Indian Journal of Dermatology
: 2019  |  Volume : 64  |  Issue : 4  |  Page : 303--310

Metabolic syndrome and dyslipidemia among Nigerians with lichen planus: A cross-sectional study

Ifeanyi Chibuzor Okpala1, Adeolu Oladayo Akinboro2, Ifeanyi Ogochukwu Ezejoifor1, Abel N Onunu3, Benson Uchechukwu Okwara3,  
1 Department of Medicine, Dermatology Unit, Nnamdi Azikiwe University Awka and Nnamdi Azikiwe University Teaching Hospital, Nnewi, Anambra State, Nigeria
2 Department of Internal Medicine, Dermatology Unit, Ladoke Akintola University of Technology, Ogbomoso and LAUTECH Teaching Hospital, Ogbomoso, Oyo State, Nigeria
3 Department of Medicine, Dermatology Unit, University of Benin and University of Benin Teaching Hospital, Benin, Edo State, Nigeria

Correspondence Address:
Adeolu Oladayo Akinboro
Department of Internal Medicine, Dermatology Unit, Ladoke Akintola University of Technology, Ogbomoso and LAUTECH Teaching Hospital, Ogbomoso, Oyo State


Background: Lichen planus (LP) is an inflammatory skin disease of unknown etiology associated with chronic inflammation, oxidative stress induction, and cardiovascular risk factors. Objectives: To document the prevalence of metabolic syndrome (MetS), dyslipidemia, and associated factors in Nigerian patients with LP. Methods: A cross-sectional design was made to evaluate 90 patients with LP and 90 controls for MetS and dyslipidemia in two Nigerian teaching hospitals. Diagnosis of LP was made with the aid of histology, and MetS and dyslipidemia were diagnosed using the National Cholesterol Education Program Adult Treatment Panel III criteria. Results: The prevalence of MetS was insignificantly higher in LP than in control (18.9% vs. 13.5, P = 0.311), and dyslipidemia was significantly associated with LP (60% vs. 40%, P = 0.007). LP was associated with higher mean of serum triglyceride (1.21 ± 0.34 vs. 1.08 ± 0.32 mmol/L, P = 0.003), low-density lipoprotein cholesterol (3.47 ± 0.89 vs. 3.12 ± 0.77 mmol/L, P = 0.007), and T-cholesterol (5.32 ± 0.88 vs. 4.92 ± 0.86, P = 0.002). LP patients with MetS were older (P < 0.001) and less likely to have Wickham's striae (P = 0.028) compared to those without MetS. Female LP patients were older (P = 0.047), obese (P = 0.043), and had insignificant increase in MetS prevalence compared to the males. Hypertrophic LP was more frequent in patients with dyslipidemia (63.0% vs. 27.8%, P = 0.002), and the family history of diabetes mellitus (DM) was an independent predictor of MetS in LP patients (odds ratio: 4.4, confidence interval: 1.0–19.1, P = 0.047). Limitation: Availability of fund is a significant factor that limited the sample size to the minimum required as always in a poor-resource setting. Conclusions: LP has an insignificant association with MetS and a significant association with dyslipidemia among Nigerians. The family history of DM is an independent predictor of MetS in LP patients. LP patients should be routinely screened for MetS and its components.

How to cite this article:
Okpala IC, Akinboro AO, Ezejoifor IO, Onunu AN, Okwara BU. Metabolic syndrome and dyslipidemia among Nigerians with lichen planus: A cross-sectional study.Indian J Dermatol 2019;64:303-310

How to cite this URL:
Okpala IC, Akinboro AO, Ezejoifor IO, Onunu AN, Okwara BU. Metabolic syndrome and dyslipidemia among Nigerians with lichen planus: A cross-sectional study. Indian J Dermatol [serial online] 2019 [cited 2022 Sep 28 ];64:303-310
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Full Text


Lichen planus (LP) is a chronic inflammatory papulosquamous disorder of the skin and mucous membrane.[1] LP is characterized by distinct clinical features that include flat-topped, glistening, hexagonal, and violaceous papules [1] that appear bluish-gray in blacks. LP affects 0.5%–1.0% of the population, and no age group, gender, or race is spared.[1],[2] Published data have associated LP with cardiovascular risk factors (CVRFs) and metabolic disorders including dyslipidemia and metabolic syndrome (MetS).[2],[3],[4],[5],[6],[7],[8],[9] MetS can be defined as a constellation of several clinical and laboratory findings that have been shown to be associated with numerous medical and dermatologic conditions. The pathogenesis of LP and these cardiovascular disorders have been linked with chronic inflammation and the induction of oxidative stress.[2],[10],[11] Studies have shown an association between LP, dyslipidemia,[2],[3],[4],[5],[8],[9] impaired glucose tolerance,[12] arrhythmias,[13] hypertension, atherosclerosis,[14],[15] and MetS.[6],[9] More recently, evidences are increasing on the association between LP, subclinical chronic inflammation, and entities such as carotid media intima thickness and epicardial fat thickness.[14],[15],[16],[17] The prevalence of MetS, dyslipidemia, and their association with LP varies in published studies.[2],[3],[4],[5],[6],[7],[8],[9],[10] Only a few published studies on MetS and dyslipidemia in LP in the available literature originated from Africa.[9],[10] In Africa, the prevalence of cardiovascular diseases (CVDs) is increasing, and the morbidity and mortality also disproportionately affect the Africans. The fact that LP is associated with CVDs which is on the rise in developing countries is a prompt for this study.

The present study was designed to document the prevalence of MetS and dyslipidemia among LP patients and to establish the patients' and disease peculiarities associated with MetS and dyslipidemia among LP patients attending the dermatology clinic of the two Nigerian teaching hospitals.


This cross-sectional study was carried out at the dermatology clinics of two Nigerian teaching hospitals in Nnewi, southeastern Nigeria, and Ogbomoso, southwestern Nigeria. The commercial town of Nnewi, Anambra state, has a population of about 4,177,828 while Ogbomosho, which is one of the Nigerian largest urban centers, has a population of approximately 1,200,000. A total of 180 patients, 90 cases, and 90 controls were selected from the two centers between December 2014 and February 2016. The study population consists of 90 consecutive patients attending the two dermatology clinics that satisfied the inclusion criteria. The control population consisted of 90 apparently healthy, age- and gender-matched participants without LP randomly selected from the general outpatient departments of the two teaching hospitals.

The inclusion criteria for cases included adult patients attending the dermatology clinics with clinical and histology features of LP who gave informed consent to participate in the study. We excluded those patients with lichenoid eruptions, patients already on steroids, patients below 18 year of age, and patients with known hypertension, diabetes mellitus (DM), or dyslipidemia. We similarly excluded all nonconsenting individuals and patients with known chronic liver disease, chronic kidney diseases, human immunodeficiency virus (HIV) infection, and familial hyperlipidemia. The inclusion criteria were same for the control population save they were without LP.

Ethical approval for the study was obtained from the ethics committees of the two teaching hospitals.

Clinical assessments

All included participants had data obtained from them using an interviewer-administered questionnaire. The data collected include sociodemographic characteristics such as age, sex, occupation, ethnicity, smoking, alcohol, and educational qualification. The survey also elicited the duration of the illness, site of onset, family history of hypertension, DM, and cardiovascular event including stroke and heart attack. In daylight, patients were clinically examined for clinical type of LP, extent of the diseases, involvement of the mouth, and nails were documented. Clinical signs such as koebnerization and Wickham striae were also noted. Skin biopsy was taken after patients' consent by a standard method. The weight of all patients and controls was obtained while patients were wearing light clothing with the aid of a weighing scale. Weight was recorded to the nearest 0.1 kg; height was obtained using a stadiometer with patients looking straight forward, head in a horizontal plane, feet apposed, with shoulder relaxed, and the arm placed at the side. Waist circumference was measured in a horizontal plane midway between the inferior margin of the ribs and the superior border of the iliac crest with the patient erect and his/her abdomen bare. All measurements were taken using a stretch resistant tape measure. Body mass index (BMI) was calculated using the formula weight/height 2 (kg/m 2).[18],[19] We measured blood pressure in the arm using standard adult arm cuff of a mercury-type sphygmomanometer (ACCOSON, England) with the patient's arm supported and at least 15 min after rest in the sitting position.[20] All measurements were repeated twice, and the average of the two measurements was taken as the research data.

Laboratory assessments

The blood samples were taken from the patients after overnight fasting for 12 h. Twelve milliliters of venous blood was drawn from a vein in the antecubital fossa for fasting blood sugar and for lipid estimation. Fasting blood glucose was determined by the glucose oxidase method described by Trinder. Fasting lipid profile was estimated using standard methods; serum triglycerides, total cholesterol (TC), and high-density lipoprotein (HDL) cholesterol were determined using enzymatic colorimetric methods. The low-density lipoprotein cholesterol (LDL-C) was determined mathematically using the Friedewald formula. The LDL-C = TC − HDL cholesterol − (Triglyceride/2.17).[21],[22],[23],[24],[25]

The diagnosis of the MetS was based on the National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATP III) working definition.[26]

  • Abdominal obesity: Waist circumference (>102 cm in males and >88 cm in females)
  • Hypertriglyceridemia (≥1.7 mmol/L)
  • Low HDL level (<1.04 mmol/L in males and <1.3 mmol/L in females)
  • High blood pressure (≥130/85 mmHg)
  • Fasting glucose level ≥6.1 mmol/L.

Using this definition, MetS is diagnosed by the presence of three or more of the above. The diagnosis of dyslipidemia was made based on the standard criteria used; dyslipidemia was diagnosed by the presence of any one of the serum triglycerides >1.7 mmol/L, total serum cholesterol >5.2 mmol/L, and serum LDL-C >3.4 mmol/L.[26]

Data analysis

Data were analyzed using Statistical Package for Social Sciences software (version 18, Chicago, IL, USA). Categorical variables were summarized using Chi-square test, and continuous variables were analyzed using Student's t-test and Mann–Whitney U statistics as indicated. Exact significance statistics was employed within the computational limit. Association between significant variables and MetS was determined using binary logistic regression. All data of interest were presented in tables. P < 0.05 was considered statistically significant.


The population studied consisted of 90 patients with LP and 90 controls. There was no significant difference in the mean age and the marital status of the study patients and the control population. More patients with LP had higher educational status than the controls (P = 0.034). The patients with LP had a significant history of alcohol ingestion (28.9% vs. 10.5%, P = 0.003) and family history of DM (16.9%, vs. 6.6%, P = 0.044) compared to the controls. Forty-eight (53.3%) of patients with LP were male while 46.7% were female. The female patients with LP were significantly older (P = 0.047) and had a higher mean BMI (P = 0.043) than the males. The males with LP, however, had a significant history of alcohol ingestion (45.8% vs. 9.5%, P < 0.001) compared to their female counterparts [Table 1].{Table 1}

The prevalence levels of MetS and its components and dyslipidemia were examined among patients with LP and controls as shown in [Table 2]. Patients with LP had a higher prevalence of high TC (60% vs. 30%, P < 0.001), high LDL-C (58.8% vs. 41.2, P = 0.004), high triglyceride (12.2% vs. 3.3%, P = 0.026), and dyslipidemia (60.0% vs. 40.0%, P = 0.007) compared to the controls. The mean TGC (P = 0.003), TC (P = 0.002), and LDL-C (P = 0.007) were also significantly higher for LP patients than controls. Meanwhile, the female patients with LP had a significantly higher frequency of low HDL-cholesterol (P = 0.041) compared to the male patients. The prevalence of MetS in LP was insignificantly higher for participants with LP (18.9% vs. 13.3%, P = 0.311) compared to controls and also insignificantly higher for females (21.4% vs. 16.7%, P = 0.565) compared to the males with LP.{Table 2}

As shown in [Table 3], the peculiarities of patients with LP were examined against the presence and the absence of MetS and dyslipidemia. Participants with LP and MetS were significantly older (49.59 ± 9.52 vs. 34.62 ± 13.23 years, P < 0.001) and had a lesser frequency of Wickham's striae (17.6% vs. 49.3%, P = 0.028) compared to those LP patients without MetS. The patients with dyslipidemia were more likely to have a significantly higher frequency of the hypertrophic type of LP (63.0% vs. 27.8%, P = 0.002) while those without dyslipidemia were more likely to have a higher incidence of classic LP (66.7% vs. 33.3%, P < 0.002) compared to those with dyslipidemia.{Table 3}

[Table 4] shows binary regression analysis of all the significant variables associated with the MetS in multivariate analysis. After correction for age, gender, and ethnicity, LP patients with family history of diabetes were 4.4 times more likely to develop MetS (odds ratio: 4.4, confidence interval: 1.0–19.1, P = 0.047) compared to those without the family history of diabetes.{Table 4}


It is clear from the present study that LP has an insignificant association with MetS and a significant association with dyslipidemia. The family history of DM is independently predictive of the occurrence of MetS in LP patients. We found that LP patients with MetS were significantly older, less likely to present with Wickham's striae, demonstrated higher levels of triglyceride, LDL-C, and high TC than the controls. However, in terms of gender, the female participants with LP had a statistically insignificant higher prevalence of MetS and dyslipidemia and were likely to be older and obese compared to the males.

The prevalence and the relationship between LP and MetS vary in published studies. The prevalence of MetS (18.9%) in a study is below 26.6% documented by Baykal et al.,[6] and below 77.0% found by Saleh et al.[10] Our prevalence is however higher than 6% found by Kuntoji et al.[5] This prevalence (18.9%) is lower, but close to the overall average of 27.9% observed in all etiologies including DM, systemic hypertension, HIV infection, asthma, and thyroid disorders in both general population and hospital settings using the NCEP-ATP III criteria.[27] About the association between LP and MetS, like ours, Arias-Santiago et al.[2] and Kotunji et al.[5] found no association between MetS and LP, but LP patients had a higher prevalence of dyslipidemia than the controls. Contrary to the present study and others,[2],[5] Saleh et al.[10] and Baykal et al.[6] found a significant association between LP and MetS. The factors that could be responsible for the observed variation in the prevalence of MetS in studies could include the different settings in which the studies were conducted, the inadequate sample size in some studies, different methods of patients' selection, and definitions of MetS used in the studies. It is worthy of mentioning that although the female participants with LP were older and more obese than their male counterparts, the females only showed an insignificant increase in the prevalence of MetS (21.4% vs. 16.7%, P = 0.565) compared to their male counterparts. This observation is similar to the findings in the study of Baykal et al.,[6] and the population variation in the prevalence of MetS was related to genetic, dietary habits and levels of physical activity of population.[6]

The frequency of oral mucosal involvement (16.7%) in association with cutaneous LP is lower in our study compared to 73.4%–90.5% reported by some authors.[6],[7] Asmita et al.,[28] however, demonstrated a lower but comparable 9% prevalence of oral involvement. In the same vein, the prevalence of MetS in LP patients with mucosal involvement (5.9%) is significantly lower compared to 34.5%[6] and 27.27% previously reported.[7] Shorter duration of LP in our study relative to other studies [6],[12] could imply a shorter length of a progressive disease such as LP. The shortness of time could have limited the spread to the oral mucosa due to the short period of inflammation, and the same could explain the lower prevalence of MetS. The severity of inflammation in LP has associated with the duration of LP.[6] However, the present study documented no association between duration of LP and MetS as found by others.[6] The factors that could be responsible might include but not limited to the inclusion of newly diagnosed LP patients who have not been exposed to any form of long-term treatment which could have implications for their metabolic status. Treatment-resistant LP are more likely to exist chronically and liable to chronic inflammation induction which has been associated with MetS and CVRFs.[6]

The anthropometric parameters are not significantly different between LP patients and controls, as found by other studies.[1],[6],[12] This finding implies that metabolic imbalance in LP patients is not obesity dependent, but might be related to chronic inflammation induction.

There was no significant difference in the mean of fasting plasma glucose of patients and controls. Our patients with LP had increased frequency of impaired fasting glucose and DM (11.1% vs. 8.9%) and the family history of DM compared to the controls. Denli et al.[29] found diabetes prevalence of 15.7% in their patients while Seyhan et al.[12] documented a much higher incidence of 26.7% in their study and attributed variation in glucose disturbance to methods of assessment. In this study, family history of DM independently predicts the occurrence of MetS after correction for confounders such as age, gender, obesity, and ethnicity.

Dyslipidemia is significantly associated with LP in the present study. Studies have consistently established a clear association between dyslipidemia and LP.[3],[4],[5],[7],[8],[9],[10],[11] The prevalence of dyslipidemia (60%) in LP patients in the present study is higher than the prevalence documented in previous studies.[5],[6],[9],[10] Significant higher levels of TGC, LDL-C, and TC seen among patients with LP are in keeping with findings of previous studies.[3],[6],[7],[8],[9],[10] However, unlike other previous studies,[3],[6],[7],[8],[9],[10] we did not find a significant difference in the levels of HDL-cholesterol between patients with LP and the controls. A systematic review by Lai et al. also found a significant elevation of triglyceride only in a large number of LP patients relative to the control population.[8] Attributed to dyslipidemia in LP is the induction of chronic inflammation, which is also the pathway to the development of other cardiovascular risks.[2],[6],[10],[11] The evidence of inflammation and oxidative induction in LP includes increasing levels of C-reactive protein, malondialdehyde, and the reduced level of catalase activity.[11] The presence of these prothrombotic and pro-atherogenic factors in addition to other cardiovascular risks might put LP patients at serious risk of CVD.

In the present study, there is no significant difference in the atherogenic indices of LP patients and the controls, though the indices are higher in patients with LP than in controls. The correlates of dyslipidemia in LP in published studies include the duration of LP, anthropometry, fasting plasma glucose, systolic blood pressure (SBP), and diastolic blood pressure (DBP).[5],[9] We found increased anthropometry, fasting plasma glucose, SBP, and DBP, but not the duration among patients of LP.

The hypertrophic type of LP [Figure 1] is associated with dyslipidemia, and the classic type [Figure 2] and [Figure 3] was found to be frequent among participants without dyslipidemia. To the best of our knowledge, this is the first report associating dyslipidemia with hypertrophic LP. The hypertrophic LP is more likely to be chronic and treatment resistant and therefore could be related to persistent induction of inflammation, in which possible consequences include dyslipidemia.[6] A recently published observation also suggested an increased suspicion of association between hypertrophic LP and squamous cell cancer.[30]{Figure 1}{Figure 2}{Figure 3}


A study of this kind is almost always limited by funding in the poor-resource settings like ours, therefore restricting the sample size to the minimum required. The strength of this study is in the fact that samples were drawn from two centers, though the second center is relatively new accounting for small number included from the site.


There is an insignificantly increased prevalence of MetS in LP patients compared to controls. The family history of DM is an independent predictor of MetS in the LP patients. Dyslipidemia is, however, significantly associated with LP. Patients with LP demonstrated a significantly higher serum level of LDL-C, TC, and TGC than the control population. Participants with dyslipidemia are more likely to have a hypertrophic variant of LP. Patients with LP should be routinely screened for components of MetS for efficient CVD prevention.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/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.


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