificity of a test concerns the percentage of patients who, certainly from the clinical perspective, show positive results but are actually false positives. The higher the number
of false positivite results, the less reliable the test.

  To understand with even more depth, here are some practical examples:

  1. Anna is a patient with celiac disease: she carries out a test for this disease and it is positive, therefore nothing to add is perfect.

  2. Loredana, who is not suffering from celiac disease, carries out a test that is positive. Here is the specificity above, it is a false positive.

  3. Roberta, of whom we have no medical history, carries out a test for celiac disease which is negative. For what has been said before regarding sensitivity, we are sure that she is not affected by celiac disease.

  In summary, for a test to be reliable it must have a sensitivity of 100% and sufficient specificity.

  Therefore, before wasting time and money, it would be best if scientific experts were transparent about the reliability of tests for food intolerances. Such tests are continually proposed by various laboratories and sometimes, even more seriously, even by "doctors".

  Clinical cases

  Case number one

  A 38 year-old patient has come to an appointment complaining about the presence of dermatitis on both hands for about a year. There are no noteworthy diseases in the patient's medical history. In the physiologic anamnesis the patient reports that she gave birth to her first child about one year ago. Patches are applied to conduct a patch test. After 48 hours patch tests are read and show a clear positive result for nickel sulphate.

  This positive result aligns with the patient's medical history as she reports using detergents and soaps for cleaning over the past year in a vastly different way than before she had a baby. It should also be considered that hormonal variations, such as those that occur during and after pregnancy, can trigger a latent allergy.

  Case number two

  Marco is a 16-year-old student who has scheduled a visit due to the appearance of dermatitis on the fingertips of his left hand. He is not left-handed. There is nothing significant in the physiologic and pathologic history and no appearance of lesions on the rest of the body. Patch tests are completed and show strong positivity to nickel sulphate. The results of the patch test does not explain why it is only on the left hand.

  However, an accurate re-examination of the physiologic anamnesis, in the light of what we have found, allows us to discover that the boy spends more time playing guitar than studying. That is the reason why dermatitis is only in the left hand.

  Case number three

  A patient suffering from a nickel allergy, established a few years earlier by patch testing, comes to the office. Today, the patient is suffering from heartburn and intestinal cramps accompanied by coughing. The patient believes that nickel is responsible for gastrointestinal symptoms which requires an adequate diet and/or therapy. A careful analysis of the patient’s medical history allows us to identify that the symptoms are more severe during the night and when fasting and not when consuming foods containing nickel. Nevertheless, we ask the patient to follow a nickel-free diet for 15 days. At the end of the diet the patient noted no improvement and, therefore, an antiacid is administered and a new diet is recommended to the patient to help with acid reflux.

  After fifteen days the patient returns and reports a significant improvement in symptoms. A subsequent gastroscopy confirms the presence of gastritis with hiatal hernia and reflux. This time the famous culprit, nickel, is innocent!

  Case number four

  A gastroenterologist orders a test for a patient with suspected food intolerance. The patient reports abdominal swelling and flatulence after eating foods with a high nickel content. In the pathologic anamnesis there are no signs suggesting nickel-related dermatitis. A patch test is administered and shows positivity to nickel sulphate. The conclusion is a diagnosis of SNAS not associated with DAC.

  Clinical case number 5

  One of our patients suffering from nickel-based dermatitis comes to the office showing sudden skin aggravation, particularly in the limbs without any known reason. The patient's physiologic history is carefully studied, but nothing suspicious emerges. After various types of therapy, with almost no results, a biopsy is ordered. The outcome of the biopsy suggests psoriasis dermatitis, but the similar appearance of lesions confuses dermatologists and allergists, suggesting an exacerbation of contact dermatitis.

  .

  The oral hypo-sensitizing treatment for nickel allergies

  Reactions to this metal, present in many objects and even foods, can be stopped with nickel hypo-sensitizing treatment (TIO NICHEL). For the more severe forms of nickel allergies, defined as systemic, an oral nickel hypo-sensitizing treatment has been successfully tested. This is not a traditional prophylaxis but, within eight to ten months, this treatment has been proven to show significant improvement in seven out of ten patients’ symptoms. Diarrhea and stomachaches are common symptoms. Of the approximately nine million Italians allergic to this metal, almost two develop the systemic form. But what does systemic mean? It means that in addition to classic contact dermatitis, caused by an infinite number of nickel-containing objects (from coins to jewels, from cell phones to cosmetics), the symptom body also reacts to oral consumption of nickel. This can cause pain, hives and eczema on the abdominal area, diarrhea, stomach swelling, bloating, vomiting, and gastroesophageal reflux. And, even in this case, avoiding metal is not easy as it is found in many fruits and vegetables and water. It can even be absorbed by eating a plate of pasta that was cooked in stainless steel pot. The oral nickel hypo-sensitizing treatment is prescribed only at the end of a complete diagnostic procedure, which starts with a patch test. In this test, a disk containing nickel sulphate is applied with a bandage to the skin and left in place for 48-72 hours. If, at the end of the examination, dermatitis is detected in the contact area, we proceed with six to eight weeks of a low nickel diet. Once the diagnosis is confirmed, oral therapy can begin which involves taking 500 nanograms of nickel (half a millionth of a gram) three times a week for six months. Therefore, in the following three months, foods containing nickel are gradually reintroduced and finally a free regime is reintroduced.

  The epidemiology of contact allergy in the general population – prevalence and main findings. Thyssen J.P., Linneberg A., Menné T., Johansen J.D.

  Contact Dermatitis 2007; 57: 287-99.

  Systemic nickel allergy syndrome: nosologic framework and diet regimen.

  Braga M., Quecchia C., Perotta C., Timpini A., Maccarinelli K., Di Tommaso L., Di Gioacchino M. Int J Immunopthol Pharmacol 2013; 26: 707–16.

  Oral hyposensitization to nickel allergy: preliminary clinical results.

  Panzani R.C., Schiavino D., Nucera E., Pellegrino S., Fais G., Schinco G., Patriarca G. Int Arch Allergy Immunol 1995; 107: 251-4.

  Expression of lymphocyte subpopulations, cytokine serum levels and blood and urine trace elements in nickel sensitized women.

  Boscolo P., Di Gioacchino M., Conti P., Barbacane R.C., Andreassi M., Di Giacomo F., Sabbioni E. Life Sci 1998; 63: 1417-22.

  Systemic effects of ingested nickel on the immune system of nickel sensitized women. Boscolo P., Andreassi M., Sabbioni E., Reale M., Conti P., Amerio P., Di Gioacchino M. Life Sci. 1999; 64: 1485-91.

  Systemic contact dermatitis after oral exposure to nickel: a review with a modified meta–analysis. Jensen C.S., Menné T., Johansen J.D.

  Contact Dermatitis 2006; 54: 79-86.

  Systemic nickel allergy syndrome. Schiavino D.

  Int J Immunopathol Pharmacol 2005; 18: 7-10.

  Nickel systemic contact dermatitis.

  Verna N., Di Claudio F., Balatsinou L., Schiavone C., Caruso R., Renzetti A., Gabriele E., Turi M.C., Feliziani A., Di Gioacchino M.

  Int J Immunopathol Pharmacol 2005; 18: 11-4.

  Serum levels of sICAM-1 in subjects affected by systemic nickel allergy syndrome. Minciullo P.L., Saija D., Trombetta D., Ricciardi L., Di Pasquale G., Gangemi S.

  It J Allergy Clin Immunol 2006; 16: 109-13.

  Appetizers

  Buttered ancho
vies

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  Ingredients:

  8 anchovies

  Butter- to taste

  Preparation:

  Start with eight anchovies in oil. Clean the fish off the bones and arrange them on a plate, layering them. For the next step, the butter must be very cold from the refrigerator and a butter curler must be very cold and wet with cold water. Use the curler on the butter to create eight curls to be placed on the anchovies and accompanied with slices of homemade bread.

  Bruschetta

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  Ingredients:

   4 slices of homemade bread

   4 tablespoons of extra virgin olive oil

  salt and pepper

  Preparation: