Journal of Clinical and Cellular Immunology

Journal of Clinical and Cellular Immunology
Open Access

ISSN: 2155-9899

+44 1223 790975

Research Article - (2014) Volume 5, Issue 3

To Compare the Safety, Efficacy and Quality of Life in Patients with Allergic Rhinitis Treated with Levocetirizine and Desloratadine

Divya Chawla1, Amandeep Singh2*, Manish Gupta3, Prithpal S Matreja4 and Khanna P M L4
1Gian Sagar Medical College and Hospital, Village Ram Nagar, District Patiala, Punjab-140601, India
2Department of Pharmacology, Shri Guru Ram Rai Institute of Medical and Health Sciences, Patel Nagar, Dehradun, Uttarakhand- 248001, India
3Department of ENT, ian Sagar Medical College and Hospital, Village Ram Nagar, District Patiala, Punjab-140601, India
4Department of Pharmacology, Gian Sagar Medical College and Hospital, Village Ram Nagar, District Patiala, Punjab-140601, India
*Corresponding Author: Dr. Amandeep Singh, Associate Professor, Department of Pharmacology, Shri Guru Ram Rai Institute of Medical and Health Sciences, Patel Nagar, Dehradun, Uttarakhand– 248001, India, Tel: +91-135 - 2522184, +91-9876102154 Exn. +91-9634172016, Fax: +91-135-2720151 Email:

Abstract

Background: Allergic Rhinitis (AR) is a very common disease that affects almost 10-30% of the world’s population. Second-generation H1 antihistaminics are the preferred drugs for treatment of patients with AR. Levocetirizine and desloratadine are commonly prescribed newer non-sedating second-generation antihistaminics. Various studies show no difference in efficacy and quality of life (QOL) between the two drugs desloratadine and levocetirizine and that the drugs are quiet safe; however, some studies show negative impact on patients’ QOL with these drugs. Studies comparing the two drugs were insufficient in India; hence, this study was designed to evaluate and compare the efficacy, safety and QOL of patients with AR, following treatment with levocetirizine or desloratadine, in the Indian scenario.
Methods: This 2-month randomized, prospective study was performed in 60 patients with AR visiting the department of Otorhinolaryngology. Patients were randomized into one of the two treatment groups, and prescribed levocetirizine 5 mg once daily for two weeks or desloratadine 5 mg once daily for two weeks. The outcome measures for the severity of AR symptoms used were Total Nasal Symptom Score (TNSS); and QOL was assessed using Rhinoconjunctivitis Quality of Life Questionnaire (RQLQ) Score.
Results: Data from 54 patients who completed the study shows that both levocetirizine and desloratadine significantly (p<0.05) improved the AR symptoms and QOL at the end of 2 weeks study period, analyzed using TNSS and RQLQ scores, respectively. However, statistically non-significant differences in analysis of TNSS score between levocetirizine and desloratadine showed that the two drugs may be equally effective in patients with AR, with patients on levocetirizine showing slightly better response. The adverse events were low in patients on levocetirizine and no adverse event was seen with desloratadine. At baseline visit, rhinorrhoea was the most common and severe symptom, whereas nasal itching was the least common and severe symptom.
Conclusion: Study findings showed that both levocetirizine and desloratadine were equally effective in patients with AR, however, desloratadine group showed better safety profile. The drugs were safe and well tolerated.

Keywords: Allergic rhinitis, Levocetirizine, Desloratadine, Efficacy, Tolerability, QOL, TNSS, RQLQ

Introduction

Systemic Lupus Erythematosus (SLE) is a systemic autoimmune disease which can cause multiple organ damage [1]. Studies carried out in different countries suggest significant variation in the survival rate of patients with SLE. Previous study reported that five-year survival rates of SLE patients in Cipto Mangukusumo hospital Indonesia was 88% from 108 SLE patients within 1990-2002 [2]. The high rates of morbidity and mortality of SLE patients is caused by the disease process or its complications. One of the long term complications in SLE is a high prevalence of premature osteoporosis. The incidence of osteoporosis in SLE patients occurs at an early onset, at an average age of 39 years [3]. It caused by prolong systemic glucocorticoids usage, chronic inflammatory processes, and metabolic factors such as homocysteine [4]. Homocysteine is a metabolic factor that associated with inflammatory diseases. Low levels of folic acid, vitamin B12, and vitamin B6 could be the reason for high homocysteine levels, because both are intrinsically involved in the metabolism of homocysteine [5,6]. Recent studies found that high levels of homocysteine was associated with decreased bone mass density and an early onset of osteoporosis [7,8]. Experimental data suggest that high homocysteine levels affect both osteoclasts and osteoblasts activity [9]. And their activities can be seen by measuring the chemical markers of bone metabolism.

The other mechanism of osteoporosis in SLE patient is stress oxidative. In an inflammatory condition, the activation of macrophage cause oxidation of lipid which is lead to the production of free radical and stress oxidative [10]. The condition of stress oxidative can be measured by calculating the level of malondialdehyde (MDA) which is the end product of lipid peroxidation. Free radicals such as reactive oxygen species (ROS) can stimulate osteoclastogenesis by causing receptor activator of NF-κB ligand (RANKL) expression on osteoblast. This RANKL expression can activate the precursor of osteoclast, macrophage-colony stimulating factor (M-CSF) to differentiate [11].

The aim of this study was to determine the association between homocysteine and biochemical parameters of bone metabolism in patients with SLE. Moreover, serum folic acid, vitamin B6, vitamin B12, MDA, and RANKL level were studied to investigate the correlation with high levels of homocysteine.

Subjects and Methods

Subjects

Thirty-nine female with SLE meeting the American College of Rheumatology 1997 criteria for SLE, aged 16-47 years, SLEDAI score >5, disease duration 2 months-96 months, average consumption of steroids (Methylprednisolone <50 mg/day), and use at least one type of immunosupresant agent were studied after giving informed consent. SLE patients who are pregnant or breast-feeding, anemia, cancer, impaired kidney function, using hormone replacement therapy, consume folic acid and vitamin B supplements, anticonvulsants agent, carbamazepine, phenytoin, xanthopterin, tamoxifen, and theophylline were excluded from the study. Subjects were obtained from Rheumatology Clinic of Dr. Saiful Anwar Hospital, Malang, Indonesia. Twelve healthy, age matched premenopausal women (medical students, resident, and healthy blood donors from the same geographical area) were studied as a control group after giving informed consent. This study used an observational analytic cross sectional approach and it was conducted in March 2012 to October 2012.

Blood sample collection

5 cc of venous blood samples were collected in test tube with aseptic precautions. After 1 h of collections, sample was centrifuged at 3000 rpm for 5 min. Serum was separated and collected in polythene tube with cork. The sera with no sign of hemolysis was stored in tubes at temperature of -70°C for further analysis.

Biochemical analysis

Various laboratory parameters including serum homocysteine, folic acid, vitamin B6, vitamin B12, bCTx, osteocalcin, and RANKL were measured by enzyme-linked immunosorbent assay (ELISA) method. The following parameters were measured by commercial ELISA Kit: homocysteine (NovaTeinBio Human ELISA Kit Total Hcy), folic acid (NovaTeinBio Human ELISA Kit Folic Acid), vitamin B6 (NovaTeinBio Human ELISA Kit Vit B6), vitamin B12 (Vit B12 NovaTeinBio Human ELISA Kit), bCTx (Cusabio bCTx Human ELISA Kit), osteocalcin (NovaTeinBio Human ELISA Kit Osteocalcin), and RANKL (NovaTeinBio Human ELISA Kit RANKL). The level of MDA was measured by Thiobarbituric Acid Reactive Substance (TBARS) method.

Statistical analysis

Statistical analysis was performed by SPSS for Windows version 16. Numerical variables were reported in terms of mean and standard deviation. In this analysis, variables showing p-value less than 0.05 were considered to be statistically significant respectively. Pearson correlation test was used to test the correlation.

Results

For every patient, data were recorded on age, SLE disease activity index (SLEDAI) scores, disease duration, glucocorticoid dose, immunosuppressant agent, and current clinical manifestations (Table 1).

Characteristics Group A (Levocetirizine 5 mg) Group B (Desloratidine 5 mg)
No. of patients 27 27
Age in years (Mean ± SD) 35.96 ± 14.31 32.33 ± 11.49
Male/ Female 13 (48.15%)/14 (51.85%) 10 (37.04%)/17 (62.96%)
TNSS 7.37 ± 0.93 7.11 ± 1.16
RQLQ score 4.17 ± 0.5 ± 0.63

Table 1: Demographic and clinical characteristics of the two treatment groups at baseline visit.

The mean age was 30 years with a range from 16 to 47 years and the mean disease duration was 26 months with a range from 2 to 96 months. At the time of the study most SLE patients had only mild disease activity as indicated by SLEDAI 6 – 26. All of the SLE patients were recieved corticosteroid therapy with the mean glucocorticoid dose was 26 mg/day with a range 4 – 48 mg/day. Nineteen SLE patients were received immunosuppresant agents. The most frequent disease manifestations were renal disorder, malar rash, and arthritis.

The mean levels of homocysteine, bCTx, osteocalcin, folic acid, vitamin B6, vitamin B12, RANKL, and MDA in SLE patient and control group were described in Table 2.

Treatment groups Baseline TNSS TNSS at the end of 2-week study Mean change from baseline Mean percentage change from baseline Statistical analysis
Group A (Levocetirizine 5 mg) 7.37 ± 0.93 4.96 ± 0.90 -2.41 ± 0.80 - 32.7% p<0.001, highly significant
Group B (Desloratidine 5 mg) 7.11 ± 1.16 5.37 ± 0.79 -1.74 ± 0.80 - 24.5% p<0.001, highly significant

Table 2: Changes in TNSS among the treatment groups over the study period.

This study found that significantly higher levels of homocysteine were found in SLE patients (p=0.010). There was also a significantly higher level of MDA and RANKL in SLE patient (p=0.042, p=0.030). But folic acid, vitamin B6, vitamin B12, bCTX, and osteocalcin levels were not statistically different between SLE patients and control group.

The correlation between parameters was observed only in SLE patients. From the correlation analysis we found that there were positive and significant correlation was observed between serum level of homocysteine and bCTx (p=0.000, r=0.943). Another positive and significant correlations were also found between serum level of homocysteine and MDA (p=0.002, r=0.731). And this level of MDA has significant and positive correlation with RANKL (p=0.000, r=0.758).

Negative and significant correlations were observed between homocysteine and osteocalcin (p=0.000, r=-0.771), homocysteine and folic acid (p=0.000, r=-0.734), and homocysteine and vitamin B6 (p=0.046, r=-0.332). But an insignificant relationship was found between serum homocysteine and vitamin B12 (p=0.080, r=-0.284) (Table 3).

Treatment groups Baseline RQLQ RQLQ at the end of 2-week study Mean change from baseline Mean percentage change from baseline Statistical analysis
Group A (Levocetirizine 5 mg) 4.17 ± 0.5 3.59 ± 0.33 - 0.58 ± 0.31 - 13.91% p<0.001, highly significant
Group B (Desloratidine 5 mg) 4.27 ± 0.63 3.76 ± 0.49 - 0.50 ± 0.29 - 11.71% p<0.001, highly significant

Table 3: Changes in RQLQ over the treatment period.

Discussion

Our finding suggest that levels of serum homocysteine are higher in SLE patients than in age-matched healthy female. Elevated levels of homocysteine in patients with SLE also reported in several researches [12-14]. Homocysteine are regulated by a number of coenzymes and cofactors that required for homocysteine metabolism, such as folic acid, vitamin B6, and vitamin B12. Increased homocysteine levels in SLE patients are caused by a chronic inflammation and abnormal immune response leading to decrease of several vitamins. In SLE patients, the inflammatory process triggered by the presence of autoantibodies that induce further inflammatory reaction resulted in tissue damage [4]. Activation of immune cells, particularly macrophages, will produce Reactive Oxygen Species (ROS) which cause the oxidation of folic acid, vitamin B6, and B12 [15]. In addition, the inflammatory process also increase the proliferation of immune cells that would lead to an increased turnover of folic acid, vitamin B6, and B12 [16]. Both are thought to be the cause of decreased levels of folic acid, vitamin B6, and B12 in inflammatory conditions. In this study, there are no significantly different of folic acid, vitamin B6, vitamin B12 level between SLE patients and control group. But the need of these vitamins is increase in SLE patients because increase of turnover and homocysteine metabolism [17].

Several studies showed that high levels of homocystein were associated with decreased bone mass density and early onset of osteoporosis [7]. Other studies mentioned that high levels of homocystiene and low levels of folic acid were associated with decreased bone mass density, whereas levels of vitamin B6 and vitamin B12 had no significant effect [8]. Elshorbagy et al. reported that decrease of vitamin B12 and folate levels contribute to increased osteoclast activity which was characterized by high levels of biochemical markers of bone resorption, whereas there was no effect of vitamin B6 [18]. In our study, a positive and significant correlation was observed between serum homocysteine and bCTx, whereas a negative and significant relationship was found between serum homocysteine and osteocalcin. It means that homocysteine contributes to the increase of bone resorption and decrease of bone formation process.

Recent studies tried to understand the mechanisms regarding the role of homocyteine, folic acid, vitamin B6, and vitamin B12 on bone metabolism. Homocysteine auto-oxidation results in increased production of intracellular ROS and stimulates p38 MAPK activation which influence the differentiation of osteoclast precursor cells [16]. Homocysteine also induces activation of RANK, a receptor for RANKL, which is a key element in the process of osteoclast differentiation [19]. There was positive and significant correlation between homocysteine level and MDA in this study. And this MDA level has positive and significant correlation with RANKL. Our result implicated that homocysteine cause an increase production of intracellular ROS that influences osteoclast differentiation through ROS-RANKL pathway.

In this study we also found a negative correlation between homocysteine and osteocalcin. It indicates that the high level of homocysteine cause decrease of osteoblast activity. Kim et al. reported that homocysteine induces apoptosis of human bone marrow stromal cells via caspase-dependent pathway [20]. The intrinsic apoptotic signals derived from DNA damage and ROS production also induced by accumulation of homocysteine [21]. In a study conducted by Park et al., reported that homocysteine induces osteoblast cell apoptosis through endoplasmic reticulum stress [22]. Other studies shown that homocysteine weaken collagen crosslink's and in large amounts it can interfere bone remodeling process [6,23].

The levels of osteocalcin were slightly more in SLE patients. Serum OC is considered a specific marker of osteoblast function, as its levels have been shown to correlate with bone formation rates. However, since it is also released from bone matrix during bone resorption, it reflects the overall turnover of bone and is considered as a bone turnover marker. In a higher activity of bone resorption such as in SLE patient, our body responds by increasing osteoclast activity to balance bone remodeling process [24]. Some studies report that there were increasing serum osteocalcin levels in postmenopausal women with osteoporosis [25-27]. So, this theory is explaining the slightly increasing of OC level in our study. Besides that, OC has a high affinity for calcium and has a compact a helical conformation. The carboxyglutamic acid (Gla) residues of OC are capable of binding to bone matrix hydroxyapatite, thus leading to bone mineralization. Osteoporotic patient may have a decreased rate of bone mineralization due to the reduction in hydroxyapatite crystal formation. In this condition, free OC may be present in the circulation, thus explaining the increased serum OC concentration in osteoporotic patient [28].

Elevated level of homocysteine in SLE patients also produce high levels of inflammatory mediators which induces thrombosis of small blood vessels, and a low level of other angiogenic factors. It causes cellular necrosis of a number of osteocytes, followed by localized to bone demineralization. Ongoing inflammation in these localized areas will diminish vascular supply on the osteoblast precursors that available to replace bone demineralization. The longer it will experience a loss of bone fracture in the weakened bone [29]. That is why osteoporosis occurs earlier in patients with SLE.

Osteoporosis in SLE patient also influenced by several kinds of drugs, such as glucocorticoids and immunosuppressants. All the subjects who contributed in this study are consuming glucocorticoids with average dose 26.87 mg/day. Approximately half of the patients who contribute to this research using immunosuppressant drugs, such as methotrexate, azathioprin, chloroquine, cyclophosphamide and mycophenolat mofetil. Among those immunosuppressants, methotrexate has the influence in decreasing bone mineral density. Study of Raghu Nadhanan et al. found that low dose of methotrexate can increase the risk of osteopenia [30]. But, other immunosuppressants such as Azathioprin, Chloroquine, Cyclophosphamide and Mycophenolat mofetil have no interference in bone mass density [31-33].

To diagnose osteoporosis we can use several methods, such as biochemical markers of bone turnover including bone formation and bone resorption. Of all the biochemical markers of bone turnover, the ones most commonly used in clinical practice are bone-specific alkaline phosphatase (BSAP), osteocalcin (OC), N-telopeptide of collagen cross-links (NTx), and C-telopeptide of collagen cross-links (CTx) [34]. Plain radiographic findings can suggest the presence of osteopenia, bone loss, or if a fracture is suspected, but they cannot be used to diagnose osteoporosis. Dual-energy X-ray Absorptiometry (DXA) is currently the criterion standard for the evaluation of bone mineral density (BMD). Compared to imaging techniques, assays for biochemical markers of bone turnover are safe, cheap, easily performed, and can detect early changes in bone metabolism [35]. In this study, we use bCTX and RANKL as bone resorption marker and Osteocalcin as bone formation marker. But, for further study we suggest to do BMD measurement to confirm the correlation.

Conclusions

Our results implicate several clinical consequences. Firstly, the high level of homocysteine was found in SLE patients. Secondly, homocysteine influences bone formation and bone resorption process which lead to bone diminution in SLE patients. In our study, we cannot conclude that giving supplementation of folic acid, B6, B12, and other antioxidant could prevent osteoporosis due to insignificant result.

Acknowledgements

The authors thank the Dean of Medical Faculty Brawijaya University Malang through Development Unit Medical Faculty of Brawijaya University Malang for providing fund to this research. We also gratefully acknowledge Prof. DR. M.D. Handono Kalim, a Rheumathologist, as a consultant of this research and for SLE patients and all those who were involved in this research.

Funding

This research was funded by Development Unit at the Medical Faculty Brawijaya University Malang, East Java-Indonesia. We certify that there is no conflict of interest with any financial organization regarding the material discussed in the manuscript.

References

  1. Pawankar R, Canonica GW, Holgate ST, Lockey RF (2011) White Book on Allergy 2011-2012 Executive Summary. World Health Organization.
  2. Bousquet J, Khaltaev N, Cruz AA, Denburg J, Fokkens WJ, et al. (2008) Allergic Rhinitis and its Impact on Asthma (ARIA) 2008 update (in collaboration with the World Health Organization, GA(2)LEN and AllerGen). Allergy 63 Suppl 86: 8-160.
  3. Gergen PJ, Turkeltaub PC (1992) The association of individual allergen reactivity with respiratory disease in a national sample: data from the second National Health and Nutrition Examination Survey, 1976-80 (NHANES II). J Allergy Clin Immunol 90: 579-588.
  4. Pradalier A, Neukirch C, Dreyfus I, Devillier P (2007) Desloratadine improves quality of life and symptom severity in patients with allergic rhinitis. Allergy 62: 1331-1334.
  5. Bachert C (2001) Decongestant efficacy of desloratadine in patients with seasonal allergic rhinitis. Allergy 56 Suppl 65: 14-20.
  6. Canonica GW, Bousquet J, Mullol J, Scadding GK, Virchow JC (2007) A survey of the burden of allergic rhinitis in Europe. Allergy 62 Suppl 85: 17-25.
  7. Woods L, Craig TJ (2006) The importance of rhinitis on sleep, daytime somnolence, productivity and fatigue. Curr Opin Pulm Med 12: 390-396.
  8. Nathan RA (2007) The burden of allergic rhinitis. Allergy Asthma Proc 28: 3-9.
  9. Crystal-Peters J, Crown WH, Goetzel RZ, Schutt DC (2000) The cost of productivity losses associated with allergic rhinitis. Am J Manag Care 6: 373-378.
  10. Schoenwetter WF, Dupclay L Jr, Appajosyula S, Botteman MF, Pashos CL (2004) Economic impact and quality-of-life burden of allergic rhinitis. Curr Med Res Opin 20: 305-317.
  11. Hansen J, Klimek L, Hörmann K (2005) Pharmacological management of allergic rhinitis in the elderly: safety issues with oral antihistamines. Drugs Aging 22: 289-296.
  12. Bachert C, Bousquet J, Canonica GW, Durham SR, Klimek L, et al. (2004) Levocetirizine improves quality of life and reduces costs in long-term management of persistent allergic rhinitis. J Allergy Clin Immunol 114: 838-844.
  13. Ciebiada M, Ciebiada MG, Kmiecik T, DuBuske LM, Gorski P (2008) Quality of life in patients with persistent allergic rhinitis treated with montelukast alone or in combination with levocetirizine or desloratadine. J Investig Allergol Clin Immunol 18: 343-349.
  14. Lee CF, Sun HL, Lu KH, Ku MS, Lue KH (2009) The comparison of cetirizine, levocetirizine and placebo for the treatment of childhood perennial allergic rhinitis. Pediatr Allergy Immunol 20: 493-499.
  15. Potter PC, Bailey MJ, Bateman M, Boyd WV, de Villiers CT, Engelbrecht I, et al. (2005) Efficacy and safety of levocetirizine on symptoms and health-related quality of life of children with perennial allergic rhinitis: a double-blind, placebo-controlled randomized clinical trial. Ann Allergy Asthma Immunol 95:175-180.
  16. Simons FE, Prenner BM, Finn A Jr; Desloratadine Study Group (2003) Efficacy and safety of desloratadine in the treatment of perennial allergic rhinitis. J Allergy Clin Immunol 111: 617-622.
  17. Kim K, Sussman G, Hébert J, Lumry W, Lutsky B, et al. (2006) Desloratadine therapy for symptoms associated with perennial allergic rhinitis. Ann Allergy Asthma Immunol 96: 460-465.
  18. Corina B, Adriana B, Miron N, Negulescu V, Cristea V (2011) Levocetirizine and Desloratadine have influence on pro-inflammatory cytokines plasmatic level in patients with persistent allergic rhinitis. Therapeutics Pharmacology and Clinical Toxicology 15: 205-210.
  19. Draft Guidance for Industry on Allergic Rhinitis: Clinical Development Programs for Drug Products. US Dept. of Health and Human Services, Food and Drug Administration; April 2000
  20. Juniper EF, Guyatt GH (1991) Development and testing of a new measure of health status for clinical trials in rhinoconjunctivitis. Clin Exp Allergy 21: 77-83.
  21. Ciprandi G, Cirillo IG, Vizzaccaro A, Tosca MA (2005) Levocetirizine improves nasal symptoms and airflow in patients with persistent allergic rhinitis: a pilot study. Eur Ann Allergy Clin Immunol 37: 25-29.
  22. de Blic J, Wahn U, Billard E, Alt R, Pujazon MC (2005) Levocetirizine in children: evidenced efficacy and safety in a 6-week randomized seasonal allergic rhinitis trial. Pediatr Allergy Immunol 16: 267-275.
  23. Benninger M, Farrar JR, Blaiss M, Chipps B, Ferguson B, et al. (2010) Evaluating approved medications to treat allergic rhinitis in the United States: an evidence-based review of efficacy for nasal symptoms by class. Ann Allergy Asthma Immunol 104: 13-29.
  24. Berger WE, White MV; Rhinitis Study Group (2003) Efficacy of azelastine nasal spray in patients with an unsatisfactory response to loratadine. Ann Allergy Asthma Immunol 91: 205-211.
  25. Raphael GD, Angello JT, Wu MM, Druce HM (2006) Efficacy of diphenhydramine vs desloratadine and placebo in patients with moderate-to-severe seasonal allergic rhinitis. Ann Allergy Asthma Immunol 96: 606-614.
  26. Khan S, Khan MI, Khan A, Abrar A (2012) Levocetrizine and desloratadine: Comparative efficacy in patients with Allergic rhinitis. Gomal J Med Sci 10: 71-75.
  27. Ciebiada M, Górska-Ciebiada M, DuBuske LM, Górski P (2006) Montelukast with desloratadine or levocetirizine for the treatment of persistent allergic rhinitis. Ann Allergy Asthma Immunol 97: 664-671.
  28. Day JH, Briscoe MP, Rafeiro E, Ratz JD (2004) Comparative clinical efficacy, onset and duration of action of levocetirizine and desloratadine for symptoms of seasonal allergic rhinitis in subjects evaluated in the Environmental Exposure Unit (EEU). Int J Clin Pract 58: 109-118.
  29. van Oene CM, van Reij EJ, Sprangers MA, Fokkens WJ (2007) Quality-assessment of disease-specific quality of life questionnaires for rhinitis and rhinosinusitis: a systematic review. Allergy 62: 1359-1371.
Citation: Chawla D, Singh A, Gupta M, Matreja PS, Khanna PML (2014) To Compare the Safety, Efficacy and Quality of Life in Patients with Allergic Rhinitis Treated with Levocetirizine and Desloratidine. J Clin Cell Immunol 5:216.

Copyright: © 2014 Chawla D, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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