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 Table of Contents  
Year : 2019  |  Volume : 8  |  Issue : 4  |  Page : 273-276

Serum lipid profiles in patients with allergic rhinitis

1 Department of ENT and Head and Neck Surgery, All India Institute of Medical Sciences, Guntur, Andhra Pradesh, India
2 Department of Biochemistry, JIPMER, Puducherry, India

Date of Submission02-Jan-2018
Date of Acceptance29-Sep-2019
Date of Web Publication15-Oct-2019

Correspondence Address:
Dr. Murugaiyan Sathish Babu
House 1A, Selvam Apartments, 71 Krishna Nagar Main Road, Krishna Nagar, Puducherry - 605 008
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijhas.IJHAS_2_18

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INTRODUCTION: Inflammation is implicated in atherosclerotic cardiovascular disease. Allergy is a systemic inflammatory condition, and this may potentiate cardiovascular disease. One of the possible mechanisms for this effect can be dyslipidemia. We aim to study the association of allergic rhinitis (AR) with dyslipidemia.
MATERIALS AND METHODS: A total of 260 patients, 134 with AR and 126 controls were included in the study. The venous samples after overnight fasting were analyzed biochemically for lipids.
RESULTS: Serum total cholesterol (P = 0.0312), low-density lipoprotein (LDL) (P = 0.0324), very LDL (P = 0.0352), and triglyceride (P = 0.0417) levels were significantly higher in patients with AR as compared to the controls. However, the values of high-density lipids were not statistically significant (P = 0.0696).
CONCLUSION: Patients with AR have abnormal lipid profiles, which may play a role in the future development of cardiovascular complications in these patients.

Keywords: Allergic rhinitis, cardiovascular disease, dyslipidemia, lipid

How to cite this article:
Bakshi SS, Babu MS. Serum lipid profiles in patients with allergic rhinitis. Int J Health Allied Sci 2019;8:273-6

How to cite this URL:
Bakshi SS, Babu MS. Serum lipid profiles in patients with allergic rhinitis. Int J Health Allied Sci [serial online] 2019 [cited 2020 Aug 6];8:273-6. Available from: http://www.ijhas.in/text.asp?2019/8/4/273/269244

  Introduction Top

The incidence of allergic rhinitis (AR) has increased markedly worldwide over the last century.[1],[2] Although there are many studies on the morbidity and disease burden of AR, we are yet to understand fully the long-term mortality burden of this condition. There are studies suggesting that asthma and allergy may represent a state of systemic immunologic response, leading to long-term consequences.[3] Again, a few observational studies have linked allergic disease with cardiovascular disease.[4] This immunologic response and consequent cardiovascular disease may lead to increased morbidity and mortality in these patients.

It is estimated that up to 78% of patients with asthma have nasal symptoms and 38% of patients with AR have asthma.[5] Adequate treatment of rhinitis might positively affect the course of asthma, and the worsening of rhinitis was associated with the persistence of asthma symptoms.[6] The association of dyslipidemia with asthma and cardiovascular morbidity has been previously studied.[7] Considering the association of AR and asthma, it is possible that the inflammatory response, dyslipidemia, and cardiovascular morbidity were seen in asthmatics may also occur in patients with AR. Early detection of these risk factors can go a long way in the prevention of future cardiovascular morbidity and mortality in these patients. The present study is aimed at evaluating the association of blood lipid levels and AR.

  Materials and Methods Top

The study was carried out in our institute and was approved by the institute ethics committee. Written informed consent was obtained from the patients. The patients were diagnosed as AR on the basis of history, clinical examination, nasal endoscopy, and a positive skin prick test. Skin prick tests were performed on the forearms using extracts of grass mix, tree mix, cockroach, mold mix, dermatophagoides pteronyssinus, dander of dog and cat, along with negative and positive control.

A total of 134 patients in the study population and 126 healthy age-matched controls were included in the study. Patients with perennial AR, body mass index ≤24, aged from 18 to 45, and allergy symptoms for >2 years were admitted to the study. Patients with diabetes mellitus, previous dyslipidemia, hypertension, previous coronary heart disease, renal failure, endocrine disorder, chronic illness, and patients on corticosteroids were excluded from the study. All the samples were taken in the morning after at least 12 h of fasting. Three ml of the venous blood sample was withdrawn in a test tube and subjected to centrifugation at 5000 rpm for 10 min. Total cholesterol (TC) was estimated by cholesterol oxidase method, triglycerides (TAGs) by glycerol kinase enzymatic method, high-density lipoprotein (HDL) by a direct colorimetric method, and low-density lipoprotein (LDL) was calculated by Friedwald's formula: LDL = TC-HDL-0.2 TAG. All reagent kits were procured from Crest Biosystems, a division of the Coral clinical system.

Statistical analysis

Statistical analyses were performed using the Statistical Package for the Social Sciences (SPSS) version 21.0 (IBM Corp.; Armonk, NY, USA) program. Descriptive statistics were used to summarize the data. Categorical variables were expressed as percentages, and continuous variables were presented as the means ± standard deviations (M ± SD). Results are expressed as M ± SD. An independent t-test was used to compare the means of the parameters showing the normal distribution, and P < 0.05 was considered significant for all statistical tests.

  Results Top

A total of 260 patient's samples were taken, 134 with AR and 126 in the age-matched healthy controls. The mean age in the AR group was 35 ± 3.8 and 34 ± 4.6 in the patient population. The control group had 69 males and 57 females, while the AR group included 78 males and 56 females. There was no statistical significant difference in terms of age (P = 0.058), gender (P = 0.575), and body mass index (P = 0.0542) of patients in both the groups [Table 1]. Serum TC (P = 0.0312), LDL (P = 0.0352), very LDL (P < 0.0001), and TAG (P = 0.0417) levels were significantly higher in the AR group as compared to the controls; however, the HDL values were not statistically significant (P = 0.0696) [Table 2].
Table 1: Baseline characteristics of the study and control population

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Table 2: Comparison of lipid profile between patients with allergic rhinitis and controls

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  Discussion Top

The prevalence of AR, which is reported to affect up to 40% of the population,[8] poses a considerable burden on public health because of its negative impact on the quality of life, its economic cost, and its asthma comorbidity.[9]

AR is now thought to be a systemic disorder, with the resulting inflammation affecting not only the respiratory passage but the whole body.[10] There is a close link between AR and allergic bronchial asthma. The lining of the airway from the nose to the lungs is similar in structure and therefore similarly affected by the allergic process, so what affects the nose also can affect the lungs. Although some AR patients do not have asthma, inflammatory changes can still be evident in their lower airway. Up to 30% of AR patients, with no history of asthma, will show bronchial hyperreactivity to methacholine.[11]

Most of the previous studies have focused on the association of asthma with cardiovascular disease. There is evidence that asthma is associated with obesity,[12] particularly early in life.[13] One theory is that chronic airway inflammation may contribute to systemic inflammation and to vulnerability to vascular disease.[14],[15] Another indicates that cytokines that are upregulated in asthma may promote migration and activation of inflammatory cells implicated in atherogenesis.[16]

The role of inflammation in atherosclerotic cardiovascular disease is well established.[17] Allergic diseases also involve systemic inflammation, which may potentiate cardiovascular disease.[18] T-lymphocytes have been implicated in the development of atherosclerosis and are found in atherosclerotic lesions.[19]

Mast cells, which are found in large concentrations in the heart and vasculature, provide another mechanism potentially linking the allergic disease with atherosclerosis.[20],[21] Pro-inflammatory mediators, released by mast cells in AR such as tryptase, chymase, and histamine, are associated with coronary artery disease.[21],[22] It has also been found that immunoglobulin E (IgE) levels are elevated in patients with myocardial infarction or unstable angina, suggesting a direct role for IgE in atherogenesis.[23],[24] In addition, AR-causing edema increases the upper airway resistance and can lead to chronic hypoxia which in turn can cause increased deoxyhemoglobin levels. Increased hypoxia and oxyhemoglobin desaturation may result in elevated cholesterol levels.[25]

AR has previously been associated with incident hypertension,[26] although those results were not duplicated in a similar study[27] and self-reported allergic rhinoconjunctivitis symptoms were associated with increased coronary heart disease in one National Health and Nutrition Examination Survey study.[28]

In a study published in 2016, Vinding et al. found blood lipid profile changes associated with asthma, airway obstruction, bronchial responsiveness, and aeroallergen sensitization in 7-year-old children. They suggested that asthma and allergy are systemic disorders with commonalities with other chronic inflammatory disorders.[29] In the present study, we find abnormal lipid profiles in adult AR patients. Deranged profiles can possibly contribute to increased atherosclerosis and cardiovascular morbidity in these patients. This is important to recognize as early intervention may prevent the development of these complications.

It is important to mention the limitations of our study. First, a direct cause-and-effect relationship cannot be determined from our results, since there are many confounding factors such as patient's diet, lifestyle, duration of disease, and genetic predisposition to cardiovascular disease which needs to be taken into account. Second, our sample size is relatively small. Third, the measurements were taken only once, when the patients visited our institution, making the study a descriptive one. Fourth, the patients were not followed up to look for the actual development of cardiovascular disease. We would like to suggest a future prospective study on the effect of AR on lipid metabolism and subsequent development of cardiovascular disease with a long-term follow-up. A study analyzing the effect of a lipid-lowering intervention in AR can also be planned to further strengthen the association and develop an action plan for preventing the development of cardiovascular complications in patients with AR.

  Conclusion Top

Patients with AR have abnormal lipid profiles, which may be a risk factor for the future development of cardiovascular disease. Therefore, it is prudent to detect and treat dyslipidemia early in these patients in order to prevent the development of cardiovascular disease.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patients have given their consent for their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

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Prescott SL. Early-life environmental determinants of allergic diseases and the wider pandemic of inflammatory noncommunicable diseases. J Allergy Clin Immunol 2013;131:23-30.  Back to cited text no. 3
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  [Table 1], [Table 2]


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