Camel Milk with Pegylated Interferon Alfa-2a and Ribavirin for Treatment-Naive Chronic Hepatitis C Genotype 2/ 3: An Open-Label, Randomized Controlled Trial


Seyyd Musa al-Reza Hosseini 1 , Said Zibaee 2 , Mahdi Yousefi 3 , Ali Taghipour 4 , Omid Ghanaei 5 , Mohammadreza Noras 6 , *

1 MD, Assistant Professor, Department of Gastroenterology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran

2 PhD in Microbiology, Assistant Professor, Razi Vaccine and Serum Research Institute, Mashhad, Iran

3 PhD in Iranian Traditional Medicine, Assistant Professor, Faculty of Persian and Complementary Medicine, Mashhad University of Medical Sciences, Mashhad

4 PhD in Epidemiology, Associate Professor, Faculty of Health, Mashhad University of Medical Sciences, Mashhad, Iran

5 MD, Department of Gastroenterology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran

6 PhD in Iranian Traditional Medicine, Faculty of Persian Traditional and Complementary Medicine, Mashhad University of Medical Sciences, Mashhad, Iran

How to Cite: al-Reza Hosseini S M, Zibaee S, Yousefi M, Taghipour A, Ghanaei O, et al. Camel Milk with Pegylated Interferon Alfa-2a and Ribavirin for Treatment-Naive Chronic Hepatitis C Genotype 2/ 3: An Open-Label, Randomized Controlled Trial, Iran Red Crescent Med J. 2017 ; 19(9):e13529. doi: 10.5812/ircmj.13529.


Iranian Red Crescent Medical Journal: 19 (9); e13529
Published Online: September 16, 2017
Article Type: Research Article
Received: March 11, 2017
Revised: May 16, 2017
Accepted: July 29, 2017




Background: Chronic hepatitis C is one of the most important causes of cirrhosis and hepatocellular carcinoma (HCC). Camel milk (CM) is a new candidate therapy for chronic hepatitis C (CHC).

Objectives: The present study assessed the safety and efficacy of pegylated interferon alfa-2a and ribavirin with CM (CM + Peg IFN/RBV) and without CM (Peg IFN/RBV) in CHC genotype 2/3 infections.

Methods: This study was an open-label, randomized, phase 2 trial. Sampling strategy and date was computer–generated randomization. The researchers randomly selected 45 adult patients (ages > 18 years), who were treatment-naive with CHC infection (non-cirrhotic) to receive Peg IFN/RBV with standard-dose alone (group A, n = 23), CM + Peg IFN/RBV: 500 cc orally per day (group B, n = 22) for 24 weeks in Iran. The primary efficacy outcomes were early virological response (EVR12) and end-of-treatment response (ETR24), the secondary efficacy outcome was sustained virological response (SVR24), and the safety outcomes were adverse events and laboratory tests at end-treatment to assess.

Results: The EVR12 was 60% (12/20), ETR24 90% (18/20), and SVR24 100% (18/18) of CM + Peg IFN/RBV therapy. The EVR12 was 15% (3/20), ETR24 70% (14/20), and SVR24 rates were 71% (10/14) in Peg IFN/RBV therapy (P < 0.05). Rates of discontinuation due to adverse events were 8.6% (2/23) in control and no discontinuation in intervention group. The most common adverse events were fatigue, anemia, and insomnia.

Conclusions: Combination of CM with Peg IFN/RBV for 48 weeks showed significant improvements in the viral response and decreased adverse effects in CHC genotype 2/3 (P < 0.05). The data of the study supported the CM synergistic antiviral activity of Peg IFN/RBV. Large clinical trials are needed to confirm the results.


Camel Milk Iran HCV Genotype 2/ 3 Chronic Hepatitis C

Copyright © 2017, Iranian Red Crescent Medical Journal. This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License ( which permits copy and redistribute the material just in noncommercial usages, provided the original work is properly cited.

1. Background

Chronic Hepatitis C is one of the most important causes of cirrhosis and hepatocellular carcinoma. It has been evaluated that there are more than 200 million patients chronically infected with hepatitis C virus (HCV). The prevalence HCV in Iran is estimated to be less than 1.5%. Standard treatments are peginterferon alfa-2a and ribavirin. Protease inhibitors (telaprevir or boceprevir) were the first oral anti-HCV drugs in combination with peginterferon and ribavirin, yet new anti-HCV drugs include: sofosbuvir, daclatasvir, and ledipasvir without peginterferon, which are very expensive (1-4). However, some patients do not respond to these treatments. Besides, the side effects of these drugs and ban on their use in some patients have made the treatment of hepatitis C difficult. Therefore, the introduction of new, safe, and effective drugs with no side effect for this disease could be considered (5, 6).

Traditional experiences of Asian, African, and Indian countries confirm many therapeutic effects of camel milk on various diseases, including liver diseases. Also, the main focus of most of the modern medicine researches conducted on camel milk effects is on the liver. Recent findings have shown antiviral effects of natural materials, such as CM against the hepatitis C virus (7). Special bio-actives along with camel immune system and its transfer to milk causes the milk to have pharmacological effects in favor of the liver, including protective effects against viral and bacterial agents, chemical, and toxic substances. Camel milk has potent immunological, anti-allergic (5), antioxidant agent (8), antibacterial (9), anti-diabetic (9), and anti-inflammatory (10), immunomodulatory (5), anti-apoptosis (11), and anticancer properties (12). It contains various mineral, vitamins, protective proteins, and essential fatty acids, indicating the potential therapeutic effects underlying the anti-HCV actions. Camel’s immune system is different from most mammals and is much stronger than the human’s immune system. For example, camel milk has a particular class of antibodies and immunoglobulins, which are only composed of heavy chains and lack light chains in their structures. These immunoglobulins (simple structure, high affinity, and specificity of these compounds, as antiviral agents) help in the reinforcement of patient’s immune system. Therefore, CM could be a new candidate for complete treatment of HCV infections.

2. Objectives

The present study assessed the safety and efficacy of CM in combination with pegylated interferon alfa-2a and ribavirin in CHC genotype 2/3 infections in Iran.

3. Methods

3.1. Study Design and Participants

For this open-label clinical trial, inclusion criteria were age of between 18 and 60 and presence of chronic infection with genotype 2 /3 HCV, with plasma HCV RNA positivity. Patients were treatment-naive in Iran (Mashhad) and non-cirrhotic, as determined by the following: Fibro scan > 12.5 kpa, or Fibro Test > 0.75. Patients with the following criteria were excluded: BMI < 18 kg/m2, autoimmune disease, evidence of cancer, human immunodeficiency virus (HIV) or HBV infection, neutropenia (neutrophils less than cells/mm3 1500), thrombocytopenia (platelets < cells/mm3 90000), creatinine levels greater than 1.5 times the normal level, clinically significant bleeding disorders, organ transplant, severe heart disease, chronic pulmonary disorder, uncontrolled psychiatric illness, epilepsy, retinopathy, active alcohol or drug abuse, pregnancy and lactation, anemia (hemoglobin less than 10), systemic bacterial or fungal infection, failure to comply with the prescribed dose of milk, discontinued participation in the study and other genotypes of HCV.

The study was based on the ethical principles of Helsinki, and was approved by the ethics committee of Mashhad University of Medical Sciences, Iran (No: 922662). All participants completed and signed an informed consent form before the start of the study. Trial registration:, NCT02216045.

3.2. Randomization and Masking

The researchers used a computer-generated randomization sequence. Patients were randomly allocated with a 1:1 ratio to 2 groups (with a block size of 4) by a centralized computer algorithm. This was an open-label clinical trial, so patients and investigators were not masked for treatment allocation.

3.3. Procedures

Among the trial patients with chronic HCV infection, there were 2 groups: Group A was the control group and received Peg IFN/RBV, and Group B was the intervention group and received CM + Peg IFN/RBV for 24 weeks. Oral consumption of CM 2 times, at 8:00 am and 20:00 am with 250 cc per serving was prescribed. Furthermore, Peg IFN and RBV with a standard dose were given. Subcutaneous injections of 180-mg of pegylated IFNa-2a (Pegasys; F. Hoffman-LaRoche) and daily weight-based oral ribavirin (Copegus; F. Hoffman-LaRoche) were also administered. Camel milk was collected from the Livestock company of Iran, and packaged in sterile bottles and then transported in cool boxes to the research center.

The primary efficacy outcomes were early virologic response (EVR12: HCV RNA ≥ 2 log10 on week 12) and end-of-treatment virologic response (ETR24: undetectable HCV RNA on week 24). Secondary efficacy outcomes were sustained virological response (SVR24: HCV RNA undetectable during week 48). Plasma HCV RNA was analyzed using quantitative Real Time-Polymerase Chain Reaction (RT-PCR) the Roche COBAS TaqMan HCV Test (v2.0). Results are expressed in copies/mL and indicate the activity of HCV and virus replication in the patient.

Safety data was collected at the beginning and end of treatment. Criteria for the side effects used “common terminology criteria for adverse events v4.0 (CTCAE)”. The data adverse events included history and physical examination, clinical laboratory tests and electrocardiogram.

3.4. Statistical Analysis

The sample size was estimated as 45 considering probable patient loss (α type error of 0.05 and β error of 0.20 on the assumption of 65% SVR24 in group A and of 90% SVR24 in group B) and formula

Equation 1.

Data were analyzed by the SPSS software (version 16). Data were expressed as mean ± standard deviation (SD). Some variables did not have a normal distribution thus the nonparametric method was used. Friedman, Mann-Whitney, and Wilcoxon test were used for analysis. P < 0.05 was considered as statistically significant.

4. Results

From June, 2014 to February, 2015, 75 patients were referred to 2 liver treatment centers (governmental) in Iran, and after screening, 45 patients were enrolled in the study. Thirty patients did not meet the study inclusion criteria for reasons of out of range age (no = 5), cirrhosis (no = 10), severe heart disease (no = 5), active drug abuse (no = 5), hyperthyroidism (no = 4), declined to participation (no = 2), and no [email protected] genotype virus (no = 2). All patients except 5 completed the treatment for reasons of loss to follow-up (no = 3) and adverse events (no = 2) (Figure 1). Baseline characteristics of patients in the 2 groups was similar and there was no difference in distribution (Table 1). The EVR12 of the intervention group was 60% and for the control group, this was 15%. The EVR24 in intervention group was 90%, and in the control group, this was 70%. The response of the intervention group was 20% higher than the control group. The analysis of results showed a significant reduction in viral load in each group (P < 0.05). The SVR24 in the intervention group was 100% (18/18) and in the control group, this was 71% (10/14). Comparison of the 2 groups showed the difference was significant (P < 0.05) (Table 2).

Table 1. Demographic, Biochemical, Serological, and Molecular Profile of Patients with Chronic Hepatitis C at Baseline
CharacteristicsCM + PegIFN/RBVPegIFN/RBVP Value
Demography No. (M/F)20 (14/6)20 (14/6)P > 0.05b
Body weight (kg)a78.65 (± 4.68)78 (± 6.49)P > 0.05c
Mean age (yr.)a47.50 (± 10.62)49.50 (± 10.14)P > 0.05c
Risk factor for transmissionP > 0.05c
Transfusion-related01 (5)
Intravenous drug abuse, No. (%)10 (50)10 (50)
Other (sexual, tattoo, occupational), No. (%)3 (15)1 (5)
Unknown, No. (%)7 (35)8 (40)
ALT, U/L106.35 (± 40.97)122.25 (± 40.99)P > 0.05c
AST, U/L92.35 (± 27.09)113.55 (± 30.59)P > 0.05c
Anti-HIV-1 and -200-
MolecularP > 0.05c
HCV genotype (2; 3)3; 175; 15
Pretreatment HCVP > 0.05b
RNAa,e, 106 copies/mL2.60 (± 3.42)2.43 (± 4.10)

aValues are expressed as mean (± SD).

bFisher’s exact test.

cChi-Square test.

dNormal reference ranges: 4 to 23 U/L for ALT, 6 to 18 U/L for AST, 3.4 to 20.5 mmol/L.

eRNA :106 copies/Ml.

Table 2. Virologic and Biochemical Responses during Treatment and End of Treatment (Week 12, 24, and 48)a
Time of StudyCM + Peg IFN/RBV No. (%)Peg IFN/RBV, No. (%)P Valuea
Virologic Response
Wk. 12 (CEVR12)12 (60)3 (15)P > 0.05
Wk. 24 (ETR24)18 (90)14 (70)P > 0.05
WK. 48 (SVR24)18/18 (100)10/14 (71)P < 0.05
Biochemical Response (ALT)
Wk. 1213 (65)15 (75)P > 0.05
Wk. 2419 (95)17 (85)P > 0.05
Biochemical Response (AST)
Wk. 1216 (80)5 (30)P < 0.05
Wk. 2419 (95)14 (70)P > 0.05

aChi-Square test (compare the two groups).

4.1. Safety and Tolerability

No patients discontinued treatment due to adverse events in the intervention group, yet 2 patients in the control group (8.7%; 2 out of 23) discontinued treatment due to a serious adverse event, including severe depression (1 patient) and hyperthyroidism (1 patient). In both groups some patients experienced a degree of loss of appetite, insomnia, fatigue and depression, yet at the end of treatment, these complaints changed in both groups. At the end of treatment, in the intervention group complaints of appetite, insomnia, and fatigue had improved, yet they had increased in the control group. Some decrease in white blood cells, platelets, and hemoglobin were observed in both groups (Table 3).

Table 3. Rates of Discontinuation of Treatment, Dose Reductions, and Adverse Events during Treatmenta
Adverse EventCM + PegIFN/RBV First of TreatmentCM + PegIFN/RBV End of TreatmentP ValuebPegIFN/RBV First of TreatmentPegIFN/RBV End of TreatmentP Valueb
Discontinuation of treatment for adverse event-0--2-
Dose reductions-0--0-
Adverse Events
Fatigue7/20 (35)6/13 (30)0.0106/20 (30)10/20 (50)P > 0.05
Insomnia4/20 (20)3/20 (15)0.5642/20 (10)7/20 (35)P < 0.05
Depression4/20 (20)5/20 (25)0.7054/20 (20)7/20 (35)P < 0.05
Loss of appetite11/20 (55)4/20 (20)0.70510/20 (50)12/20 (60)P < 0.05
Laboratory Abnormalities
Hemoglobin, < 12 g/dL0/202/20 (10.0)0.1570/208/20 (40)P < 0.05
Platelet, < 120000 cells / mm30/203/20 (15.0)0.8300/207/20 (35)P < 0.05
White blood cell, < 4000 cells / mm30/206/20 (30.0)0.0140/208/20 (40)P < 0.05

aValues are expressed as No. (%).

bWilcoxon test (compare the intergroup).

5. Discussion

The results presented here indicate that 24 weeks of 250 cc of CM twice a day with Peg IFN/RBV achieved EVR12, ETR24, and SVR24 of 60%, 90%, and 100%. Peg IFN/RBV achieved EVR12, ETR24, and SVR24 of 15%, 70%, and 71%. Higher levels of ETR24 and SVR24 could be attributed to differences in immunity status between various populations. All of the patients were white Iranians, therefore, race had no impact on the results of the current study.

Patients with viral load of < 2 × 106 Copy/mL showed better therapeutic responses, yet in the current study no significant correlation was found between viral load and therapeutic response due to the normal distribution of the 2 groups, and mean viral loads were higher than 2600771.25 in the case and 2438350 in the control group (higher than 2 × 106 Copy/mL).

Consumption of alcohol is associated with lower therapeutic response. In the current sample, alcohol intake was not common and alcohol intake in both groups was excluded. It seems that the mean age of the patients (< 50 years) in the current study was another reason for higher therapeutic response. However, due to the normal distribution, age had no significant effect on the results.

Receiving a proper dose of ribavirin is effective in treatment response. In the current study, 25% of the patients in both groups were over 75 kg and received a full dosage. With observing the appropriate dosage and normal distribution of the patients in both groups, weight had no confounding effect on the outcome.

Another probable reason for stronger response to the treatment could be attributed to the use of CM. Camel immunoglobulins are secreted in the blood and then into milk, and it is known as a substance that empowers the immune system (13).

Several studies reported the protective and therapeutic effects of camel milk on the liver of mice exposed to carbon tetrachloride (14), alcohol (15), and gentamicin (16). In all cases, normalization of liver enzymes and recovery of live tissue has been accessed. Therefore, decreased aspirate aminotransferase (AST) and Alanine Transferase (ALT) is associated with the ability of camel milk to protect the structural integrity of the hepatocytes and to recover the damaged hepatocytes.

Redwan et al. (2014) showed that camel milk’s lactoferrin might be one of the main components of CM that has anti-viral properties. They also stated that camel milk’s lactoferrin is much more efficient than lactoferrin from human and cow’s milk, which prevents the HCV to enter leukocytes and human HepG2 cells (17, 18). El-Fakharany from Egypt (2012) showed that camel milk polyclonal antibody has destructive viral peptides and growth inhibitory effects yet human immunoglobulin and casein have not been affected (19).

Yalin Liao et al. (2012) showed the inhibitory effect of native and recombinant lactoferrin of camel milk on HCV infection on the Huh7.5 cells. This study suggests that lactoferrin prevents the entry of virus in the cell through direct interaction with HCV and inhibition of virus amplification (20). The current results are also consistent with the findings of a study by Seher Abbas et al. (2014) that explored the potential of camel milk on blood parameters and liver function of patients with hepatitis. Similar to the current study, ALT, AST, and ALP levels were reduced and inhibited the reduction of platelets, white blood cells, and hemoglobin (21).

In a human study on hepatitis B, it was shown that taking CM improves cellular immunity and interferon level, and inhibits viral proliferation, resulting in greater improvement in chronic hepatitis B patients (22). In another human study on 25 patients with HCV in Egypt, in was shown that drinking CM for 60 days as an adjunctive therapy to the standard treatment of PEG/RBV significantly elevated the serum levels of albumin, ant apoptotic protein BCL-2, total antioxidant capacity, interleukin-10, and vitamin D (P < 0.001) (23).

Furthermore, CM, as a supplement food, containing the substances required for the body, is an effective element in therapeutic response improvement. Results of a study conducted on 31 patients to investigate the role of vitamin D, suggested that the intake of 2000 units of vitamin per day, significantly decreased AST enzyme and viral load. According to this study, deficiency of vitamin D effects the response to treatment; therefore, vitamin D supplementation could contribute to better responses (24). Vitamin content of camel milk could play a role in response improvement. Results reported that camel milk contained higher levels of B2, C, D, and niacin (5).

The current study is consistent with Al-Hashem et al.’s (2009) report that addressed the role of camel milk in rates of exposure to aluminum chloride, a substance that destructs red blood cells and hemoglobin and leads to hematocrit reduction. In this study, daily consumption of CM for 30 days effectively increased the number of red blood cells and corrected hemoglobin and hematocrit level (25).

The strength of this study was the use of natural acceptable food with conventional treatment and the limitation of this study was the low number of patients. Results suggested that the therapeutic response of pegylated interferon alfa-2a and ribavirin was acceptable, however, camel milk could be used to increase therapeutic response and decrease complications. Camel milk is recommended as a safe complementary therapy that could be added to standard antiviral drugs to increase their safety and effectiveness in CHC.




  • 1.

    Aghemo A, Dore GJ, Hatzakis A, Wedemeyer H, Razavi H. Estimating HCV disease burden - volume 3 (editorial). J Viral Hepat. 2015; 22 Suppl 4 : 1 -3 [DOI][PubMed]

  • 2.

    Alfaleh FZ, Nugrahini N, Maticic M, Tolmane I, Alzaabi M, Hajarizadeh B, et al. Strategies to manage hepatitis C virus infection disease burden - volume 3. J Viral Hepat. 2015; 22 Suppl 4 : 42 -65 [DOI][PubMed]

  • 3.

    Taherkhani R, Farshadpour F. Epidemiology of hepatitis C virus in Iran. World J Gastroenterol. 2015; 21(38) : 10790 -810 [DOI][PubMed]

  • 4.

    Guidelines for the Screening, Care and Treatment of Persons with Hepatitis C Infection. 2014; [PubMed]

  • 5.

    Zibaee S, Hosseini SM, Yousefi M, Taghipour A, Kiani MA, Noras MR. Nutritional and Therapeutic Characteristics of Camel Milk in Children: A Systematic Review. Electron Physician. 2015; 7(7) : 1523 -8 [DOI][PubMed]

  • 6.

    Corouge M, Pol S. New treatments for chronic hepatitis C virus infection. Med Mal Infect. 2011; 41(11) : 579 -87 [DOI][PubMed]

  • 7.

    Coon JT, Ernst E. Complementary and alternative therapies in the treatment of chronic hepatitis C: a systematic review. J Hepatol. 2004; 40(3) : 491 -500 [DOI][PubMed]

  • 8.

    Arab HH, Salama SA, Eid AH, Omar HA, Arafa el SA, Maghrabi IA. Camel's milk ameliorates TNBS-induced colitis in rats via downregulation of inflammatory cytokines and oxidative stress. Food Chem Toxicol. 2014; 69 : 294 -302 [DOI][PubMed]

  • 9.

    el Agamy EI, Ruppanner R, Ismail A, Champagne CP, Assaf R. Antibacterial and antiviral activity of camel milk protective proteins. J Dairy Res. 1992; 59(2) : 169 -75 [PubMed]

  • 10.

    Korish AA. The antidiabetic action of camel milk in experimental type 2 diabetes mellitus: an overview on the changes in incretin hormones, insulin resistance, and inflammatory cytokines. Horm Metab Res. 2014; 46(6) : 404 -11 [DOI][PubMed]

  • 11.

    Alhaider AA, Abdel Gader AG, Almeshaal N, Saraswati S. Camel milk inhibits inflammatory angiogenesis via downregulation of proangiogenic and proinflammatory cytokines in mice. APMIS. 2014; 122(7) : 599 -607 [DOI][PubMed]

  • 12.

    Almahdy O, El-Fakharany EM, El-Dabaa E, Ng TB, Redwan EM. Examination of the activity of camel milk casein against hepatitis C virus (genotype-4a) and its apoptotic potential in hepatoma and hela cell lines. Hepat Mon. 2011; 11(9) : 724 -30 [DOI][PubMed]

  • 13.

    Korashy HM, Maayah ZH, Abd-Allah AR, El-Kadi AO, Alhaider AA. Camel milk triggers apoptotic signaling pathways in human hepatoma HepG2 and breast cancer MCF7 cell lines through transcriptional mechanism. J Biomed Biotechnol. 2012; 2012 : 593195 [DOI][PubMed]

  • 14.

    Yadav AK, Kumar R, Priyadarshini L, Singh J. Composition and medicinal properties of camel milk: A review. Asian J Dairy Food Res. 2015; 34(2) : 83 -91 [DOI]

  • 15.

    Althnaian T, Albokhadaim I, El-Bahr SM. Biochemical and histopathological study in rats intoxicated with carbontetrachloride and treated with camel milk. Springerplus. 2013; 2(1) : 57 [DOI][PubMed]

  • 16.

    Darwish HA, Abd Raboh NR, Mahdy A. Camel's milk alleviates alcohol-induced liver injury in rats. Food Chem Toxicol. 2012; 50(5) : 1377 -83 [DOI][PubMed]

  • 17.

    Al-Asmari AK, Abbasmanthiri R, Al-Elewi AM, Al-Omani S, Al-Asmary S, Al-Asmari SA. Camel milk beneficial effects on treating gentamicin induced alterations in rats. J Toxicol. 2014; 2014 : 917608 [DOI][PubMed]

  • 18.

    Redwan EM, El-Fakharany EM, Uversky VN, Linjawi MH. Screening the anti infectivity potentials of native N- and C-lobes derived from the camel lactoferrin against hepatitis C virus. BMC Complement Altern Med. 2014; 14 : 219 [DOI][PubMed]

  • 19.

    El-Fakharany EM, Sanchez L, Al-Mehdar HA, Redwan EM. Effectiveness of human, camel, bovine and sheep lactoferrin on the hepatitis C virus cellular infectivity: comparison study. Virol J. 2013; 10 : 199 [DOI][PubMed]

  • 20.

    Liao Y, El-Fakkarany E, Lonnerdal B, Redwan EM. Inhibitory effects of native and recombinant full-length camel lactoferrin and its N and C lobes on hepatitis C virus infection of Huh7.5 cells. J Med Microbiol. 2012; 61 : 375 -83 [DOI][PubMed]

  • 21.

    Abbas S, Imran R, Nazir A, Qamar MF, Sarfraz L. Effect of camel milk supplementation on blood parameters and liver function of hepatitis patients. Am J Ethnomed. 2014; 1(3) : 129 -46

  • 22.

    Saltanat H, Li H, Xu Y, Wang J, Liu F, Geng XH. [The influences of camel milk on the immune response of chronic hepatitis B patients]. Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2009; 25(5) : 431 -3 [PubMed]

  • 23.

    Mohamed WA, Schaalan MF, El-Abhar HS. Camel Milk: Potential Utility as an Adjunctive Therapy to Peg-IFN/RBV in HCV-4 Infected Patients in Egypt. Nutr Cancer. 2015; 67(8) : 1305 -13 [DOI][PubMed]

  • 24.

    Eltayeb AA, Abdou MA, Abdel-aal AM, Othman MH. Vitamin D status and viral response to therapy in hepatitis C infected children. World J Gastroenterol. 2015; 21(4) : 1284 -91 [DOI][PubMed]

  • 25.

    Al-Hashem F, Dallak M, Bashir N, Abbas M, Elessa R, Khalil M, et al. Camel's milk protects against cadmium chloride induced toxicity in white albino rats. Am J Pharmacol Toxicol. 2009; 4(3) : 107 -17 [DOI]