E-IJD® - ORIGINAL ARTICLE
|Year : 2022 | Volume
| Issue : 2 | Page : 205
|Insulin resistance in moderate to severe acne vulgaris
Monika Singh1, Dikshant Shri2
1 From the Department of Dermatology, Sawai Man Singh Medical College, Jaipur, Rajasthan, India
2 Department of Medicine, JNU Medical College, Jaipur, Rajasthan, India
|Date of Web Publication||13-Jul-2022|
Consultant Dermatologist, Department of Dermatology, Amar Jain Hospital, Jaipur, Rajasthan
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Introduction: Acne vulgaris is a chronic inflammatory disease of the pilosebaceous unit usually affects adolescents. It is seen on the face, neck, trunk and arms. The main pathogenic factors of acne are high sebaceous gland secretion, follicular hyper proliferation, high androgen effects, propionibacterium acnes colonization and inflammation. Objectives: To determine the presence of insulin resistance in moderate to very severe acne vulgaris. Material and Methods: One hundred sixty subjects were enrolled in the study consisting of 80 patients with moderate to very severe acne vulgaris and 80 age and sex-matched controls without acne. Fasting serum insulin and glucose levels were measured and insulin resistance was calculated by Homeostasis Model Assessment- Insulin Resistance (HOMA-IR) Index. The values were compared with the healthy control group. Results: Significant difference was observed in HOMA values and fasting insulin among the two groups (P < 0.001). The levels were significantly higher in the patient group than in the control group, whereas no significant difference was present in fasting glucose levels between the two group. Conclusions: In conclusion, insulin resistance was seen in majority of patients with acne. These results can add to the evidence regarding a potential association between metabolic dysregulation and acne.
Keywords: Acne vulagris, HOMA-IR, insulin resistance
|How to cite this article:|
Singh M, Shri D. Insulin resistance in moderate to severe acne vulgaris. Indian J Dermatol 2022;67:205
| Introduction|| |
Acne vulgaris is a chronic inflammatory disease of the pilosebaceous unit. It usually affects adolescents. It is seen on the face, neck, trunk and arms. Most cases of acne present with a pleomorphic variety of lesions consisting of comedones, papules, pustules, nodules and cyst. Four major factors play role in the pathogenesis of acne vulgaris, that is, hyperplasia of sebaceous glands and increased sebum production, hyperkeratinisation of pilosebaceous ducts, propionibacterium acnes colonization and periglandular inflammation and high androgen effects.
The role of insulin in acne is that it induces the production of androgens, which play a major role in the production of excessive sebum, hyperkeratinisation and proliferation of sebaceous glands. Therefore, insulin may have a role in aetiology and severity of the acne.
As there is lack of studies to find out insulin resistance in acne patients especially among the Indian population, the present study was aimed at to observe insulin resistance in moderate to very severe acne patients without having any other systemic complains, which may affect body insulin level.
| Aim and Objectives|| |
The present study was done to determine the presence of insulin resistance in patients with acne for which HOMA-IR was calculated, which is a composite outcome based on the product of fasting glucose and insulin.
| Material and Methods|| |
It was a cross-sectional observational study of a cohort of patients with and without acne, conducted in the Department of Dermatology, STD & Leprosy at a tertiary care hospital at Jaipur, Rajasthan, India from March 2016 to October 2017 with a sample size 160 of total study subjects. Eighty eligible male and female untreated patients with moderate to very severe acne vulgaris with normal body mass index (BMI) were included in the study and 80 age, and sex-matched controls attended the OPD with minor cutaneous complains unrelated to acne were recruited in the study. While subjects on any medications known to affect insulin metabolism, previous treatment with oral retinoids or any hormonal treatment for any reason in previous 3 months, cigarette smoking, history of thyroid dysfunction or a history of diabetes mellitus, hypertension, known case of malignancy, pregnancy, atherosclerotic vascular disease, psoriasis, polycystic ovarian disease or any other known metabolic disorders were excluded from the study. Written consent was taken from all the participants. Peripheral venous blood sample was collected from all the participants under aseptic conditions after >8 h of fasting. Insulin resistance was assessed using Homeostasis model assessment of insulin resistance (HOMA-IR). All baseline routine investigations were done at the beginning of the study including fasting blood glucose, fasting insulin level, complete blood count, ESR, total lipid profile, liver function test, renal function test, routine urine examination and a written informed consent was taken from all the participants. A detailed demographic data along with clinical history was recorded on a predesign proforma with the following points mentioned such as duration of acne, any aggravating factors, family history of acne, history of previous treatment for acne, any systemic illness, occupational history, diet history, BMI. Cutaneous examination including site of acne, type of acne (comedones/papules/pustules/nodules/cysts) and severity of acne. Patients of acne vulgaris were examined under good illumination and graded on the basis of severity as described by Global acne grading system (GAGS). HOMA and GAGS were calculated by using the following formula:
HOMA-IR = fasting glucose × fasting insulin/405
Fasting glucose was measured in mg/dL and insulin in μIU/mL. Values of more than 2.7 were taken as an indicator of insulin resistance.
Statistical analysis was performed with the SPSS, Trial version 23 for Windows statistical software package (SPSS Inc., Chicago, IL, USA) and Primer for the generation of descriptive and inferential statistics. Continuous variables were summarized as mean ± standard variation (SD). The Categorical data were presented as numbers (percent). Chi- square test was used for data analysis. Student's 't' test was calculated by taking into consideration the difference between the mean values and the standard deviation of each group. Probability P value < 0.05 was considered statistically significant.
| Results|| |
In our study, we included 80 cases and 80 controls, male outnumbered the females in both the groups making 72% of cases and 59% in controls. The GAGS was used for assessing the severity of acne [Table 1]. Among cases, 17.5% had moderate, 32.5% severe and majority belonged to the very severe acne vulgaris with 50% of the involved patients. There was no significant difference between the patient and control groups regarding sex or age (P > 0.05). The mean ± SD of age was 21 ± 3.9 years in cases and 22 ± 4.9 in controls. There was no difference between two groups in terms of weight, height or BMI (all P values > 0.05). While fasting, blood glucose levels were not different among the two groups (P > 0.05) [Table 2]; the fasting insulin levels were significantly higher in the patient group than in the control group (P < 0.001), and a significant difference is found in P values of HOMA between the two groups (P < 0.001) [Table 2]. Our study concluded that insulin resistance was present in patients with acne but no direct relationship was found between acne severity and insulin resistance [Table 3].
| Discussion|| |
Acne vulgaris is a self-limiting chronic inflammatory condition of the pilosebaceous follicles and is characterized by comedones, papules, pustules, nodules and scars. It can manifest at any time during life but usually present between ages of 12–24 years. Pathogenesis of acne is known since a very long time as hyperseborrhea, follicular hyperkeratinization, Propionibacterium acne colonization and inflammation, yet the mechanism of acne is not fully understood. In this study, we aim at investigating the relationship between moderate to very severe acne vulgaris and insulin resistance.
Previous studies suggest that high insulin level because of intake of high glycemic load diet may trigger acne by inducing hyperinsulinemia.,, Low glycemic load diet is having a role in the prevention of hyperinsulinemia by lowering the postprandial insulin., Another clinical example about the relation between acne and IGF is Laron syndrome (LS). LS is characterized by congenital IGF-1 deficiency. In his study, Ben-Amitai and Laron observed that IGF-1 deficiency prevents the occurrence of acne. They suggested that IGF-1 and androgens are necessary for the development of acne.
Studies done by Anderson et al. and by Adebamowo et al. showed the same results that hyperinsulinemia induced by giving increasing amount of chocolates day by day to the patients resulted in the flaring of acne.
Acne is also a common occurrence in PCOS patients, as are high levels of IGF-1 and androgens. Both insulin and IGF induce the production of androgens while simultaneously inhibiting the hepatic synthesis of sex hormone-binding globulin (SHBG); therefore, the bioavailability of androgens increases. Hyperinsulinemia increases serum levels of IGF-1 and reduces serum levels of insulin-like growth factor binding protein 3. These two factors directly influence proliferation and apoptosis of keratinocytes. Insulin-like growth factor may also stimulate some comedogenic factors such as androgens, growth hormone and glucocorticoids.,, The incidence of acne corresponds more closely to insulin and IGF-1 levels than plasma androgens.,
Insulin resistance may occur during various clinical conditions such as physiological conditions, for example, puberty, pregnancy, old age or as a side effect of certain medications, for example, corticosteroids, some oral contraceptives, diuretics or as a symptom of certain diseases, for example, type 2 diabetes, cardiovascular disease, essential hypertension, PCOS, nonalcoholic fatty liver disease, certain cancer.
In our study, the average age of the subjects enrolled was 20 years; hence, it is unlikely that most of the abovementioned chronic conditions are the causes of insulin resistance found in our patients and apart from that the diseases that had also been ruled out by the physical examinations and investigations advised as set in predesigned proforma.
Study done by Munichandrappa et al. did not find any significant correlation between acne and insulin resistance in Indian population, which contradicts the many of studies; the reasons for that can be the small population size and bulk of patients mainly belonged to the mild category of acne, while in our study, we have taken patients having moderate to very severe acne vulgaris. While the study conducted by Nagpal et al. concluded that postadolescent male patients with acne are more prone to have higher mean HOMA-IR values, higher mean fasting plasma glucose levels and higher prevalence of insulin resistance compared with the controls in their study. And Kartal et al. did a study where they enrolled only female patients with acne and found a positive relationship between female acne and insulin resistance.
Here, in our study, we used HOMA-IR index for evaluating insulin resistance. The HOMA-IR index has been an accepted formula for measuring insulin resistance since its original publication by Matthews et al. in 1985. There are many various methods to describe insulin sensitivity. Among other models, gold standard methods are euglycemic clamp and modified minimal model, but they are used for research only because they are too invasive for general epidemiologic studies., Therefore, methods such as fasting insulin level, fasting glucose/insulin ratio, HOMA-IR and quantitative insulin-sensitivity check index are suggested to be used in population studies. HOMA-IR is a frequently used parameter in clinical research.
In taken view of our study, there was no difference between the two groups in terms of demographic profile including, sex, age, BMI etc. In our study, patients with acne were showing insulin resistance as compared to the controls. There are only a few studies done to assess insulin resistance in acne patients. In our study, we found statistically significant values of serum insulin despite of normal fasting glucose levels in patients with moderate to very severe acne in compare to the control group.
The study showed a significant difference between mean insulin and HOMA-IR between the two groups, but no significant difference was obtained in terms of fasting glucose level in between the two groups. The rising insulin may initiate the earliest change of acne before hyperandrogenism. This trend can be seen in cases that develop acne before other signs of puberty. This insulin resistance in these patients may be due to the adoption of western diet rich in carbohydrate and other factors like sedentary lifestyle, spending more time on electronic gadgets and lack of outdoor activities. It may be one of the possible mechanisms involved in pathogenesis of acne. These results can add to the evidence regarding potential association between metabolic dysregulation and acne. Hence, we believe that insulin resistance should be determined in acne especially on those patients who are not responding to the conventional treatment. These patients should be advised to take low glycaemic diet along with the drugs that reverse insulin resistance.
| Conclusion|| |
In our study, we found statistically significant values of serum insulin despite of normal fasting glucose levels in our patients compared to the control group and concluded that insulin resistance was present in our study in acne patients. Therefore, with conventional treatment of acne, anti-insulin drugs may be used as an adjunctive to treat moderate and severe acne vulgaris. Food with high glycaemic index are advised to avoid. Insulin resistance may be a stage of prediabetes, and the patients may develop type 2 diabetes or metabolic syndrome in future, so those patients showing insulin resistance should be followed-up to determine whether they develop any other conditions associated with insulin resistance.
This result cannot be generalised to all patients as mild acne patients were excluded from the study.
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.
| References|| |
Doshi A, Zaheer A, Stiller MJ. A comparison of current acne grading systems and proposal of a novel system. Int J Dermatol 1997;36:416-8.
Bataille V, Snieder H, MacGregor AJ, Sasieni P, Spector TD. The influence of genetics and environmental factors in the pathogenesis of acne: A twin study of acne in women. J Invest Dermatol 2002;119:1317-22.
Jenkins D, Kendall C, Augustin L, Franceschi S, Hamidi M, Marchie A, et al
. Glycemic index: Overview of implications in healthy and disease. Am J Clin Nutr 2002;76:266S-73S.
Carnethon MR, Loria CM, Hill JO, Sidney S, Savage PJ, Liu K, et al
. Risk factors for the metabolic syndrome: The coronary artery risk development in young adults (CARDIA) study, 1985-2001. Diabetes Care 2004;27:2707-15.
McKeown N, Meigs J, Liu S, Saltzman E, Wilson PW, Jacques PF. Carbohydrate nutrition, insulin resistance and the prevalence of the metabolic syndrome in the Framingham offspring cohort. Diabetes Care 2004;27:538-46.
Ben-Amitai D, Laron Z. Effect of insulin-like growth factor-1 deficiency or administration on the occurrence of acne. J Eur Acad Dermatol Venereol 2011;25:950-4.
Anderson PC. Foods as the cause of acne. Am Fam Physician 1971;3:102-3.
Adebamowo CA, Spiegelman D, Berekey CS, Danby FW, Rockett HH, Colditz GA, et al
. Milk consumption and acne in adolescents girls. Dermatol Online J 2006;12:1.
Ludwig DS. The glycemic index: Physiological mechanisms relating to obesity, diabetes, and cardiovascular disease. JAMA 2002;287:2414-23.
Arora MK, Yadav A, Saini V. Role of hormones in acne vulgaris. Clin Biochem 2011;44:1035-40.
Del Prete M, Mauriello MC, Faggiano A, Di Somma C, Monfrecola G, Fabbrocini G, et al
. Insulin resistance and acne: New risk factor for men? Endocrine 2012;42:555-60.
Stern MP. The insulin resistance syndrome. In: International textbook of diabetes mellitus. 2nd
ed. Alberti KGMM, Zimmet P, De Fronzo RA, Keen H. John Wiley and Sons, Ltd. Chichester 1997. p. 255-83.
Cordain L, Lindeberg S, Hurtado M, Hill K, Eaton SB, Brand-Miller J. Acne vulgaris – a disease of Western civilization. Arch Dermatol 2002;138:1584-90.
Melnik BC, John SM, Plewig G. Acne: Risk indicator for increase body mass index and insulin resistance. Acta Derm Venereol 2013;93:644-9.
Munichandrappa P, Manjunath KG, Kiran C, Variyar A. A comparative study of insulin resistance in acne vulgaris. Int J Res Dermatol 2017;3:403-6.
Nagpal M, De D, Handa S, Pal A, Sachdeva N. Insulin resistance and metabolic syndrome in young men with acne. JAMA Dermatol 2016;152:399-404.
Kartal D, Yildiz H, Ertas R, Borlu M, Utas S. Association between isolated female acne and insulin resistance: A prospective study. G Ital Dermatol Venereol 2016;151:353-7.
Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: Insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 1985;28:412-9.
DeFronzo RA, Tobin JD, Andres R. Glucose clamp technique: A method for quantifying insulin secretion and resistance. Am J Physiol 1979;237:214-23.
Bergman RN. Towards physiological understanding of glucose tolerance-minimal model approach. Diabetes 1989;38:1512-27.
Kurtoğlu S, Hatipoğlu N, Mazıcıoğlu M, Kendirici M, Keskin M, Kondolot M, et al
. Insulin resistance in obese children and adolescents: HOMA-IR cut-off levels in the prepubertal and pubertal periods. J Clin Res Pediatr Endocrinol 2010;2:100-6.
[Table 1], [Table 2], [Table 3]
| Article Access Statistics|
| Viewed||310 |
| Printed||10 |
| Emailed||0 |
| PDF Downloaded||54 |
| Comments ||[Add] |