Abstract
This cohort study evaluates the association between lichen planopilaris, hyperlipidemia, and metabolic syndrome.
Lichen planopilaris (LPP) is a lymphocytic cicatricial alopecia characterized by follicular hyperkeratosis, perifollicular erythema, and loss of follicular orifices.1 The pathogenic mechanism is uncertain but thought to be due to an autoimmune, cell-mediated cytotoxic immune reaction against follicular antigens.2 The pathogenesis is similar to that of lichen planus, with some considering LPP a follicular variant of lichen planus.1 Chronic inflammatory skin diseases, including lichen planus, have been associated with dyslipidemia and metabolic syndrome.3,4 This association is likely due to a combination of increased immunologic activity of type 1 helper T cells and the cytokines tumor necrosis factor and interleukin 6.5 However, to our knowledge, there have been no studies evaluating the association between LPP, hyperlipidemia, and metabolic syndrome.
Methods
Patients with LPP seen at the Cleveland Clinic during the period from January 1, 2003, to June 12, 2011, were identified using the Cleveland Clinic alopecia registry (n = 187). For inclusion into the LPP registry, patients must have received a scalp biopsy with results showing histopathologic characteristics of LPP. The characteristics of these patients were compared with the characteristics of patients with seborrheic dermatitis (n = 56). The electronic health record was reviewed for demographic (age, sex, and body mass index [calculated as weight in kilograms divided by height in meters squared]), clinical (type 1 diabetes, hypertension, and dyslipidemia), and laboratory characteristics. Hypercholesterolemia was defined as a serum low-density lipoprotein level of higher than 130 mg/dL (to convert to millimoles per liter, multiply by 0.0259) or a serum total cholesterol level of higher than 200 mg/dL (to convert to millimoles per liter, multiply by 0.0259), or was based on the use of lipid-lowering medications. Hypertriglyceridemia was defined as a serum triglyceride level of higher than 150 mg/dL (to convert to millimoles per liter, multiply by 0.0113). Statistical analysis was performed from July 8 to 29, 2011. Continuous variables were analyzed with the Mann-Whitney test. Differences between categorical variables were assessed using the χ2 and Fisher exact tests when appropriate. Statistical significance was set as P < .05. This study was approved by the Cleveland Clinic Institutional Review Board. Patient consent was waived by the Cleveland Clinic Institutional Review Board, as the data were collected retrospectively.
Results
The study included 243 participants: 187 patients with LPP and 56 controls (Table). No differences were observed between the patients with LPP and the controls in mean (SD) age (57 [12] vs 54 [15] years; P = .09), sex (16 men and 171 women vs 6 men and 50 women; P = .60), and mean (SD) body mass index (29.0 [7.3] vs 28.0 [7.6]; P = .24), mean (SD) serum glucose levels (102 [31] vs 102 [24] mg/dL [to convert to millimoles per liter, multiply by 0.0555]; P = .19), and mean (SD) serum glycosylated hemoglobin (5.9% [0.6%] vs 5.9% [0.7%] [to convert to proportion of total hemoglobin, multiply by 0.01]; P = .86). The presence of hypertension was noted in 46 patients with LPP (24.6%) and 20 controls (35.7%) (P = .18).
Table. Demographic, Laboratory, and Clinical Characteristics of Patients With LPP vs Controls.
| Characteristic | LPP (n = 187) | Controls (n = 56) | P Valuea |
|---|---|---|---|
| Age, y | |||
| Mean (SD) | 57 (12) | 54 (15) | .09 |
| Median (range) | 58 (24-84) | 57 (22-86) | |
| Race, No. (%) | |||
| White | 118 (63.1) | 33 (58.9) | .69 |
| African American | 47 (25.1) | 14 (25.0) | |
| Other or unknown | 22 (11.8) | 9 (16.1) | |
| Sex, No. (%) | |||
| Male | 16 (8.6) | 6 (10.7) | .60 |
| Female | 171 (91.4) | 50 (89.3) | |
| BMI | |||
| Mean (SD) | 29 (7.3) | 28 (7.6) | .24 |
| Median (range) | 27 (16-55) | 29 (18-54) | |
| Serum glucose, mg/dL | |||
| Mean (SD) | 102 (31) | 102 (24) | .19 |
| Median (range) | 93 (67-357) | 96 (68-198) | |
| HbA1c, % | |||
| Mean (SD) | 5.9 (0.6) | 5.9 (0.7) | .86 |
| Median (range) | 5.8 (4.9-8.3) | 5.8 (4.3-7.6) | |
| Hypertension, No. (%) | 46 (24.6) | 20 (35.7) | .18 |
| Serum total cholesterol, mg/dL | |||
| Mean (SD) | 192 (40) | 189 (37) | .84 |
| Median (range) | 191 (68-305) | 187 (100-308) | |
| Serum HDL-C, mg/dL | |||
| Mean (SD) | 66 (20) | 64 (18) | .70 |
| Median (range) | 64 (28-126) | 63 (31-110) | |
| Serum LDL-C, mg/dL | |||
| Mean (SD) | 113 (36) | 105 (27) | .28 |
| Median (range) | 105 (38-221) | 105 (45-193) | |
| Serum triglycerides, mg/dL | |||
| Mean (SD) | 100 (62) | 102 (55) | .89 |
| Median (range) | 84 (29-478) | 85 (38-265) | |
| Statin use, No. (%) | 35 (18.7) | 15 (26.8) | .19 |
Abbreviations: BMI, body mass index (calculated as weight in kilograms divided by height in meters squared); HbA1c, hemoglobin A1c; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; LPP, lichen planopilaris.
SI conversion factors: To convert total cholesterol, HDL-C, and LDL-C to millimoles per liter, multiply by 0.0259; triglycerides to millimoles per liter, multiply by 0.0113; glucose to millimoles per liter, multiply by 0.0555; and HbA1c to proportion of total hemoglobin, multiply by 0.01.
Wilcoxon test (Mann-Whitney test) for continuous variables, and χ2 and Fisher exact tests for categorical variables.
Lipid-lowering drugs were used for 35 patients with LPP (18.7%) and 15 controls (26.8%) (P = .19). No differences were observed between the patients with LPP and the controls in mean (SD) total cholesterol levels (192 [40] vs 189 [37] mg/dL; P = .84), mean (SD) high-density lipoprotein cholesterol levels (66 [20] vs 64 [18] mg/dL [to convert to millimoles per liter, multiply by 0.0259]; P = .70), mean (SD) low-density lipoprotein cholesterol levels (113 [36] vs 105 [27] mg/dL; P = .28), and mean (SD) triglyceride levels (100 [62] vs 102 [55] mg/dL; P = .89).
Discussion
Despite the connection between hyperlipidemia and lichen planus, no differences were found in this group of patients with LPP. Confounding factors such as age, body mass index, and hypertension were homogeneous in both groups. This study has several limitations. The different ranges of LPP duration in this study may have influenced the lipid profiles and could potentially bias the estimates toward a smaller difference between patients with LPP and healthy controls. In addition, this study was conducted at a tertiary care center renowned for its cardiology department, and the composition of patients may be different compared with the general population. Our study cannot definitively exclude the possibility of a correlation between dyslipidemia and LPP. Prospective studies with larger numbers of patients are required to further investigate the potential correlation between dyslipidemia and LPP.
References
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