IBN AL- HAITHAM J . FO R PURE & APPL. SC I VO L. 22 (4) 2009 Study of Some Biochemical Parameters in Iraqi Male Children with Thalassemia H. K. Al-Hakeim *,T. Al-Madani **,M. M. R.Mahammad *** D. A. Kate b *,S. A. Nassir *,S, Kareem * * Department of Chemistry, College of Science, Al-Kufa Unive rsity ** Department of Pediatrics, College of Medicine, Al-Kufa Unive rsity ***Departme nt of Chemistry, College of Medicine, Al-Kufa Unive rsity Abstract Thalassemia is a term that refers to a group of genetic disorders characterized by a defect in the sy nthesis of hemoglobin. It is sometimes called M editerranean anemia. M any biochemical changes in the blood accomp any this disease. In this research, some biochemical p arameters were measured in thalassemic p atients and comp ared with healthy control group . These p arameters include serum Iron, ferritin, TIBC, hemoglobin, uric acid, albumin, calcium, transferrin, and transferrin saturation percentage. The results of the research showed that there is a significant increase (P<0.05) in serum iron and ferritin in thalassemic p atients group in comp arison with healthy control group . A significant decrease (P<0.05) in serum uric acid, TIBC, transferrin p rotein concentration, and hemoglobin. There is no significant difference (P>0.05) in serum albumin and calcium in both group s. The results of this research can be exp lained by different mechanisms involving the hemolysis of ery throcytes and consequence precipitation of iron in the tissues. In addition, the hy p oxia may be one of the reasons about the biochemical changes in thalassemic p atients. M onitoring the measured p arameters may be useful in the p rognosis and follow up of the thalassemic patients. Introduction Thalassemia is a term that refers to a group of genetic disorders characterized by insufficient p roduction of hemoglobin, wherein there is a defect in the sy nthesis of hemoglobin. It is sometimes called M editerranean anemia. To understand how thalassemia affects the human body , we must first understand a little about how blood is made. If the body doesn't p roduce enough of alp ha and a beta chains of globin, the red blood cells do not form p rop erly and cannot carry sufficient oxy gen. The result is anemia that begins in early childhood and last s throughout life. Genes involved are those that control the p roduction of alp ha and beta globins contained in hemoglobin [1]. The two main ty p es of thalassemia, alpha and beta, are named for the two p rotein chains that make up normal hemoglobin. Since thalassemia is not a single disorder but a group of related disorders that affect the human body in different ways. T halassemia can be classified according to sy mptoms or to the genes affected. Thalassemia major that is st udied in this work is inherited from both p arents. Beta thalassemia tends to be more common in p eople from many ancestry including M editerranean and Arabian Peninsula. Thalassemia in Iraq is a real p roblem due mainly to the deficiency in the equip ments and drugs during different p eriods of lack of security and wars. Thalassemia is a p roblem in many areas in Iraq [2]. Of 1064 coup les recruited from the Public Health Laboratory in Basra, sout hern Iraq, about 5% had beta-thalassemia trait and the carriers of major beta-gobin disorders comp rised 11.48%. These defects constitut e a real health p roblem and necessitate a management p lan and public health education for early diagnosis and therap y . In Iraq-Najaf IBN AL- HAITHAM J . FO R PURE & APPL. SC I VO L. 22 (4) 2009 Government, till October-2007 there are 288 p atients' files who are still treating in the thalassemia Unit in AL-Zahra'a Teaching Hosp ital. The p atients are more dependent on blood transfusions, the more likely he or she is t o be classified as thalassemia major. Biochemical changes may include; serum iron, increased/normal total iron binding cap acity (TIBC), decreased/normal ferritin, increased/normal and increased transferrin saturation p ercentage (TISP). These factors in addition to others are st udied in Iraqi p atients in this work in addition to uric acid, calcium and albumin which are not st udied extensively in thalassemic p atients. Transferrin acts as iron transp ort p rotein between sites of absorp tion, storage, and use . Ferritin is a ubiquitous p rotein in which the only clearly defined function is t he sequest ration and st orage of iron [3]. Ferritin sy nthesis may be induced by iron . The serum ferritin is a universally available and well-st andardized measurement that has been the single most imp ortant laboratory measure of iron st atus during the past quarter century . The well-known limitation of the serum ferritin is the elevation in values indep endent of iron status that occur with acute or chronic inflammation, malignancy , liver diseases, and alcoholism .Therefore, transferrin-bound iron and transferrin saturation must be measured in the same serum sample with ferritin p rotein to distinguish iron st atus from inflammation. Just as a high serum ferritin p rotein may mean inflammation rather than iron overload, a low serum iron may mean inflammation rather than iron deficiency . Only if both serum iron and serum ferritin p rotein go in the same direction (i.e., both go up or down) can reasonably assess iron st atus from them. There is no treatment when asy mptomatic. Different methods for t reating Thalassemia are available Partial sp lenectomy was associated with a dramatic reduction of mortality in the Iraqi p atients [2]. Thalassemia in Iraq was st udied in different areas at different fields of st udy [4], but the comp lete p icture about the chemical changes in Iraqi thalassemic p atients is not understood y et. The aim of the st udy is to identify variation in biochemical changes in thallasemic p atients in comp arison with healthy control group . These p arameters include serum Iron, ferritin, TIBC, hemoglobin, albumin, calcium, uric acid and TISP. Materials and Methods 1-Patie nts: Fort y -five male children with thalassemias have p articip ated in this research. Age range was (6-10 y ears) from AL-Zahraa Teaching Hosp ital for Obstetrics and Children during the p eriod from 1-7-2007 till 1-10-2007. Thirty non-thalassemic children were taken as control group . 2-Biochemical (me asureme nts): Blood was asp irated from individuals in the morning and collected in p lain tubes for serum in order to est imate the following p arameters. Hemoglobin electrop horesis shows; Hgb A decreased, Hgb F increased, and Hgb A2 variable. Biochemical Analysi s Serum Iron was estimated by using colorimetric method[5], total Iron Binding Capacity were estimated by using colorimetric method by the following method: An excess of iron is added to the serum iron to saturate the transferrin. The unbound iron is p recipitated with basic magnesium carbonate. Aft er centrifugation the iron in the sup ernatant is determined). Hemoglobin was estimated by using colorimetric method. Calcium was estimated by using colorimetric method using O-Cresolp htaleine comp lex comp ound, at alkaline p H, Albumin was estimated by using colorimetric method by binding to the BCG dy e to p roduce a blue green color. Uric acid was used for estimation by using colorimetric method. The Ferritin Quantitative Test is based on a solid phase enzy me-Linked IBN AL- HAITHAM J . FO R PURE & APPL. SC I VO L. 22 (4) 2009 immunosorbent assay (ELISA). T he assay sy st em utilizes one rabbit anti-ferritin antibody for solid p hase (microtitre wells) immobilization and a mouse monoclonal anti-ferritin antibody in the antibody -enzy me (horseradish p eroxidase) conjugate solution. Transferrrin saturation p ercentage (TISP) was calculated by dividing serum iron concentration by TIBC (17) concentrations, using the formula: serum iron (µmol/L)/transferrin (g/L) x 3.98. The formula is based on the maximal binding of 2 mol Fe 3+ /mol of transferrin and a molecular weight of 79,570 Dalton for transferrin [6]. As shown in the formula : 98.3*%. )/(. )/( saturationnTransferri LumolIronS LgnTransferri  Biostati sti cal analysi s: The results were exp ressed as (mean±st andard deviation ). Pooled t-t est was used for the comp arison of a significant difference between the healthy and control group s in the measured p arameters. Correlation coefficient (r) was also used for searching about any correlation between the p arameters. Re sults The results of the research exp ressed as mean ±standard deviation are shown in Table (1). There is a significant increase (P<0.05) in serum iron, ferritin, and TISP in thalassemic p atients group in comp arison with healthy control group .. A significant decrease (P<0.05) in serum uric acid, TIBC, transferrin p rotein concentration, and hemoglobin. There is no significant difference (P>0.05) in serum albumin and calcium in both group s. The correlation coefficient values (r-value) of serum iron versus different measured p arameters for healthy and thallasemic group s are shown in Table (2). There was no st rong correlation, either p ositive or negative, between serum iron and the p arameters excep t for the TISP, which is st rongly correlated with serum, iron in both group s. Discussion Some hematological and biochemical characterist ics of our thalassemic p atients are list ed in Table (1) and comp ared with those of healthy controls. Iron indices, with the excep tion of TIBC and transferrin p rotein concentration, were markedly increased, and the mean concentration of serum ferritin was more than seven times higher than normal (Table 1). In st ates of iron overload or excess, the iron comp osition of ferritin increases and this may be the most imp ortant cause for the elevation of serum ferritin. The results of our research on Iraqi thallasemic p atients are comp arable with the result of Fairbanks (1999) [7]. In that research the following results were obtained in thalassemic p atients; serum iron is normal or increased, TIBC is normal, TISP is 30-100%, Serum ferritin is Increased. Some researches showed a higher level of ferritin in thalassemic p atients than healthy children and the ferritin level was t wenty times higher than normal . Serum Ferritin was found to be 5506 +/- 635 microg/l in thallasemic p atients in one st udy [8]. . In one st udy carried out in one of Iraqi neighboring country , Iran, the serum ferritin showed a higher concentration ( 3503 ± 201 ng/ml) in thalassemia major in many thalassemic patients which is absent in our Iraqi sample group [9]. These differences may be due to the difference in mutation defects, causes thalassemia in Iraqi's, differs from those reported in the surrounding countries and the difference between races and subp op ulations in transferrin saturation and ferritin data [10] IBN AL- HAITHAM J . FO R PURE & APPL. SC I VO L. 22 (4) 2009 Serum ferritin concentration results from the leakage of tissue ferritin. While tissue ferritin clearly p lay s a role in intracellular iron handling. The level of ferritin in p lasma rep resents the balance between its secretion, which is directly related to intracellular iron sy nthesis, and its clearance, mainly in liver and other organs [11]. Serum ferritin p rotein levels >400 ng/ml define iron overload in most clinical laboratories, but, in fact, such interp retation requires confirmation by finding a high p ercentage of saturation with iron of iron binding cap acity (transferrin). . While other researches have suggest a higher serum ferritin values (>2000 mg/dl) which are much more likely to be an indicator of iron overload as shown in different disorders including those in thalassemic p atients with haemochromatosis [11]. Hence, the Iraqi p atients in this work are less likely to correlate with haemochromatosis as a sy ndrome but instead they suffer from mild increase in serum iron (Table 1) and subsequent events of this increaser which are not well documented. These changes in some hematological and biochemical changes may be mainly due to iron overload and p recipitation of iron as different ions or complex in hep atocy tes. In one research, all the p atients were iron overloaded. M arkers of free radical injury such as malondialdehyde (M DA) and antioxidant enzy mes levels were significantly elevated in thalassemic children while mean glutathione p eroxidase levels were decreased in p atients comp ared to controls .All these markers are significantly correlated with serum ferritin levels. . Anot her significant fact is obtained from the effective chelation therap y , when initiated, the serum ferritin falls more rapidly than body iron. This may happ en p artly because of the imp rovement in liver function and p artly because serum ferritin may reflect p redominantly reticular endothelial iron rather than parenchymal iron in the liver and other organs [12] The other imp ortant p rove for the result of our work is the TISP that is an app roach to saturation (95.6±22.9) as shown in Table (1). Suominnen et al (1998) (34) found that p lasma ferritin iron increases markedly in those with fully saturated transferrin. Furt hermore, there was a significant difference (p = 0.01) between mean serum ferritin in thalassemic p atients with endocrine comp lications and thalassemic p atients without endocrinopathies in many p revious researches [13]. This indicates the involvement of the harmfull effect of increase iron st orage and precipitation on the endocrine glands t hat must be studied in the future works in details. From Table (1) a high serum ferritin is accomp anied by a high p ercentage of saturation of a normal serum transferrin which usually indicates iron overload. These two p arameters are p ositively correlated (Table (2) at which iron overload clearly app ears clinically and biochemically in our p atients. Transferrin level showed a decrease in thalassemic p atients as comp ared with healthy controls T able (1). This result may be due to the fact t hat t ransferrin is a reverse acute p hase reactant. Thus the decrease in hemoglobin in thalassemic p atients is accomp anied by an acute p hase resp onse confirmed by the decrease in transferrin concentration and increase in serun ferritin level as an antagonist cause of the elevation of serum ferritin in addition to the increase in serum iron in thalassemic p atients. For examp le, during the acute p hase resp onse, inflammatory cytokines such as interleukin 1 beta and tumor necrosis factor alp ha increase the sy nthesis of both subunits of ferritin [14]. Hence, serum ferritin can be elevated in inflammation. In Table (2) there is no significant difference in blood hemoglobin indicating that thalassemia is not related to iron within hemoglobin molecule but instead it correlates with iron librated from the hemoglobin molecules after hemolysis and degradation. Statist ically significant correlations were found between serum Fe, serum ferritin (5). Under various p athological conditions associated with iron overload, including thalassemia, there is an evidence of an increase in low molecular weight iron in serum and in the intracellular transit p ool of iron. This is the same in our thalassemic p atients (Table 1). This p romotes p eroxidative damage to cell and organelle membranes" in organs that IBN AL- HAITHAM J . FO R PURE & APPL. SC I VO L. 22 (4) 2009 accumulate excess iron, including liver, p ituitary gland, p ancreas, and heart (40). Iron p lay s a key role in the formation of toxic oxy gen radicals that can att ack all biological molecules. Hence, sp ecialized molecules for the acquisition, transp ort (transferrin), and st orage (ferritin) of iron in a soluble nontoxic form have evolved [15]. Transferrin saturation can be elevated by increased iron st ores and a variety of other conditions . In p atients with severe iron overload, p lasma can contain transferrin comp letely saturated with iron and also a chelatable low molecular weight iron fraction not associated with transferrin . Hence, over saturation in some other thalassemic patients may be due to the p resence of these sp ecies of non-transferrin bound iron where the TISP range is (95.6±22.9) as shown in Table (1). Nonsp ecific, non-transferrin–bound iron is rapidly cleared from the p lasma, mainly by the liver [16]. Non-t ransferrin-bound iron (NTBI) app ears in the serum of individuals with iron overload and in a variety of other p athologic conditions. Because NTBI constitut es a labile form of iron, it might underlie some of the biologic damage associated with iron overload. Thalassemic sera contained NT BI in 80% of the cases (range, 0.9-12.8 micromole/L).[17] Total iron-binding cap acity (a measure of p lasma transferrin levels) is app roximately 56 umol/liter; thus, t ransferrin is about one-third saturated with iron, with app roximately 10% p resent as a diferric transferrin. [18]. Hence, there seems to be a control mechanism that guarantees that rate of iron release from st ores which p erfectly matches the one with which the iron is taken up by tissues, but the nature of this regulation is unknown. Table (1) showed a significant decrease in serum hemoglobin as comp ared with healthy control group . This result is exp ected mainly due to the hemolysis of RBC and the release of iron from the degraded abnormal hemoglobin molecules chain. (Hb) Anemia can occur in severe iron overload . A number of st udies also indicate that RE cells release significant amounts of erythrop hagocytosed iron in the form of hemoglobin , or ferritin. It has been sp eculated that hemoglobin release results from macrophage cell death after the ingestion of too many erythrocytes, whereas others argue that hemoglobin release represents a normal p hy siological p rocess . Interest ingly, M oura et al. (1998b) [19] noted that most early release consists of hemoglobin, whereas ferritin and low-molecular-weight iron are the main forms released subsequently. It has also been p rop osed that iron and oxy gen radicals may p lay a key role in the p rogression of chronic renal failure, the fact that may be related to the changes in kidney excretionb of different substances . Prot einuria, resulting from the glomerular injury , may p erpetuate renal injury , and it has generally been assumed that the tubulointerstitial injury is induced by albumin. Patients with Hemoglobinop athies including thalassemia would develop albuminuria and this may affect the blood concentration of albumin. We concluded that renal disorders are not rare in p atients with beta-thalassemia major . The albuminuria or decrease in serum albumin are not shown in our work neither any correlation between albumin and iron st atus. M any works obtained the same results [20] also noticed no correlation between seum ferritin with serum albumin. Nut ritional deficiencies are common in thalassemia secondary to the use of desferrioxamine, the hemolytic anemia, and iron overload that accomp anies this disease. Calcium in our work is changed and this result differs from the results obtained from other thalassemic p atients group in M osul-Iraq [21] at which the mean serum level of calcium had no significant difference as comp ared with healthy control group . In the M osul st udy , the thalassemic p atients was 105 p atients while in the p resent study only 45 p atients are involved due to the variation in samp ling between the centers. IBN AL- HAITHAM J . FO R PURE & APPL. SC I VO L. 22 (4) 2009 Some calcium metabolism markers were measured in another st udy . Serum levels of calcium, p hosp hate, p arathy roid hormone (PT H), calcitonin and 25-OH vitamin D were measured. Average serum levels of PT H and vitamin D were significantly lower in thalassemic patients than in control group . [22] It is suggested that increasing the circulating IGF-I concentration through aggressive nutritional therap y and/or GH/IGF-I therap y with sup p lementation with vitamin D and/or calcium might imp rove bone growt h and mineralization and p revent the development of ost eoporosis and consequent fractures in thalassemic p atients. Secondary gout is a well-recognised comp lication of disorders characterized by increased nucleic acid catabolism and disordered renal function. However, in the p resent work, there is a significant decrease in serum uric acid in comp arison with control group (Table 1). This results agrees with a st udy carried out in Turkey . While, In Italian st udies t hat carried out by Gallerani et al (1989 ) [23] showed that uric acid levels in Beta Thalassemia were higher than in the control group . Hyp eruricemia and microscopic hematuria are more common in thalassemia intermedia than thalassemia major. M icroscop ic hematuria in thalassemia intermedia might be related to either hyp ercalciuria or hyp eruricosuria (9). Conclusion Our st udy should be qualified for its relatively small sample size (n =45) and its cross- sectional design. While causality cannot usually be detected in cross-sectional st udies, associations can be examined. M oreover, the markers of inflammation were not measured in this st udy , nor were other measures of malnutrition. Therefore, it is imp ortant t o understand iron metabolism not only at the molecular and cellular levels but also at the level of the whole organism. In thalassemia p atients, the iron absorp tion is increased and the excretion rates of iron should be achieved to maintain a "safe" level of body iron. M onitoring of iron st atus requires: estimation of the iron content of different body organs, and assessment of the function of the organs p articularly damaged by iron overload namely ; heart, liver, and endocrine glands,. Thus, the monitoring of iron st atus is of imp ortance to overcome the p ossible consequences that could occur in vital organs. These asp ects are of imp ortance and they are the targets of our future works. References .894: 90Blood . )1997(. G,her S;. G,oren K;.T ,Einarson;.P ,oghertyD.1 2.Sheikh a ,A.K.; Salih, Z.T.; Kasnazan, K.H.; Khoshnaw, M.K.; Al-M aliki, T.; Al-Azraqi, T.A.andZafer, M .H. (2007) Can J Surg. Oct;50(5):382-6. .1−40: 1331; Biochim Biop hy s Acta)1997(. P , Ponkaand .R.D ,Richardson.3 4.Al-Kubaisy , W.A.; Al-Naib, K. T .and Habib, M . (2006)East M editerr Health J. Jan- M ar;12(1-2):204-10. 5.Richer, Stuart; Rudy , David ; Statkut e, Laisvy de; Karofty, Kurt ; Frankowski, Jim, (2002) .February/January, 28-25):1(9. American Journa l of Therapeutics 6.M organ, E.H. T ransferrin. Haeberli A eds. (1992)Human p rotein data VCH Weinheim. .95-6:198341)1999( Engl J M ed .N. F.V,Fairbanks .7 8.M ourad,F.H.; Hoffbrand, A.V.; Sheikh-Taha, M .; Koussa, S.; Khoriaty , A.I.and Taher, Br- 9-187): 1(121; Ap r)2003(. Haematol -J 9.(Ali D, M ehran K, M oghaddam AG.. Saudi J Kidney Dis T ransp l. 2008 M ar- Ap r;19(2):206-9 .104-:98140)2000(. Am Heart J. Schwartz, Woloshin S, Ornstein DL, Zacharski LR(.10 11.Kattamis A, ;Dinop oulos, A.; Ladis, V.; Berdousi, H.and Kattamis, C. Am J Hematol .224–221 : 68 )0012( IBN AL- HAITHAM J. FO R PURE & APPL. SC I VO L. 22 (4) 2009 .:293492 )1998(B lood . et al, Suominn en P.12 13.Saka, N.; Sukur, M .; Bundak, R.; Anak, S. ; Neyzi, O.and gediko glu, G. J Pediatr Endocrinol M etab. 1995;8:181–186. PubM ed 14.Rogers, J.T .; Brid ges, K.R.; Durmowicz, G.P.; Glass, J.; Auron, P.E.and M unro, H.N . J Biol Chem 1990 ; 265: 14572–14578. x.69002.Sup p l1755.1999.055-1523.j/.104610:do i; 11S–2S:55) 1999 (onkaP remP.15 16.Craven, C.M .; Alexander, J.; Eldridge, M .; Kushner, H.P.; Bernst ein, S. and Kaplan, J. ;1987 .3461−3457: 84Proc Natl Acad Sci U SA )1987 ( 17.Breuer,W.; Ronson,A.; Slotki,IN.; Abramov,A.; Hershko,C.; Cab antchik,ZI (2000)Blood. 82-2975): 9(95; 1M ay 18.Bothwell, T.A.; Charlton, R.W.; Cook, J.D. and Finch ,C.A. (1979) Iron M etabolism in M an Oxford, Blackwell Scientific. 19.M oura, E.; Noordermeer, M .A.; Verhoeven, N.; Verheu l, A.F. and M arx, J.J. (1998). .2519–:251192Blood .)1076-:106648)2002(. Clinical Ch emistry. 1a and Loth ar Thomas1Christ ian Thomas.20 21. (Al-Samarrai AH, Adaay MH, Al-T ikr it i KA, Al-An zy MM . Saudi Med J. 2008 Jan;29(1) :94- 97). 22.Pratico,-G; Di-Gregorio,-F; Caltabiano,-L; Palano,-G-M [ Pediatr-M ed-Chir. (1998) Jul- Aug; 20(4): 265-8. 23.Gallerani M, Faggioli M, Martinelli L, Ricci A, Colett i M.Minerv a Med. (1989) Nov.80(11):1199-204. Table (1): The biochemical parameters of thal assemic patients as compared with healthy control group. Biochemical Parameter Thalassemic M ±SD Control M±SD Significance S.Ferritin (u g/L) 556.5±103 73.8±31.2 Significant S.Calcium (u mol/L) 2.58±0.13 2.46±0.22 NonSignificant S.Albumin ( g/L) 41.5±10.5 43.8±5.7 NonSignificant S.TIBC (umol/L) 51.9±8.9 61.6±8.3 Significant S.Iron (umol/L) 49.1±12.3 20±5.5 Significant Hemoglobin (g/L) 72±17 135±21 Significant TISP % 95.6±22.9 32.9±9.1 Significant Trans ferrin Conc.g/L) 0.131±0.023 0.155±0.021 Significant S.Uric acid (umo l/L) 278.8±53.6 319.9±67.9 Significant (*): Significant only when p <0.05. IBN AL- HAITHAM J . FO R PURE & APPL. SC I VO L. 22 (4) 2009 Table (2): Correl ation coefficie nt of serum iron versus different biochemical parameters concentration in both thal assemic patients and healthy control group. The Comp ared Parameters Thallasemic patients Healthy Control S.Iron vs. Ferritin 0.66 0.54 S.Iron vs. TISP 0.67 0.89 S.Iron vs. Trans ferrin 0.52 0.15 S.Iron vs. Album in 0.19 -0.04 S.Iron vs. Uric acid 0.04 0.10 S.Iron vs. Calcium 0.08 0.27 S.Iron vs. TIBC -0.52 -0.47 S.Iron vs. Hb 0.17 0.10 2009) 4(22مجلة ابن الھیثم للعلوم الصرفة والتطبیقیة المجلد بین ادراسة بعض المتغیرات الكیموحیاتیة في مصول االطفال العراقیین المص میابمرض الثاالسی *ضرغام عزیز كاتي *** محمدرضامھدي محمد ،**ني طالب المد، *حسین كاظم الحكیم * سرور كریم ،*صفاء عبد المھدي ناصر ة جامعة الكوف–كلیة العلوم ، قسم الكیمیاء * ة جامعة الكوف–كلیة الطب ، قسم األطفال ** ة جامعة الكوف–كلیة الطب ، قسم الكیمیاء *** الخالصة یطلـق مــصطلح الثاالســیمیا علــى مجموعـة مــن االضــطرابات الوراثیــة التــي تـؤثر فــي عملیــة تــصنیع الهیموكلــوبین . یرافـق هـذا المـرض الكثیـر مـن التغیـرات الكیموحیاتیـة فـي الـدم. ویسمى هذا المرض أحیانـا بفقـر دم البحـر األبـیض المتوسـط شـــملت . یــة المهمـــة فــي المرضــى وقورنــت نتــائجهم بمجموعــة الــسیطرة بعــض المتغیــرات الكیموحیاتتفــي هــذا البحــث قیــس و ، وحـامض الیوریـك ، و الهیموكلـوبین،و سـعة ارتبـاط الحدیـد الكلیـة،و الفیـریتین ،الحدید : القیاسات العملیة المتغیرات التالیة . و نسبة تشبع الترانسفرین،و الترانسفرین ،و الكالسیوم ،األلبومین بینمـا لـوحظ انخفاضـا معنویـا فـي تراكیـز ،في تراكیز الحدید و الفیریتین (P<0.05)ارتفاعا معنویا أظهرت النتائج حـامض الیوریــك و ســعة ارتبــاط الحدیــد الكلیــة و الهیموكلــوبین و الترانــسفرین و نــسبة تــشبع الترانــسفرین و لــم تتغیــر تراكیــز .ع مجموعة السیطرةاأللبومین و الكالسیوم في مصول مرضى الثاالسیمیا مقارنة م یمكن تفسیر نتائج هذا البحث من خالل میكانیكیات مختلفة تتـضمن تحلـل كریـات الـدم الحمـر وترسـب الحدیـد فـي . كـذلك ان قلــة نقـل األوكــسجین لألنـسجة قــد یكـون ســببا فـي التغیــرات الكیموحیاتیـة التــي لوحظـت فــي هـذا البحــث. األنـسجة . اكیز هذه المتغیرات قد یكون مفیدا في عملیة متابعة تطور المرضیمكن االستنتاج بان قیاس ومتابعة تر