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ORIGINAL ARTICLE
Year : 2020  |  Volume : 33  |  Issue : 3  |  Page : 1050-1054

Lipid profile in cases of lichen planus


1 Department of Dermatology, Andrology and STIs, Faculty of Medicine, Menoufia University, Menoufia, Egypt
2 Department of Medical Biology, Faculty of Medicine, Menoufia University, Menoufia, Egypt
3 Department of Dermatology, Shebi El-Kom Dermatology and Leprosy Hospital, Menoufia, Egypt

Date of Submission07-Mar-2019
Date of Decision15-Apr-2019
Date of Acceptance27-Apr-2019
Date of Web Publication30-Sep-2020

Correspondence Address:
Eman M. H Abd El Hamid El Khateeb
Department of Dermatology, Shebi El.Kom Dermatology and Leprosy Hospital, Menoufia
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/mmj.mmj_92_19

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  Abstract 


Objective
The aim of this work is to measure serum lipid profile in lichen planus) LP (cases for assessment of possible myocardial ischemia in these cases.
Background
LP is a chronic inflammatory disease that affects the skin and mucous membranes. It occurs mostly in individuals older than 45 years, and it is more common among women. Lipids are a broad group of naturally occurring molecules. High levels of triglycerides in the blood stream have been linked to atherosclerosis and, by extension, the risk of heart disease and stroke. Atherogenic lipid profile leads to atherosclerosis, which may be complicated by cerebral stroke, myocardial infarction, and/or peripheral vascular disease.
Patients and methods
This case–control study was carried out on 20 nonobese cases with LP as patient group and 20 age-matched, sex-matched, and BMI-matched healthy participants as a control group. All participants were subjected to full history taking, clinical examination, and laboratory investigations (blood lipid profile).
Results
Our results showed no significant difference between cases and controls regarding age and sex. There was no significant difference between cases and controls regarding blood pressure and BMI. There was a highly significant difference between case and control groups regarding serum cholesterol, high-density lipoprotein, and low-density lipoprotein.
Conclusion
Serum cholesterol, high-density lipoprotein, and low-density lipoprotein may be better predictors of cardiovascular risk in patients with LP.

Keywords: cholesterol, lichen planus, lipid profile, obesity, triglycerides


How to cite this article:
Hammam MA, Bakry OA, Soliman SE, Abd El Hamid El Khateeb EM. Lipid profile in cases of lichen planus. Menoufia Med J 2020;33:1050-4

How to cite this URL:
Hammam MA, Bakry OA, Soliman SE, Abd El Hamid El Khateeb EM. Lipid profile in cases of lichen planus. Menoufia Med J [serial online] 2020 [cited 2020 Oct 22];33:1050-4. Available from: http://www.mmj.eg.net/text.asp?2020/33/3/1050/296717




  Introduction Top


Lichen planus (LP) is the prototypical lichenoid tissue reaction that affects ∼1% of the population worldwide. Classic LP is characterized by violaceous, flat-topped, polygonal papules, which favor the flexor aspects of the body. LP can affect any ectodermally derived tissues (skin, hair, nail, mucous membranes, and esophagus) [1].

Microscopically the disease is characterized by dense subepithelial lympho-histiocytic infiltrate, increased numbers of intraepithelial lymphocytes, and degeneration of basal keratinocytes. Degenerating basal keratinocytes form colloid (civatte, hyaline, and cytoid) bodies that appear as homogenous eosinophilic globules [2]. Epithelial basement membrane changes include breaks, branches, and duplications. Degeneration of basement membrane causes weaknesses at the epithelial-connective tissue interface which may result in histological cleft formation (Max-Joseph space) and, rarely, clinical blistering of the oral mucosa (bullous LP). Parakeratosis, acanthosis, and 'saw-tooth' rete peg formation may be seen [3].

The cause of LP is unknown. In general, activated T-lymphocytes are recruited to the dermoepidermal junction and induce apoptosis in basal keratinocytes. Both CD4+ and CD8+ T-lymphocytes are found in the lichenoid infiltrate of LP, with a predominance of the latter cell type being present in established lesions [4].

Epidermal cells in LP have shown abnormalities in enzymatic activity, as well as defective carbohydrate expression. An increased prevalence of diabetes and carbohydrate intolerance has been observed in patients with LP, suggesting its possible role in the pathogenesis of this etiologically obscure disease [5].

As LP is a chronic inflammatory disease, patients with LP may have increased cardiovascular (CV) risk factors in the long term [6].

Patients with LP were found to have higher makers of both metabolic and CV risk factors in relation to controls most probably owing to long-standing inflammation [7].

Dyslipidemia refers to a disruption of lipid metabolism with exceeding serum levels of total cholesterol (TC), triglycerides (TGs), and low-density lipoprotein-cholesterol (LDL-C) and/or lower level of high-density lipoprotein-cholesterol (HDL-C). Serum levels of lipids and lipoprotein lipids are among the most potent and best substantiated risk factors for atherosclerotic diseases, particularly coronary heart disease [8].

LP has been associated with dyslipidemia and metabolic syndrome. This association is likely owing to a combination of increased immunologic activity of type 1 helper T-cells and the cytokines tumor necrosis factor and interleukin [9].

Therefore, we evaluated serum level of lipid profile in LP cases for assessment of possible myocardial ischemia in these cases.


  Patients and Methods Top


The study was approved from the ethical committee of Faculty of Medicine Menoufia University and the patients gave an informed consent. This is a case–control study that included 40 participants who were attending the Menoufia Skin and Andrology Outpatient Clinic.

They were classified into two groups:

  1. Group 1 (LP group) included 20 nonobese with LP patients
  2. Group 2 (control group) included 20 age-matched, sex-matched, and BMI-matched healthy participants.


All study participants were subjected to the following after taking written consent: thorough history tacking focusing on age of onset, course and duration of LP, family history, history of precipitating/initiating factors, or drug intake.

Moreover, all patients and control were subjected to through general examination, detailed dermatological examination, assessment of disease severity among cases and controls, measurement of blood pressure, and determination of BMI.

Overall, 5 ml of blood sample was collected from each individual under aseptic condition by clean venipuncture without venous stasis. Blood sample was added to a sterile plain tube. The blood was left to clot at 37°C (for 30 min) and rapidly centrifuged at 4000 rpm for 10 min, and then stored at −20°C for assessment of serum lipid profile.

Inclusion criteria were as follows:

  1. Patients with LP.
  2. Nonobese patients.


Exclusion criteria were as follow:

  1. Obese patients.
  2. Dermatologic diseases other than LP.


The results were statistically analyzed by SPSS, version 20 (SPSS Inc., Chicago, Illinois, USA). Statistics were calculated in terms of percentage, mean, SD, Student's t test, Mann–Whitney test, χ2, Spearman and Pearson, P value, and Wilcoxon.


  Results Top


This study included 20 cases with LP (11 males and nine females) aged 21–57 years and 20 age-matched and sex-matched healthy controls (11 males and nine females). There were no significant differences between cases and controls regarding age and sex (P > 0.05) [Table 1].
Table 1: Comparison between cases and controls regarding age and sex

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There were no significant differences between cases and controls regarding blood pressure (systolic and diastolic) and BMI (P > 0.05) [Table 2].
Table 2: Comparison between cases and controls regarding blood pressure and BMI

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Regarding serum cholesterol level in cases, it ranged between 106 and 444.8 mg/dl, with mean ± SD of 273.4 ± 100.6; HDL ranged 38 and 57 mg/dl, with mean ± SD of 45.6 ± 7.71; LDL ranged from 87.3 to 666.8, with mean ± SD of 247.2 ± 134.2; and serum TG level ranged from 53.1 to 226.1 mg/dl, with mean ± SD of 122.9 ± 52.1 [Table 3].
Table 3: Laboratory investigations of studied cases (n=20)

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There was a highly significant difference between case and control groups regarding serum cholesterol level, as the mean ± SD was 273.4 ± 100.6 in cases and 172.2 ± 39.0 in controls (P < 0.001) [Table 4].
Table 4: Comparison between cases and controls regarding lipid profile

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Regarding serum HDL level, there was a highly significant difference between case and control with significantly higher mean values in cases (45.6 ± 6.71) than in controls (37.2 ± 7.85) (P < 0.001) [Table 4].

Regarding serum LDL level, there was a highly significant difference between case and control groups with significantly higher mean values in cases (247.2 ± 134.2) than in controls (111.6 ± 37.4) (P < 0.001) [Table 4].

Regarding serum TG level, there was a nonsignificant difference between case and control groups, with mean values of 122.9 ± 52.1 in case and 115.7 ± 27.8 in controls (P < 0.914) [Table 4].


  Discussion Top


LP is a common T-cell mediated chronic inflammatory disease of the stratified squamous epithelium, with unknown etiology. It can affect oral mucosa, genitalia, hair follicle, nail, esophagus, larynx, and even the eyes. It is reported in ∼1–2% of all dermatologic patients [10].

It typically affects middle-aged adults of both sexes. It can occur at any age; however, more than two-thirds of patients with LP are aged between 30 and 60 years. An Egyptian study showed that most patients (66%) fall in the age group from 21 to 50 years [11].

LP was reported in some studies to affect females more than males [12]. In other studies, LP affects men and women equally; however, oral lichen planus (OLP) affects women twice as often as men [13].

Because of the predominant secretion of interferon-c and tumor necrosis factor-a, LP is characterized by a type 1 cytokine pattern [14].

LP can be divided into a lot of types according to configuration and morphology of the lesions, site of involvement, and the presence of special forms [15].

'Pruritic, purple, polygonal, planar, papules, and plaques' are the traditional 6 'P's' of LP. The lesions are typically bilateral and relatively symmetric [16]. The classic LP lesion is a shiny, red/purple-colored, flat-topped papule. Lesions may also have a thin, transparent, and adherent scale. Wickham striae, which are defined as fine whitish points or lacy lines, may be seen on the surface of well-developed papules [10].

LP can also be divided into various types according to the configuration of lesion (annular LP and linear LP) and according to the morphology of the lesions (hypertrophic LP, atrophic LP, vesiculobullous LP, ulcerative LP, follicular LP, actinic LP, and LP pigmentosus) [15].

Although the exact etiology of LP is unknown, several pathogenic factors have been implicated in the pathogenesis of LP. The main theories are genetic, autoimmune, infective, and psychogenic [16].

The existence of familial cases of LP may suggest a possible genetic predisposition. Gene polymorphisms of different human leukocyte antigen markers as well as the inflammatory cytokines and chemokines have been associated with the presence of LP. Some authors even mention the possibility of familial LP being an isolated entity, with frequent expression of human leukocyte antigen-B7 antigens [17].

HCV has been implicated in triggering LP, and patients with LP were observed to have significantly higher risk of being HCV seropositive [18].

Anxiety is a well-established risk factor or accompanying factor in patients with LP, such that certain intense and prolonged emotional stress such as anxiety, shock, traumatic childhood, sadness, disappointment, failure, and humiliation may initiate the process of LP [19].

LP may be associated with other immune-mediated diseases including alopecia areata, dermatomyositis, lichen sclerosis et atrophicus, morphea, myasthenia gravis, primary biliary cirrhosis, ulcerative colitis, and vitiligo. OLP is also reported in association with hepatitis C infection and chronic active hepatitis. However, the association between OLP and systemic disease may be coincidental [20].

The association between HCV infection and LP comes from epidemiological studies that have shown that the prevalence of antibodies against HCV antigens is higher in patients with LP than in general population. The high-risk patients of HCV infections are drug users, those who share needles, those treated with unsterilized dental instruments, and health care workers [21].

Increased LDL-C/HDL-C ratio has already been considered as a sensitive predictor of CV risk, and recently, TC/HDL-C ratio has been found an even better predictor metabolic index for CV risk in a large study [22].

High-sensitivity C-reactive protein (hs-CRP) was significantly higher in patients with type 2 diabetes. Significant correlations were seen between IMA and fasting glucose and IMA and hs-CRP. Significant correlations between IMA and TC, LDL cholesterol, oxidized LDL antibodies and hs-CRP levels have also been noted [23].

The aim of the work of this study was to measure serum level of lipids in LP cases for assessment of possible myocardial ischemia in these cases.

In the present study, there was a highly significant difference between case and control groups regarding serum cholesterol level, serum HDL level, serum LDL level.

The abnormal lipid profile in cases compared with control owing to LP has been associated with metabolic disorders such as dyslipidemia and diabetes mellitus [24]. Antioxidant defense mechanisms are significantly altered in LP causing an increase in oxidative damage to lipids, protein, and DNA, which may be involved in inflammatory processes of the disease [25].

Sharrett et al. [26] stated that higher values of TGs and low levels of HDL-C were associated with the transition from atheroma to atherothrombosis, and therefore, control of these two CV risk factors is essential in patients with subclinical disease.

However, the enormous contributions of TGs to CV risk have been underestimated [27]. Indeed high levels have been associated with an increased incidence of coronary artery disease [28] and an increased population of small dense LDL-C particles [29].

Higher values of TGs and low levels of HDL-C were associated with the transition from atheroma to atherothrombosis and therefore control of these two CV risk factors is essential in patients with subclinical disease [30]. Low serum levels of HDL-C and elevated levels of TGs also increase the risk of coronary artery disease, even in patients treated with statins and with low LDL-C levels [30].


  Conclusion Top


Lipid profile (cholesterol, HDL, and LDL) is significantly elevated in patients with LP and dyslipidemia is prevalent among patients with LP, with no sex differences.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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