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 Table of Contents  
ORIGINAL ARTICLE
Year : 2019  |  Volume : 32  |  Issue : 3  |  Page : 1051-1058

Study of adipocytokines (visfatin and resistin) levels in children with β-thalassemia major and intermedia


1 Department of Pediatrics, Faculty of Medicine, Menoufia University, Menoufia, Egypt
2 Department of Medical Biochemistry, Faculty of Medicine, Menoufia University, Menoufia, Egypt
3 Department of Pediatrics, Ministry of Health, Cairo, Egypt

Date of Submission06-Dec-2017
Date of Acceptance29-Jan-2018
Date of Web Publication17-Oct-2019

Correspondence Address:
Yasser F. M. Wasel
Department of Pediatrics, Ministry of Health, Cairo
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/mmj.mmj_835_17

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  Abstract 

Objective
The objective of this study was to assess visfatin and resistin levels in children with β-thalassemia major and intermedia.
Background
β-Thalassemia represents a major public health problem in Egypt. Adipocytokines are bioactive mediators released from the adipose tissue including adipocytes and other cells present within fat tissues.
Patients and methods
This study was conducted on 70 patients with β-thalassemia diagnosed by both clinical and laboratory criteria. They were divided into two groups: group I included 50 patients with β-thalassemia major and group II consisted of 20 patients with β-thalassemia intermedia. Moreover, 20 healthy individuals were included as a control group. All the participants were included from February 2016 to February 2017. Full history, routine physical examination, and special investigations were taken.
Results
BMI (kg/m2) was significantly lower in patients with β-thalassemia than control group, and it was higher in β-thalassemia intermedia group than β-thalassemia major group. Lipid profile and serum resistin and visfatin levels were significantly higher in patients with β-thalassemia than control group. Resistin was positively correlated with total leukocyte count, ferritin, urea, serum glutamic pyruvic transaminase, and serum glutamic oxaloacetic transaminase and negatively correlated with BMI and hemoglobin. Serum visfatin was positively correlated with total leukocyte count, urea, serum glutamic pyruvic transaminase, serum glutamic oxaloacetic transaminase, lipid profile, and glucose and negatively correlated with BMI and hemoglobin.
Conclusion
The adipocytokines (resistin and visfatin) were significantly higher in patients with β-thalassemia (major and intermedia) than control group. The measurement of these adipocytokines may be helpful in differentiating the degree of inflammation. Moreover, a novel association was found between the increasing concentrations of proinflammatory adipocytokines (resistin and visfatin) and the severity of β-thalassemia types.

Keywords: adipocytokines, resistin, visfatin, β-thalassemia


How to cite this article:
Deeb MM, Dawoud AA, El-Hawy MA, Wasel YF, Elsayed EA. Study of adipocytokines (visfatin and resistin) levels in children with β-thalassemia major and intermedia. Menoufia Med J 2019;32:1051-8

How to cite this URL:
Deeb MM, Dawoud AA, El-Hawy MA, Wasel YF, Elsayed EA. Study of adipocytokines (visfatin and resistin) levels in children with β-thalassemia major and intermedia. Menoufia Med J [serial online] 2019 [cited 2019 Nov 16];32:1051-8. Available from: http://www.mmj.eg.net/text.asp?2019/32/3/1051/268855




  Introduction Top


β-Thalassemia syndrome is a group of hereditary blood disorders characterized by reduced or absent β-globin chain synthesis, resulting in reduced hemoglobin (Hb) in red blood cells, decreased red blood cell production, and anemia. Global annual incidence is estimated at one in 100 000. β-Thalassemia is caused by mutations in the HBB gene on chromosome 11 and inherited in an autosomal recessive fashion. The severity of the disease depends on the nature of the mutation [1]. β-thalassemia includes three main forms: thalassemia major, variably referred to as Cooley's anemia and Mediterranean anemia; thalassemia intermedia; and thalassemia minor, also called β-thalassemia carrier, β-thalassemia trait, or heterozygous β-thalassemia [1].

All types of thalassemia can be fatal in some cases, particularly when there are multiple gene mutations that affect the production of the globin chains. In 2013, 25 000 deaths were attributable to thalassemia, which was an improvement upon the 36 000 deaths recorded in 1990. The major causes of morbidity and mortality in β-thalassemia are anemia and iron overload. The severe anemia resulting from this disease, if untreated, can result in high-output cardiac failure; the intramedullary erythroid expansion may result in associated skeletal changes such as cortical bone thinning. The long-term increase in red-cell turnover causes hyperbilirubinemia and bilirubin-containing gallstones [2].

β-Thalassemia is a significant public health problem in Egypt, where more than one million newborns are expected to be affected with this disorder, and it is considered the most common genetically determined chronic hemolytic anemia (85.1%) in our locality. A high frequency of carriers has been reported in Egypt, ranging from 4 to 10%. This is owing to high rate of consanguineous marriage, which leads to accumulation of deleterious genes in Egyptian families [3].

Adipocytokines are bioactive mediators released from the adipose tissue including adipocytes and other cells present within fat tissues. These include several novel and highly active molecules released abundantly by adipocytes like leptin, adiponectin, resistin, or visfatin. Visfatin is an insulin-mimicking adipocytokine secreted from visceral adipose tissue, which plays an essential role in several biological processes affected glucose uptake regulation, inflammation, immunity, insulin resistance, vascular calcification, capillary tube formation, endothelial cell function, and angiogenesis [4].

Resistin is a member of the resistin-like molecule family of cysteine-rich secretory 12 kDa proteins. Resistin is regulated by insulin, glucose, growth hormone, and thiazolidinediones. Resistin is one of the placental hormones, which seemingly has a substantial role in the homeostasis of pregnancy and fetal development. However, there are insufficient data revealing the role of resistin in this regard [5].

Visfatin is an insulin-mimicking adipocytokine secreted from visceral adipose tissue, and it can be considered a new proinflammatory adipocytokine. It dose-dependently upregulates the production of the proinflammatory and anti-inflammatory cytokines interleukin (IL)-1, IL-1Ra, IL-6, IL-10, and tumor necrosis factor in human monocytes. These cytokines play a substantial role in a wide range of infectious and inflammatory diseases. The role of visfatin in the pathogenesis of other diseases such as diabetes mellitus, insulin resistance, atopic dermatitis, chronic kidney diseases, and rheumatic disease has been reported [6].

The aim of this study was to assess adipocytokines concentration (resistin and visfatin) in patients with different types of β-thalassemia and to determine any possible correlations with disease severity.


  Patients and Methods Top


A prospective randomized comparative study was conducted on 70 patients with β-thalassemia (major and intermedia) diagnosed by both clinical and laboratory criteria. They were enrolled from the Hematology and Oncology Unit, Pediatrics Department, Menoufia University. The study was approved by the local medical ethical committee. Cases were selected during the study period from February 2016 to February 2017, and all study patients were divided in two groups:

  1. Group I (β-thalassemia major) included 50 patients (30 male and 20 females) with β-thalassemia major.
  2. Group II (β-thalassemia intermedia) included 20 patients (15 male and five female) with β-thalassemia intermedia.
  3. Group III (control group) included 20 healthy individuals (13 male and seven female) who were clinically free of any disease and volunteered to participate in the study.


Ethical consideration

The study was approved by the ethical committee of Menoufia Faculty of Medicine, and an informed consent was obtained from all patient's guardian before the study was commenced.

Selection criteria

The patients included in this study were selected according to inclusion and exclusion criteria.

Inclusion criteria

Patients with β-thalassemia major and intermedia from age 1 to 18 years were included from the study.

Exclusion criteria

The exclusion criteria were patients with infectious diseases, those with liver diseases, those on steroid therapy, or those on immunosuppressive drugs.

Method of sampling

Sample size was calculated using computer sample block randomization type. Samples were obtained during routine investigations. Overall, 5 ml sample of venous blood was drained by sterile syringes and put in a tube containing dipotassium EDTA reagent. The sample were shaken gently and analyzed by Medonic 20 (Domnarvsgatan, Spånga, Sweden).

All cases were subjected to the following:

  1. Complete history: personal, present, past and family history such as, age, relative, consanguinity, blood transfusion per year, and drug history
  2. Clinical examination: general including anthropometric measurements such as, height, weight and BMI and local including cardiovascular system, central nervous system, abdominal, and chest
  3. Investigations:


    1. Routine investigations.


      1. Complete blood count, including total leukocyte count (TLC) (×103), platelet count, and Hb, using Sysmex KX-21 automatized hematology analyzer (Sysmex Corporation, Kobe, Japan)


      2. Reference value for TLC × 103 was 4.5–10.5 mm 3, Hb was 11–14 g/dl, and platelets was 150–440 mm 3

      3. Kidney functions including blood urea and serum creatinine using the open system Autoanalyzer Synchron CX5 (Beckman Coulter Inc., California, USA)


      4. Reference value for creatinine in males was 0.6–2.5 mg/dl and in females was 0.6–1.5 mg/dl, and for urea was 15–45 mg/dl

      5. Liver enzymes test, including serum glutamic pyruvic transaminase (SGPT) and serum glutamic oxaloacetic transaminase (SGOT) measured using a biochromatic (405–510 nm) rate technique


      6. Reference value for SGPT was 15–37 U/l and SGOT was 30–65 U/l

      7. Lipid profile: cholesterol, triglyceride (TG), low-density lipoprotein (LDL), and high-density lipoprotein (HDL) using the open system Autoanalyzer Synchron CX5 (Beckman Coulter Inc.)


      8. Reference value for cholesterol was 103–190 mg/dl, TG was 45–189 mg/dl, LDL was 36–195 mg/dl, and HDL was 7–36 mg/dl

      9. Random blood sugar: measured using Sysmex KX-21 automatized hematology analyzer (Sysmex Corporation) (reference value: 70–120 mmol/l)


    2. Specific investigations.


      1. Serum ferritin: measured using ELISA Kit 'EIA-01-Ferritin' (New England Immunology Associates Inc., Cambridge, Massachusetts, USA) (reference value was 30–100 ng/ml)
      2. Serum resistin and visfatin: measured using human resistin and visfatin ELISA kit [7]. Reference value for resistin was 2.35–4.45 ng/ml and visfatin was 0.71–2.68 ng/ml.


Methods

Human resistin ELISA kit

Principal of the assay: The assay max human resistin ELIZA kit is designed for detection of human resistin in plasma, serum, urine, and cell culture supernatants. This assay employs a quantitative sandwich enzyme immunoassay technique, which measures resistin in less than 5 h. A murine monoclonal antibody specific for resistin has been precoated onto a microplate. Resistin standards and samples are sandwiched by the immobilized antibody and a biotinylated polyclonal antibody specific for resistin, which is recognized by a streptavidin-peroxidase conjugate [7].

Assay procedure: The assay is performed at room temperature (20–30°C). Remove excess microplate strips from the plate frame and return them immediately to the foil pouch with desiccant inside. Add 50 ml of standard or sample per well. Cover wells with a sealing tape and incubate for 2 h. Start the timer after the last sample addition. Wash five times with 200 ml of wash buffer manually. Invert the plate each time and decant the contents; hit it four to five times on absorbent paper towel to completely remove the liquid. If using a machine, wash six times with 300 ml of wash buffer and then invert the plate, decant the contents, and hit it four to five times on absorbent paper towel to completely remove the liquid. Add 50 ml of biotinylated resistin antibody to each well and incubate for 2 h and then wash the microplate as described before. Add 50 ml of streptavidin-peroxidase conjugate per well and incubate for 30 min. Add 50 ml of chromogen substrate per well and incubate for ∼10 min or till the optimal blue color density develops [7].

Statistical analysis

Results were tabulated and statistically analyzed by using a personal computer using Microsoft Excel 2016 and SPSS, v. 21 (SPSS Inc., Chicago, Illinois, USA). Statistical analysis was done using the following: descriptive, for example, percentage, mean, and SD, and analytical, which includes χ2-test, t-test, Mann–Whitney test, and Pearson's correlation coefficient (r). A value of P less than 0.05 was considered statistically significant.


  Results Top


There was a nonsignificant difference between patients with thalassemia and control group regarding age (P > 0.05). In contrast, BMI (kg/m 2) was significantly lower in patients with β-thalassemia (major and intermedia) than the control group. However, BMI was higher in patients with β-thalassemia intermedia than those with β-thalassemia major. Moreover, there was a significantly higher difference (P < 0.01) between patients with β-thalassemia (major and intermedia) and the control group regarding serum resistin and visfatin levels (P > 0.05). Serum resistin was significantly higher in patients with β-thalassemia (major and intermedia) than the control group and was higher in patients with β-thalassemia major than those with β-thalassemia intermedia, whereas serum visfatin was significantly higher in patients with β-thalassemia major (2.69 ± 4.39) than those with β-thalassemia intermedia (2.1 ± 3.39), and both were more than the control group (1.03 ± 0.42) [Table 1].
Table 1: Comparison between patients with β-thalassemia (major and intermedia) and control groups regarding their age, BMI, serum resistin level, and serum visfatin level

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The current study shows that there was no statistical significant difference between patients with β-thalassemia (major and intermedia) and control groups regarding TLC and serum creatinine levels (P > 0.05), whereas highly significant differences (P < 0.01) were observed among the studied groups regarding serum platelet, serum ferritin, serum urea, and liver enzymes, which were increased in both patient groups and were significantly higher in patients with β-thalassemia (major and intermedia) than the control group. However, the Hb level was significantly higher in control group than patients with β-thalassemia (major and intermedia) [Table 2].
Table 2: Comparison between patients with β-thalassemia (major and intermedia) and control groups regarding complete blood count, renal function, and liver enzymes (n=70)

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Regarding lipid profile (cholesterol, TG, LDL, and HDL) and glucose, there was a statistically significant difference (P < 0.05) between patients with β-thalassemia (major and intermedia) and the control group. Moreover, these were significantly higher in patients with β-thalassemia major than those with β-thalassemia intermedia [Table 3].
Table 3: Comparison between patients with β-thalassemia (major and intermedia) and control groups regarding lipid profile (cholesterol, triglyceride, low-density lipoprotein, and high-density lipoprotein) and glucose

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In addition, the current study shows that resistin was significantly positive correlated with TLC (r = 0.69, P = 0.034), ferritin (r = 0.853, P = 0.000), urea (r = 0.348, P = 0.03), SGPT (r = 0.54, P = 0.014), SGOT (r = 0.78, P = 0.002), lipid profile (0.832, P = 0.001), and glucose (r = 0.55, P = 0.041) and negatively correlated with BMI (r=−0.78, P = 0.002) and Hb (r=−859, P = 000). However, resistin was not correlated with sex, age, and creatine. In addition, serum visfatin was significantly positive correlated with TLC (r = 0.541, P = 0.05), creatinine (r = 0.61, P = 0.047), urea (r = 0.95, P = 0.001), SGPT (r = 0.77, P = 0.005), SGOT (r = 0.63, P = 0.014), lipid profile (r = 0.902, P = 0.001), and glucose (r = 0.58, P = 0.045). However, BMI (r = −0.73, P = 0.002) and Hb (r = −0.62, P = 0.035) were significant negative correlated with visfatin. In addition, visfatin was not correlated (P > 0.05) with sex, age, and ferritin [Table 4] and [Figure 1].
Table 4: Pearson's correlation (r) between resistin and visfatin levels and complete blood count, renal function, and liver enzymes of studied groups

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Figure 1: BMI percentile for age. A 115 cm tall, 23 kg, 18-year-old patients had a BMI of 17.4, which is at the fourth percentile for age. This suggests that this patient is underweight.

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  Discussion Top


In the current study, it was found that there was no statistical significant difference between patients with β-thalassemia (major and intermedia) and control groups regarding age (years) and BMI (kg/m 2). The study conducted by Elsayh et al. [8] revealed that height, weight, and BMI in patients with thalassemia were significantly lower than their respective values in the control group.

In addition, the current study shows that there was highly significant difference (P < 0.01) between patients with β-thalassemia (major and intermedia) and the control groups regarding serum resistin and visfatin levels. Serum resistin and visfatin levels were significantly higher in patients with β-thalassemia (major and intermedia) than the control group and were higher in patients with β-thalassemia major than those with β-thalassemia intermedia. This comes in agreement with Enli et al. [9] who found in their study that resistin concentrations were significantly higher in patients with β-thalassemia major than in controls. Resistin and visfatin concentrations were significantly higher in both patients with β-thalassemia intermedia and those with β-thalassemia major than in controls. Moreover, Silswal et al. [10] found that the concentrations of resistin and visfatin in patients with β-thalassemia major and those with β-thalassemia intermedia were higher than in the other two groups (control and patients with β-thalassemia minor). In another recent study, Dehkordi et al. [11] found that the mean value of visfatin was significantly higher in patients with β-thalassemia than control group (133.9 ± 60.1 vs. 43.3 ± 27.9, P < 0.001). This finding indicates that similar results with adiponectin and resistin and visfatin concentration changes according to the disease severity.

In the current study, it was found that platelet, serum ferritin, serum urea, SGPT, and SGOT were significantly higher in patients with β-thalassemia (major and intermedia) than the control group, but Hb level was significantly higher in control group than patients with β-thalassemia (major and intermedia) groups. However, no statistical significant difference was found between patients with β-thalassemia (major and intermedia) and control groups regarding their TLC and serum creatinine (P > 0.05). This comes in agreement with Elsayh et al. [8] who found that Hb was significantly lower in patients with thalassemia than control. Furthermore, as expected, serum ferritin levels of all patients with thalassemia were significantly higher than those of the healthy controls. Moreover, Younus et al. [12] found a significant increase in serum urea level in patients with β-thalassemia, receiving only regular blood transfusion, when compared with controls. In addition, Sarai et al. [13] found in their study a significant increase in the levels of serum iron and a significant decrease in total iron binding capacity in patients with β-thalassemia. Serum urea levels were significantly higher in patients with β-thalassemia when compared with controls.

Another study done in Northern Iran, Ameli et al. [14] was in agreement with our results, which also means that liver enzymes in patients with thalassemia, as reflected by elevated ALT, are affected or deteriorated by increasing serum iron overload, as reflected by elevated serum iron. According to Mohammad and Al-Doski [15] a significant increase in activity of AST, ALT, and bilirubin level was found in patients with thalassemia as compared with control participants. A significant alteration in liver enzymes of patients with thalassemia shown by changes in biochemical markers (elevated ALT and AST) and hepatomegaly, both with the close association with iron overload. In contrast to our results Younus et al. [12] found a significant decrease in serum creatinine level. Moreover, Sarai et al. [13] found that the activities of the liver enzymes in serum (SGPT and SGOT) were significantly decreased in patients with β-thalassemia as compared with controls.

In the current study, it was found that lipid profile (cholesterol, TG, LDL, and HDL) was significantly higher (P < 0.5) in patients with β-thalassemia (major and intermedia) than control groups. Moreover, these were significantly higher in patients with β-thalassemia major than those with β-thalassemia intermedia. This comes in agreement with Hartman et al. [16] who found in their study that lipid profile is altered in patients with β-thalassemia major and β-thalassemia intermedia. Serum total cholesterol (TC) and LDL-cholesterol levels are lower in patients with thalassemia than the normal controls. In addition, Haghpanah et al. [17] found that TC and LDL-cholesterol were significantly lower in patients with BTM and those with BTI in comparison with controls. HDL-cholesterol was significantly higher in patients with BTI than in control. Moreover, Amendola et al. [18] showed that TC and LDL-cholesterol levels were lower in patients with β-thalassemia major and those with β-thalassemia major intermedia than in the control group, although these values were similar in patients with BTM and those with BTI. In contrast, our results disagree with Haghpanah et al. [17] who revealed that the levels of TG, HDL, and LDL were significantly lower among children with β-thalassemia intermedia compared with those with β-thalassemia major and healthy controls.

In the current study, it was found that resistin was significantly positively correlated (P < 0.05) with TLC, ferritin, urea, SGPT, SGOT, lipid profile, and glucose and negatively correlated with BMI and Hb. However, resistin was not correlated with sex, age, and creatine. This comes in agreement with Janke et al. [19] who found that resistin serum levels were found to be related to BMI in human participants. Moreover, Dan [20] reported a significant negative correlation between the serum resistin levels and BMI. Resistin has been shown to be influenced by BMI. Moreover, Fonseca and Santos [21] did not reveal a correlation between BMI and resistin levels in blood. However, Zein et al. [22] found that there was a nonsignificant positive correlation between resistin level and serum creatinine level.

Furthermore, the current study shows that serum visfatin was significantly positively correlated (P < 0.05) with TLC, creatine, urea, SGPT, SGOT, lipid profile, and glucose. However, BMI and Hb were significantly negatively correlated with visfatin. Moreover, visfatin was not correlated (P > 0.05) with sex, age, and ferritin. This comes in agreement with Haider et al. [23] who concluded that plasma visfatin did not correlate with age and sex. In another study, Krzyzanowska et al. [24] found that there was no correlation between visfatin concentrations and age or sex. In contrast, our results are in disagreement with Fernandez-Real et al. [25] who found that serum visfatin concentration was not found to be significantly associated with blood Hb and serum ferritin. In addition, Krzyzanowska et al. [24] found that there was no correlation between visfatin concentrations and BMI, fasting plasma glucose, and plasma insulin. Moreover, Yuksel et al. [26] found that no significant correlation was found between visfatin and glucose, ALT, AST, and BMI. These differences between our results and other studies may be related to the relatively low number of participants in the later mentioned studies.


  Conclusion Top


The adipocytokines (resistin and visfatin) were significantly higher in patients with β-thalassemia (major and intermedia) than control group. These adipocytokines measurement may be helpful in differentiating the degree of inflammation. Moreover, a novel association was found between the increasing concentrations of proinflammatory adipocytokines (resistin and visfatin) and the severity of β-thalassemia types.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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  [Table 1], [Table 2], [Table 3], [Table 4]



 

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