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View of Correlation between Zinc and Iron with Psoriatic Patients in Al-Anbar Governorate

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Correlation between Zinc and Iron with Psoriatic Patients in Al-Anbar Governorate

Abdullah Salih Al-Hasan

Assistant Professor, University of Anbar, College of Medicine, Department of Medicine

Abstract

Psoriasis is a common chronic, immune-mediated, inflammatory disease of the skin. It is relapsing, non-contagious disorder characterized by red patchy lesions, with grey or silvery-white, dry scales. Lesions are typically distributed symmetrically on the scalp, elbows, knees and essentially any part of the body. It is a disease with an unpredictable course, prone for flareups and remissions and can affect the joints and nails.The study included 60 patients (35 male and 25 female) and 30 healthy individuals (18 male and 12 female) as a control group. Their ages ranged from 10 to 60 years with a mean of 32 years. All had psoriatic lesions that involved less than 30% of body surface. Family history of psoriasis was positive in a percentage of (20%) of the patients. The majority of patients (n= 60, 100%) had plaque type psoriasis. The duration of disease ranged between 1 month to 30 years with a mean of 6.9 years. The sera of patients and control were collected in the dermatologist clinic and tested for the concentration of zinc and iron. The statistical analysis results showed a significant decrease in the concentrations of iron and zinc for psoriatic patients compared with healthy individuals.

Keyword: Psoriasis, plaque psoriasis, zinc, iron.

Introduction

Psoriasis is a common chronic, immune-mediated, inflammatory disease of the skin (1). It is relapsing, non-contagious disorder characterized by red patchy lesions, with grey or silvery-white, dry scales (2). Lesions are typically distributed symmetrically on the scalp, elbows, knees and essentially any part of the body. It is a disease with an unpredictable course, prone for flareups and remissions and can affect the joints and nails(3).

Psoriasis is generally categorized into one of three severities based on the extent of body surface covered. Where 2% of the body is affected, it is classified as mild, where 3-10% of the body is covered, it is classified as moderate and where more than 10% of the body is affected, the disease is classified as severe. Based on these criteria, approximately 25-30% patients have psoriasis, which is considered moderate to severe (4).

It can afflict both men and women, and usually begins in early adulthood

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although it has been reported at birth. There is a bimodal distribution in the age of onset. Type I or early onset psoriasis typically appears in individuals between ages 15 to 20 years and shows a tendency to disseminate, greater number of relapses, and higher frequency of familiar history of psoriasis when compared with Type II or late onset psoriasis during or after the fifth decade of life (5, 6, 7).

Psoriasis is distributed worldwide but its prevalence varies among different geographical areas and ethnic groups (8). In Iraq, approximately 2.3% of the population is affected (9). The immune system has been strongly implicated in the pathogenesis of psoriasis that resembles a T cell-mediated disease (10). T cells are found in the dermis and epidermis and are accompanied by increased numbers of dermal dendritic cells, macrophages and mast cells(11).

Several environmental factors are recognized as triggers and exacerbators for psoriasis among which: infections (12), alcohol and smoking (13), family history (genetics) (14), trauma (15), stress (16), drugs (17) and diet (18). Clinical types of psoriasis can be classified according to phenotype-based classification that intended for use in both clinical practice and researches: plaque psoriasis, guttate (Eruptive) psoriasis, generalized pustular psoriasis, palmoplantar pustular psoriasis, psoriatic arthropathy, eryth-rodermic psoriasis, scalp psoriasis, nail psoriasis(19).

Iron is a trace element that is essential for life, being required for important cell processes such as DNA synthesis, energy production and defense. Many different structural and enzymatic proteins contain iron, which is essential to their function. In some of these proteins, iron (in the ferrous or Fe2+form) is found in the center of a porphyrin ring, forming a heme prosthetic group(20).

Serum iron is a medical laboratory test that measures the amount of circulating iron that is bound to transferrin. Clinicians order this laboratory test when they are concerned about iron deficiency, which can cause anemia and other problems. 65% of the iron in the body is bound up in hemoglobin molecules in red blood cells. About 4% is bound up in myoglobin molecules. Around 30% of the iron in the body is stored as ferritin or hemosiderin in the spleen, the bone marrow and the liver. Small amounts of iron can be found in other molecules in cells throughout the body. None of this iron is directly accessible by testing the serum.

However, some iron is circulating in the serum. Transferrin is a molecule produced by the liver that binds one or two iron(III) ions, i.e. ferric iron, Fe3+; transferrin is essential if stored iron is to be moved and used. Most of the time, about 30% of the available sites on the transferrin molecule are filled. The test for serum iron uses blood drawn from veins to measure the iron molecules that are

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bound to transferrin, and circulating in the blood(21).

Zinc is an essential mineral that is naturally present in some foods, added to others, and available as a dietary supplement. Zinc is involved in numerous aspects of cellular metabolism. It is required for the catalytic activity of approximately 100 enzymes(22,23), and it plays a role in immune function(24), protein synthesis(25), wound healing(26), DNA synthesis, and cell division. Zinc also supports normal growth and development during pregnancy, childhood, and adolescence(27,28,29), and is required for proper sense of taste and smell(30). A daily intake of zinc is required to maintain a steady state because the body has no specialized zinc storage system(31).

Materials and methods Determination of Iron

Serum iron was determined by the using of colorimetric method, by a ready kit from reliable scientific company.

Principle

The Fe+3 bound to serum ferritine once dissociated in a week-acid medium by Teepol and guanidium chloride, is reduced by hydroxylamine to Fe+2, forming the ferrous ion a colored complex with ferrozine proportional to the concentration of iron present in the sample(32).

Samples

Serum or heparinized plasma. Centrifuge specimen as soon as possible after collection. Hemolyzed samples are rejected. Ruptured red cells falsely elevate the serum results. Iron in serum is stable for 3 weeks at 28ºC and for about 7 days at 20- 25ºC. Freeze for longer storage.

Procedure

Bring reagents and samples to room temperature and pipette into sample labeled tubes 1 ml of reagent and 200µl of sample, mix and let the tube stands for 5 minutes at room temperature. Read the absorbance (A) of the samples and the standard at 560 nm against the blank. The standard tube is made by the addition of 200 µl of standard solution to 1 ml of sample. Eventually calculate the concentration of iron by the comparison with the standard solution absorbance.

Determination of zinc

Serum zinc was determined by the using of colorimetric method, by a ready kit from reliable scientific company.

Principle

Zinc reacts with the chromogen present in the reagent forming a colored compound which color intensity is proportional to the zinc concentration present in the sample

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Samples

Serum or heparinized plasma. Hemolyzed samples are rejected. zinc in serum is stable for 1 weeks at 2-8ºC. Freeze for longer storage.

Procedure

Bring reagents and samples to room temperature and pipette into sample labeled tubes 1 ml of reagent and 50µl of sample, mix and let the tube stands for 5 minutes at room temperature. Read the absorbance (A) of the samples and the standard at 578 nm against the blank. The standard tube is made by the addition of 50 µl of standard solution to 1 ml of sample. Eventually calculate the concentration of zinc by the comparison with the standard solution absorbance.

Results and Discussion

The concentrations of iron and zinc are shown in the table 1 below:

(Table 1) the concentration of iron and zinc in µg/dl

No. Iron µg/dl

Zinc µg/dl

No. Iron µg/dl

Zinc µg/dl

No. Iron µg/dl

Zinc µg/dl

1. 25 93.2 31 47 178 61 59 67.8 2. 142 119 32 22 33.9 62 113 508 3. 63 153 33 39 178 63 97 678 4. 13 33.9 34 29 8.47 64 182 593 5. 52 67.8 35 29 42.4 65 42 678 6. 27 67.8 36 50 186 66 73 373 7. 109 16.9 37 44 16.9 67 75 398 8. 32 25.4 38 71 25.4 68 83 153 9. 84 67.8 39 14 93.2 69 103 288 10. 85 8.47 40 106 76.3 70 48 525 11. 18 84.7 41 48 84.7 71 168 144 12. 59 50.8 42 44 84.7 72 55 305 13. 22 33.9 43 61 76.3 73 30 42.4 14. 58 93.2 44 29 76.3 74 47 254 15. 39 102 45 64 25.4 75 75 119 16. 34 119 46 11 25.4 76 27 339 17. 37 203 47 25 59.3 77 61 288 18. 51 93.2 48 39 50.8 78 74 559 19. 72 169 49 71 84.7 79 62 288

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20. 93 8.47 50 81 67.8 80 51 483 21. 60 67.8 51 20 76.3 81 85 508 22. 19 16.9 52 62 76.3 82 75 508 23. 14 84.7 53 17 25.4 83 83 492 24. 86 50.8 54 67 25.4 84 113 644 25. 30 169 55 54 59.3 85 42 271 26. 42 59.3 56 127 50.8 86 148 229 27. 54 33.9 57 68 84.7 87 55 432 28. 83 2.54 58 80 67.8 88 39 475 29. 48 322 59 26 76.3 89 47 212 30. 89 203 60 66 59.3 90 74 153

The statistical analysis results showed a significant decrease in the concentrations of iron and zinc for psoriatic patients compared with healthy individuals (p<0.05) as shown below table 2:

No. parameters factor mean Std.

deviation

t- value

Pvalue

1 Iron µg/dl

patient 52.5167 29.15214

-3.235 0.002 control 76.3103 38.66533

2 Zinc µg/dl

patient 78.2675 59.91635

-10.92 0.000 control 366.6966 186.58224

The figures below also explain the significant decrease of both iron and zinc in psoriatic patients compared with healthy individuals.

Figure 1 the mean values of patient's Zn and Fe.

0 100 200 300 400

1 2

3

52.5 iron 78.2

zinc

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Figure 2 the mean values of control Zn and Fe.

Zinc and many other trace metals are known to be among the constituents of the skin and to play essential roles in maintenance of its function in association with the enzyme systems activated by trace metals(34,35). Therefore most of psoriatic patients obtained benefit from oral zinc treatment(36). Many other studies showed also significant decrease in the level of serum zinc but the administration of oral zinc changes nothing, therefore they believed that systemic zinc deficiency is unlikely to be the basic error in psoriasis(37).

Accelerated loss of nutrients from the hyperproliferation and desquamation of the epidermal layer of skin in psoriasis has been reported(38). It can be speculated that Fe may be lost due to desquamation. Fe is an important requirement of cell division, therefore it is depleted during the rapid turnovers of skin cells.

The presence of excess Fe in skin tissues has been demonstrated in many skin diseases involving an inflammatory response including psoriasis(39,40). From these facts and our results it seems that psoriasis is a rapid cell divisions and Fe is an important requirement of cell division, therefore it is depleted.

References

1. Pariser D., Bagel J. and Gelfand J. "National psoriasis foundation clinical consensus on disease severity" Arch Dermatology; 143:239–242. (2007).

2. Picardi A., Mazzotti E., Gaetano P., et al. (2005). Stress, social support, emotional regulation, and exacerbation of diffuse plaque psoriasis psychomatics; 46:556–564.

3. Campalani E. and Barker J. (2005). The clinical genetics of psoriasis; 6:51-60.

4. Gilliard S. and Finlay A. (2005). Current management of psoriasis in the United Kingdom: patterns of prescribing and resource use in primary care. Int J Clin Pract; 59 (11): 1260-1267.

0 100 200 300 400

1 2

3

76.3 iron 366.6

zinc

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5. Langley R., Krueger G. and Griffiths C. (2005). Psoriasis: epidemiology, clinical features, and quality of life. Ann Rheum Dis; 64 (Suppl. II): 18-23.

6. Kormeili T., Lowe N. and Yamauchi P. (2004) Psoriasis: immunopathogenesis and evolving immunomodulators and systemic therapies; U.S. experiences. Br J Dermatol; 151:3-15.

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8. Raychaudhuri S. and Farber E. (2001). The prevalence of psoriasis in the world J Eu Acad Dermatol Venereol; 15:16-7.

9. Alsamarai A. (2008). Prevalence of skin diseases in Iraq. Int J Der.

10. Bowcock A. (2005). Getting under the skin: the immunogenetics of psoriasis.

Nat Rev Immunol; 5:699–711.

11. Nickoloff B. and Nestle F. (2004). Recent insights into the immunopathogenesis of psoriasis provide new therapeutic opportunities. J Clin Invest; 113:1664–

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13. Cohen A. and Halevy S. (1999). Alcohol intake, immune response, on the skin.

Clin Dermatol ; 17(4): 411-412.

14. Neimann A., Porter S. and Gelfand J. (2006). The epidemiology of psoriasis.

Future Drugs Ltd.

15. Miller R. (1982).The Koebner phenomenon. Int J Dermatol; 21:192197.

16. Mease P. and Menter M. (2006). Quality-of-life issues in psoriasis and psoriatic arthritis, outcome measures and therapies from a dermatological perspective. J Am Acad Dermatol; 54:685-704.

17. Hunter J., Savin J. and Dahi M. (1996). London Blackwell science Clinical dermatology 2nd edition: 51-54.

18. Horrobin D. (1987). Low prevalence of coronary heart disease, asthma, psoriasis, rheumatoid arthritis in Eskimos are caused by high dietary intake of eicosapentanoic acid, a genetic variation of essential fatty acids metabolism or a combination of both .Med hypothesis;22 :421-428.

19. Griffiths C., Christophers E., Barker J., et al. (2007). A classification of psoriasis vulgaris according to phenotype. Br J Dermatol; 156:258– 262.

20. Reproduced with permission from Andrews NC, New Engl J Med. 341:1986- 1995, Copyright © 1999 Massachusetts Medical Society.

21. Serum iron levels in Shetland Ponies with experimentally-induced acute inflammation (commencing day zero) compared to normal control animals.

Reproduced with permission from Smith and Cipriano, Vet Pathol. 24:354-356

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(1987).

22. HH. Understanding zinc: recent observations and interpretations. J Lab Clin Med 1994;124:322-7.

23. Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington, DC: National Academy Press, 2001.

24. Solomons NW. Mild human zinc deficiency produces an imbalance between cell-mediated and humoral immunity. Nutr Rev 1998;56:27-8.

25. Prasad AS. Zinc: an overview. Nutrition 1995;11:93-9.

26. Heyneman CA. Zinc deficiency and taste disorders. Ann Pharmacother 1996;30:186-7.

27. Simmer K, Thompson RP. Zinc in the fetus and newborn. Acta Paediatr Scand Suppl 1985;319:158-63.

28. Fabris N, Mocchegiani E. Zinc, human diseases and aging. Aging (Milano) 1995;7:77-93.

29. Maret W, Sandstead HH. Zinc requirements and the risks and benefits of zinc supplementation. J Trace Elem Med Biol 2006;20:3-18.

30. Prasad AS, Beck FW, Grabowski SM, Kaplan J, Mathog RH. Zinc deficiency:

changes in cytokine production and T-cell subpopulations in patients with head and neck cancer and in noncancer subjects. Proc Assoc Am Physicians 1997;109:68-77.

31. Rink L, Gabriel P. Zinc and the immune system. Proc Nutr Soc 2000;59:541-52.

32. Artiss, J.D., Vinogrador, S., and Zak, B. Clin. Biochem. 14 :311 (1981).

33. Tetsuo Makino, Chemica Clinica Acta 197, 209-220 ( 1991 ).

34. Molokhia MM, Portnoy B : Neutron activation analysis of trace elements in skin. I. Copper in normal skin. Br J Dematology 81:110-114, 1969.

35. Michaelsson G, Edqvist L-E : Erythrocyte glutathione peroxidase activity in acne vulgaris and the effect of selenium and vitamin E treatment. Acta Derm Venereol (Stockh) 64:9-14, 1984.

36. Bor NM : Copper supplementation in treatment of zinc deficiency diseases.

JIASci, 2:5-6, 1989.

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37. Withers AF, Baker H, Musa M, Dormandy TL : Plasma zinc in psoriasis. Lancet 2:278, 1968.

38. Update on nutrition and psoriasis. Prystowsky JH, Orologa A, aylor S Int J Dermatol. 1993 Aug; 32(8):582-6.

39. In vivo assessment of iron and ascorbic acid in psoriatic dermis. Leveque N, Robin S, Muret P, Mac-Mary S, Makki S, Berthelot A, Kantelip JP, Humbert P Acta Derm Venereol. 2004; 84(1):2-5.

40. iron content in normal and psoriatic epidermis. Molin L, Wester PO Acta Derm Venereol. 1973; 53(6):473-6.

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