الفهرس 
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Abstract
A
cne vulgaris is a chronic inflammatory disease of the pilosebaceous unit, and it is one of the most common dermatological conditions worldwide. Some of the key mechanisms of pathogenesis are the disturbed sebaceous gland activity associated with excess sebum production and alterations in sebum fatty acid composition, dysregulation of the hormone microenvironment, interaction with neuropeptides, follicular hyperkeratinization, and induction of inflammation and dysfunction of the innate and adaptive immunity.
Apelin is a new peptide identified as the endogenous ligand of the G protein-coupled receptor, APJ. Apelin is secreted from brain, placenta, lungs, heart, kidneys also from the veins of coronary artery, saphenous vein, kidneys and adrenal gland. Apelin is secreted as preproapelin, that has the sequence of 77 amino acids, preproapelin is then fragmented by protease and apelin will be named as Apelin-13, Apelin-17 and Apelin-36, depending on the number of amino acids it contains. Apelin-36 and apelin-13 represent the predominant and most active isoforms.
The increase in blood glucose stimulates insulin secretion which decreases the availability of binding protein for insulin-like growth factor 1 (IGF-1) which facilitates its effects on basal keratinocyte proliferation. Also, insulin induces the synthesis of androgens which in turn cause acne, and this explains the relation between acne vulgaris and insulin resistance.
In our study we aimed to evaluate the serum apelin levels and its relation to insulin resistance in acne vulgaris patients in comparison with healthy controls.
All patients were subjected to full history taking, general examination and dermatological examination. We excluded pregnant and lactating females, diabetic and renally impaired patients, patients on hormonal treatment, patients with history of previous treatment with oral retinoids, and patients with psoriasis and atopic dermatitis and patients who have had any hormonal disturbances like polycystic ovary as well as patients on medications known to aggravate acne.
In the current study, we recorded waist and hip circumference, BMI and GAG score for acne patients and healthy controls. Also, we measured serum apelin, fasting insulin, and fasting glucose and we calculated HOMA-IR.
We conducted a study on 32 acne vulgaris patients and 32 age- and sex- matched healthy controls who were recruited from the Outpatient Dermatology Clinic at Ain Shams University. The patients group was divided into three groups (mild, moderate, severe) according to the global acne grading system (GAG).
The current study was the first to report the higher level of Apelin in the serum of acne vulgaris patients as compared to healthy controls.
We found that acne patients had significantly higher serum levels of apelin compared to their age-, sex-, body mass index- matched controls. These high serum levels did not differ significantly between acne cases of different severity grades and were not correlated to body mass index or HOMA-IR scores of the acne patients.
Finally, we concluded that serum levels of apelin is significantly higher in acne vulgaris patients compared to control subjects, but there is no significant difference in its levels between mild, moderate and severe acne cases. HOMA-IR values also show significant higher levels in acne patients compared to controls, which suggest the link between insulin resistance and acne. Despite of these higher levels of HOMA- IR values, there is no significant relation with the detected higher levels of apelin in sera of acne vulgaris patients.
More studies are required to provide a detailed explanation about the role of apelin in acne vulgaris patients and its relation to the pathogenesis of the disease.