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Polymorphism of Extrapituitary Promoter of PRL Gene and Relationships With Serum Prolactin Levels in Acne Vulgaris.

A

Assiut University

Status

Unknown

Conditions

Acne Vulgaris

Treatments

Diagnostic Test: blood sample

Study type

Observational

Funder types

Other

Identifiers

NCT03186222
POEPOPRGAGARWSPLIAV

Details and patient eligibility

About

Acne vulgaris is one of the most common skin diseases. It is a disease of the pilosebaceous units, clinically characterized by seborrhea, comedones, papules, pustules, nodules and, in some cases, scarring.

Full description

The pathogenesis of acne has been attributed to multiple factors such as increased sebum production, alteration of the quality of sebum lipids, regulation of cutaneous steroidogenesis, androgen activity, interaction with neuropeptides, exhibition of pro- and anti- inflammatory properties, follicular hyperkeratinization and the action of Propionibacterium acnes (P. acnes) within the follicle .

Central or peripheral stress may induce the development of clinical inflammation in the pilosebaceous unit, leading to the development of acne lesions or to exacerbation of pre-existing acne . Prolactin is one of the major hormonal signals that are immediately upregulated on psychoemotional and physical stress .

The discovery of locally produced extrapituitary prolactin and that human skin is both a source and target of prolactin production has increased interest in cutaneous prolactin research . Prolactin and prolactin receptors expression have now been demonstrated in several cutaneous cell populations, including keratinocytes, fibroblasts, sweat glands and sebaceous glands. Hence, prolactin is likely to be involved as a mediator in the ''brain-skin axis'' .

Given that the mammary gland is an epidermal derivative, it is not surprising that the pilosebaceous unit, another epidermal derivative, has also surfaced as a prominent, non-classical prolactin target organ expressing prolactin receptors .

In human skin, Prolactin and prolactin receptors are both expressed in the sebaceous gland , and prolactin stimulates sebum production . These effects are evident in women with hyperprolactinemia, who develop hirsutism and seborrhea, not uncommonly associated with female pattern balding . Patients treated with hyperprolactinemia-inducing neuroleptic agents also develop seborrhea . As sebocytes are prominent target cells of neuroendocrine signaling , prolactin might also contribute to the aggravating effect of psychoemotional stress on acne vulgaris. Besides the stimulation of sebocyte proliferation, which enhances holocrine secretion of this gland, this might also be related to effects on peripheral androgen metabolism .

The secretion of extrapituitary prolactin is regulated by the alternative promoter of prolactin gene , and the G/T polymorphism in position -1149 seems to be associated with level of prolactin expression .

In view of the recognized increase of human prolactin serum levels upon psychoemotional stress and the exacerbating effect of psychological stress on acne, together with a proposed role of prolactin in acne pathogenesis, it would be interesting to investigate the role of prolactin in acne vulgaris

Enrollment

200 estimated patients

Sex

All

Ages

12 to 40 years old

Volunteers

Accepts Healthy Volunteers

Inclusion and exclusion criteria

Inclusion Criteria: patients with acne vulgaris.

Exclusion Criteria:

  • patients below 12 years of age
  • patients recieving disorders and drug that could alter levels of prolactin such as thyroid disorders, renal and/or hepatic failure and drug use.

Trial design

200 participants in 2 patient groups

cases with acne vulgaris
Description:
A group of 100 patients with acne vulgaris. blood sample are taken in the morning hours, between 08:00 and 10:00 am.
Treatment:
Diagnostic Test: blood sample
control group
Description:
control group of 100 age and sex matched healthy volunteers. blood sample are taken in the morning hours, between 08:00 and 10:00 am.
Treatment:
Diagnostic Test: blood sample

Trial contacts and locations

0

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Central trial contact

Yasmin Tawfik, MD; Sara Awad, MD

Data sourced from clinicaltrials.gov

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