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ORIGINAL ARTICLE
Year : 2021  |  Volume : 34  |  Issue : 1  |  Page : 18-22

Lipid profile in androgenetic alopecia


1 Department of Dermatology, Andrology and STDs, Faculty of Medicine, Menoufia University, Menoufia, Egypt
2 Department of Medical Biochemistry, Faculty of Medicine, Menoufia University, Menoufia, Egypt
3 Department of Dermatology, El-Shohada Central Hospital, Menoufia, Egypt

Date of Submission24-Mar-2019
Date of Decision02-Apr-2019
Date of Acceptance08-Apr-2019
Date of Web Publication27-Mar-2021

Correspondence Address:
Amira M Amer
Department of Dermatology, El-Shohada Central Hospital, Menoufia
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/mmj.mmj_125_19

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  Abstract 


Objective
The aim of this work is to evaluate lipid profile in patients with androgenetic alopecia and to correlate their levels with disease severity.
Background
Androgenetic alopecia (AGA) is the most common form of alopecia which is an androgen hormone-dependent process with continuous miniaturization of hair follicles in both genetically predisposed men and women. Lipids are a broad group of naturally occurring molecules. AGA has been found to be associated with coronary artery disease (CAD). The well-known risk factors of CAD are family history of CAD, hypertension, increased BMI, central obesity, hyperglycemia, and dyslipidemia.
Patients and methods
This case–control study was carried out on 30 men with early-onset AGA and 30 age-matched and sex-matched healthy subjects as the control group. All patients were subjected to full history taking, general examination, and laboratory investigations (fasting blood sugar and blood lipid profile).
Results
Our results showed no significant difference between cases and controls regarding age and sex. There were statistically significant differences regarding mean values of body weight, waist circumference, and BMI between cases and controls. There were statistically significant differences regarding mean values of fasting blood sugar, triglycerides, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol between cases and controls.
Conclusion
Patients with AGA appear to be at an increased risk of developing CAD and high blood lipids.

Keywords: alopecia, androgenetic alopecia, coronary artery disease, lipid profile, obesity


How to cite this article:
Bakry OA, El-Shafey SM, Amer AM. Lipid profile in androgenetic alopecia. Menoufia Med J 2021;34:18-22

How to cite this URL:
Bakry OA, El-Shafey SM, Amer AM. Lipid profile in androgenetic alopecia. Menoufia Med J [serial online] 2021 [cited 2021 Jun 21];34:18-22. Available from: http://www.mmj.eg.net/text.asp?2021/34/1/18/311991




  Introduction Top


Alopecia is the loss of hair from skin areas where it is normally present. There are many different types of alopecia which are attributed to the underlying cause. Hair loss is a common problem for both men and women. The most common form of hair loss is androgenetic alopecia (AGA) [1].

AGA is the most common form of alopecia which is an androgen hormone-dependent process with continuous miniaturization of hair follicles in both genetically predisposed men and women [2]. AGA is hereditary thinning of the hair induced by androgens in genetically susceptible men and women. This condition is also known as male-pattern hair loss or common baldness in men and as female-pattern hair loss in women. Thinning of the hair usually begins between the ages of 12 and 40 years in both sexes, and approximately half the population expresses this trait to some degree before the age of 50 years [3].

The incidence and the severity of AGA tend to be highest in Whites, second highest in Asians and African Americans, and lowest in Native Americans and Eskimos. Whites are four times more likely to develop baldness than African Americans [4].

The diagnosis of AGA is usually made clinically. The finding is typical especially in patients with a positive family history (FH) of gradual hair loss [5]. The clinical appearance of male AGA is universally and instantly recognizable in most cases. The progression of hair loss occurs in an orderly manner and ranges from the bitemporal recession of hair, to thinning of the frontal and vertex regions of the scalp, to complete baldness and loss of all hair except the occipital and temporal fringes. In some cases, men have diffuse thinning all over the scalp [5].

Dyslipidemia refers to a disruption of lipid metabolism with exceeding serum levels of total cholesterol (TC), triglycerides (TGs), low-density lipoprotein cholesterol (LDL-C), and/or lower levels 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 [6].

AGA has been shown to be associated with several diseases such as coronary heart disease, hyperinsulinemia, and insulin resistance-associated disorders such as obesity, hypertension, and dyslipidemia. AGA is a risk factor for prostate cancer and benign prostatic hyperplasia [7].

Severe early onset AGA in young patients before their 30s may have a higher risk for ischemic heart disease. In a retrospective study, subjects who had predominantly vertex balding as opposed to frontal hair loss were shown to be at an increased incidence of myocardial infarction. This pattern was especially true among men with hypertension or high cholesterol levels [8].

So, we assess the serum level of lipid profile in patients with AGA and to correlate their levels with disease severity.


  Patients and methods Top


The study was approved by the ethics committee of Faculty of Medicine, Menoufia University and the patients gave an informed consent. This is a case–control study that included 60 patients who were attending the Menoufia Dermatology and Andrology Outpatient Clinic.

They were classified into two groups:

Group 1 (AGA group): included 30 men with early-onset AGA

Group 2 (control group): included 30 age-matched, sex-matched and BMI-matched healthy individuals.

All study participants were subjected to the following after taking written consent: thorough history tacking focusing on the age of onset, course, and duration of AGA, or history of previous treatment, FH AGA, and/or FH of cardiovascular diseases.

Also, all patients and control were subjected to through general examination, detailed dermatological examination, assessing grading of AGA based on the Hamilton-Norwood classification. Cases and controls will undergo measurement of blood pressure (BP) and determination of anthropometric measures including weight, height, waist circumference, and BMI). The degree of alopecia was classified according to the Hamilton-Norwood classification.

After a 12 h fasting period, 5 ml of venous blood was collected from each patient by the use of disposable, sterilized plastic syringes. The blood was allowed to clot for half an hour in a water bath at 37°C and then it was centrifuged for 15 min at 3000 rpm for separation of serum by means of a clean dry Pasteur pipette. The serum was fractionated into two clean dry tubes and frozen at −80°C till used for determination of fasting blood glucose and complete serum lipid profile.

Inclusion criteria were as follows: men with early-onset AGA.

Exclusion criteria were as follows: congenital adrenal hyperplasia, thyroid disease, Cushing's disease, hepatic and renal failure, androgen or antiandrogen therapy, slimming, insulin-sensitizing drugs or insulin treatment, glucocorticoid treatment within the previous 6 months, and changes related to body weight within last 3 months.

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-test, Spearman's and Pearson's tests, P value, and Wilcoxon's test.


  Results Top


This study included 60 patients: 30 men with early-onset AGA (onset before 35 years) with mean age (40.6 ± 10.9) and 30 age-matched and sex-matched healthy volunteers as a control group with mean age (35.8 ± 10.5). There were no significant difference between cases and controls regarding age (P > 0.05).

All cases had gradual onset of disease with progressive course; 53.3% of cases were smokers; and 93.3% of cases had positive FH with statistically significant difference between both groups. The mean age of onset was 24.9 ± 6.32, of the disease/months was 15.3 ± 7.39, of systolic blood pressure was 136 ± 18.7, and of diastolic blood pressure was 86.0 ± 8.03 [Table 1].
Table 1: Clinical data of the studied cases (n=30)

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All men in the control group had grade I (physiological) AGA, while cases had variable grades that ranged from II to VI (according to the Norwood-Hamilton classification). Metabolic syndrome was present in 80% of cases [Table 1].

There were statistically significant differences regarding mean values of body weight (P < 0.001), waist circumference (P < 0.001), and BMI (P < 0.001) between cases and controls [Table 2].
Table 2: Comparison between cases and controls regarding anthropometric measures (n=60)

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There were statistically significant differences regarding mean values of FBS (P = 0.001), TGS (P = 0.001), HDL-C (P < 0.01), LDL-C (P < 0.001) between cases and controls [Table 3].
Table 3: Comparison between cases and controls regarding lipid profile and fasting blood sugar (n=60)

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  Discussion Top


AGA is characterized by follicular miniaturization in a patterned manner occurring due to systemic androgens and genetic factors. The disease is multifactorial, with several lines of evidence suggesting it most likely functions by a genetic predisposition (diathesis). Since androgens and androgen receptors are the initiating cause of androgenic alopecia, their genetic corollaries are a subject of much research [9].

The concentration of DHT levels and 5α-reductase activity are increased on balding areas of the scalp in these patients. Some authors stated that nearly all men affected with AGA have normal circulating androgen levels [10]. On the contrary, others demonstrated that there are more androgen receptors in the dermal papillae of the scalp in patients with severe AGA and higher levels of total and free testosterone in the serum [11].

Patients with AGA might be at an increased risk of CAD which increases with increasing grade of AGA. Thus, clinical evaluation of cases of AGA for risk factors of CAD can help in preventing a dreaded disease [12].

The aim of this study was to investigate the possible association between AGA and serum lipid profile.

This finding can be explained by the presence of metabolic syndrome in 80% of the studied cases. The presence of metabolic syndrome was significantly associated with cases compared with controls.

Metabolic syndrome is a clustering of at least three of the five following medical conditions: central obesity, high BP, high blood sugar, high serum TGs, and low serum HDL. Metabolic syndrome is associated with the risk of developing cardiovascular disease and type 2 diabetes [13].

Insulin resistance, metabolic syndrome, and prediabetes are closely related to one another and have overlapping aspects. Insulin resistance (IR) is considered as a pathological condition in which cells fail to respond normally to insulin. IR is associated with declining insulin production by the pancreas, the emergence of type 2 diabetes and increasing risk of cardiovascular disease. Clinical markers of IR include elevated plasma glucose concentration under fasting conditions or following ingestion of an oral glucose challenge. IR and hyperinsulinemia produce a number of effects that promote CVD, including adverse effects on blood pressure, endothelial cell function, lipid profile, platelet function, and blood coagulation [14].

Insulin resistance plays a pathogenetic role in the miniaturization of hair follicles. Vasoactive substances associated with endothelial dysfunction in insulin resistance lead to microcirculatory disturbance, perifollicular vasoconstriction, and proliferation of smooth muscle cells in the vascular wall. This condition leads to microvascular insufficiency, local-tissue hypoxia, favoring the effect of DHT on follicular miniaturization [15].

The current study showed that AGA cases have abnormal lipid profile manifesting as significantly elevated TGs and LDL-C.

The association of abnormal serum lipid profiles and AGA has been reported in previous studies with controversial results. Şaşmaz et al. [16] compared the serum TC, HDL-C, LDL-C, TGs, and lipoprotein A levels in 41 male vertex-type AGA patients and 36 controls with and lipoprotein A in the AGA group, and higher but not statistically meaningful TC and LDL-C levels. Animal experiments have also shown that androgens can cause hyperlipidemia that poses a risk for CAD [17].

Greger et al. [18] showed that when external dihydrotestosterone was administered to castrated male monkeys, their HDL-C levels dropped. In another study, administering testosterone to monkeys resulted in an increase in TC and LDL-C levels, and a decrease in HDL-C levels. In a meta-analysis conducted by Shepherd et al. [19], a 1 mmol/l increase in the TG values was shown to increase the possibility of CAD by 30% in men and by 69% in women.

Sharrett et al. [20] 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 cardiovascular risk factors is essential in patients with subclinical disease.

Contrary to our results, Guzzo et al. [21] compared the serum lipid profile of 50 Hamilton III and IV vertex alopecia patients with a control group, and found no difference in HDL-C, LDL-C, TC, TGs, and TC/LDL rates. This inconsistency may be partially attributed to the different target populations studied and to the failure to control for other confounding factors, such as FH and smoking status.

Therefore, moderate or severe AGA may be considered as a marker of increased probability of CAD. Investigation and control of lipid profiles in patients with AGA may be important to reduce this risk. Therefore, serum lipid indices should be evaluated in these patients.

In the present study, FBS was significantly higher among cases than controls. This is similar to Ekmekci et al. [22] but was against Acibucu et al. [8] who found a nonsignificant difference in FBS between cases and controls.

In the present study, there were statistically significant differences between cases and control subjects regarding body weight and waist circumference. Similar results were reported previously by Arias-Santiago et al. [23] regarding waist circumference although they found a nonsignificant difference regarding body weight.

Regarding BMI, the current study showed a statistically significant difference between cases and healthy controls. This is in line with Matilainen et al. [24] who found higher mean BMI values in patients with AGA, but was not consistent with the study done by Arias-Santiago et al. [23].

We reported statistically significant differences between cases and controls regarding mean systolic BP values. Contrary to our results, Acibucu et al. [8] and Arias-Santiago et al. [23] demonstrated a nonsignificant correlation between hypertension and AGA.

Similar results were reported in previous studies by Ahouansou et al. [25] who demonstrated a significant correlation between hypertension and AGA, irrespective of age.

Arias-Santiago et al. [23] found that the mean systolic BP values were higher in patients with AGA than in controls.

There are androgen-mediated receptors accelerating the atherosclerotic process in the vascular endothelium. Androgens can accelerate atherosclerosis by proliferation of smooth muscle cells in vessels [26]. In addition, androgens implicated in AGA bind with mineralocorticoid receptors, favoring BP increase [27].

Another possible explanation for such association is the presence of hyperaldosteronism in AGA cases. Hyperaldosteronism underlies most hypertension cases and directly participates in the development of alopecia. This was observed in transgenic mice with skin overexpression of mineralocorticoid receptors [28].


  Conclusion Top


Lipid profile (TGs, HDL-C, and LDL-C) is significantly elevated in AGA patients. This means that their elevation in these cases may be a result of its pathogenesis.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Randall VA. The use of dermal papilla cells in studies of normal and abnormal hair follicle biology. Dermatol Clin 2005; 14:585–594.  Back to cited text no. 1
    
2.
Birch MP, Messenger AG. Genetic factors predispose to balding and non-balding in men. Eur J Dermatol 2001; 11:309–314.  Back to cited text no. 2
    
3.
Sinclair RD. Common baldness and androgenetic alopecia. In: Burns T, Breathnach S, Cox N, Griffiths CH, editors. Rook's textbook of dermatology. 7th ed. London: Blackwel Publishing Co Oxford; 2004; pp. 18–63  Back to cited text no. 3
    
4.
Tosti A, Camaeho-Martinez F, Dawber R. Management of androgenetic alopecia. J Eur Acad Dermatol Venereol 1999; 12:205–214.  Back to cited text no. 4
    
5.
Norwood OT. Male pattern baldness: classification and incidence. South Med J 1975; 68:1359–1365.  Back to cited text no. 5
    
6.
Hawk E, Brewslow RA, Graubard BI. Male pattern baldness and clinical prostate cancer in the epidemiologic follow-up of the First National Health and Nutrition Examination Survey. Cancer Epidemiol Biomark Prev 2000; 9:523–527.  Back to cited text no. 6
    
7.
Matilainen VA, Koskela P, Keinanen-Kiukaanniemi SM. Early onset of androgenetic alopecia associated with early severe coronary heart disease: a population-based, case control study. J Cardiovasc Risk 2001; 8:147–151.  Back to cited text no. 7
    
8.
Acibucu F, Kayatas M, Candan F. The association of insulin resistance and metabolic syndrome in early androgenetic alopecia. Singapore Med J 2010; 51:931.  Back to cited text no. 8
    
9.
Inui S, Itami S. Androgen actions on the human hair follicle: Perspectives. Experimental Dermatology 2012; 22:168–171.  Back to cited text no. 9
    
10.
Chumlea WC, Rhodes T, Girman CJ, Johnson-Levonas A, Lilly FR, Wu R, et al. Family history and risk of hair loss. Dermatology, 2004;209 (1):33-39.  Back to cited text no. 10
    
11.
Demark-wahnefried WE, lesko S, Conaway MR, Robertson CN, Clark RV, Lobaugh B, et al. Serum androgens: associations with prostate cancer risk and hair patterning. J Androl 1997; 18:495–500.  Back to cited text no. 11
    
12.
Sharma L, Dubey A, Gupta PR, Agrawal A. Androgenetic alopecia and risk of coronary artery disease. Indian Dermatol Online J 2013; 4:283.  Back to cited text no. 12
    
13.
Felizola SJ. Ursolic acid in experimental models and human subjects: Potential as an anti-obesity/overweight treatment? Research 2015; 3:294–303.  Back to cited text no. 13
    
14.
Wang G. Raison d'être of insulin resistance: the adjustable threshold hypothesis. J Royal Society Interf 2014; 11:10-21.  Back to cited text no. 14
    
15.
Isomaa BO, Almgren P, Tuomi T, Forsén B, Lahti K, Nissen M, et al. Cardiovascular morbidity and mortality associated with the metabolic syndrome. Diabetes Care 2001; 24:683–689.  Back to cited text no. 15
    
16.
Sasmaz S, Senol M, Ozcan A, Dogan G, Tuncer C, Akyol O, et al. The risk of coronary heart disease in men with androgenetic alopecia. J Eur Acad Dermatol Venereol 1999; 12:123–125.  Back to cited text no. 16
    
17.
Weyrich AS, Rejeski WJ, Brubaker PH, Parks JS. The effects of testosterone on lipids and eicosanoids in cynomolgus monkeys. Med Sci Sports Exerc 1992; 24:333–338.  Back to cited text no. 17
    
18.
Greger NG, Insull JW, Probstfield JL, Keenan BS. High-density lipoprotein response to 5-α-dihydrotestosterone and testosterone in Macaca fascicularis: a hormone-responsive primate model for the study of atherosclerosis. Metabolism, 1990; 39:919–924.  Back to cited text no. 18
    
19.
Shepherd J, Hunninghake DB, Barter P. Guidelines for lowering lipids to reduce coronary artery disease risk: a comparison of rosuvastatin with atorvastatin, pravastatin, and simvastatin for achieving lipid-lowering goals. Am J Cardiol 2003; 91:11–17.  Back to cited text no. 19
    
20.
Sharrett AR, Sorlie PD, Chambless LE, Folsom AR, Hutchinson RG, Heiss G, et al. Relative importance of various risk factors for asymptomatic carotid atherosclerosis versus coronary heart disease incidence: the Atherosclerosis Risk in Communities Study. Am J Epidemiol 1999; 149:843–852.  Back to cited text no. 20
    
21.
Guzzo CA, Margolis DJ, Johnson J. Lipid profiles, alopecia, and coronary disease: any relationship? Dermatol Surg 1996; 22:481.  Back to cited text no. 21
    
22.
Ekmekci TR, Ucak S, Basat O, Koslu A, Altuntas Y. The presence of insulin resistance and comparison of various insulin sensivity indices in women with androgenetic alopecia. Eur J Dermatol, 2007; 17:21–25.  Back to cited text no. 22
    
23.
Arias-Santiago S, Gutiérrez-Salmerón MT, Castellote-Caballero L, Buendía-Eisman A, Naranjo-Sintes R. Androgenetic alopecia and cardiovascular risk factors in men and women: a comparative study. J Am Acad Dermatol 2010; 63:420–429.  Back to cited text no. 23
    
24.
Matilainen V, Laakso M, Hirsso P. Hair loss, insulin resistance, and heredity in middle-aged women. A population-based study. J Cardiovasc Risk 2003; 10:227–231.  Back to cited text no. 24
    
25.
Ahouansou S, Le Toumelin P, Crickx B. Association of androgenetic alopecia and hypertension. Eur J Dermatol 2007; 17:220–222.  Back to cited text no. 25
    
26.
Fujimoto R, Morimoto I, Morita E, Sugimoto H, Ito Y, Eto S. Androgen receptors, 5 alpha-reductase activity and androgen-dependent proliferation of vascular smooth muscle cells. J Steroid Biochem Mol Biol 1994; 50:169–174.  Back to cited text no. 26
    
27.
Sainte Marie Y, Toulon A, Paus R, Maubec E, Cherfa A, Grossin M, et al. Targeted skin overexpression of the mineralocorticoid receptor in mice causes epidermal atrophy, premature skin barrier formation, eye abnormalities, and alopecia. Am J Pathol 2007; 171:846–860.  Back to cited text no. 27
    
28.
Arias-Santiago S, Gutiérrez-Salmerón MT, Castellote-Caballero L, Naranjo-Sintes R. Elevated aldosterone levels in patients with androgenetic alopecia. Br J Dermatol 2009; 161:1196–1198.  Back to cited text no. 28
    



 
 
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