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Status unknownNCT03186222Updated Jun 14, 2017

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

An observational study in Acne Vulgaris, sponsored by Assiut University. Status unknown. Open to participants aged 12 Years to 40 Years, including healthy volunteers. Per ClinicalTrials.gov, last updated 2017-06-14.

Sponsored by Assiut University · Observational

The sponsor has not verified this record recently (last verified Jun 2017), so the status shown — last known as Not yet recruiting — may be out of date.
Study type
Observational
Model
Case-control
Time perspective
Prospective
Enrollment
200
Ages
12 Years to 40 Years
Sex
All
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Study summary

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.

Read the detailed 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

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Conditions studied

  • Acne Vulgaris

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03

In context

Acne Vulgaris

730 studies on the registry are indexed under Acne Vulgaris; 86 are open to participants now.

This study's planned enrollment of 200 is above the median of 90 across 81 observational studies indexed under Acne Vulgaris.

Browse Acne Vulgaris studies →

Lead sponsor

Assiut University is the lead sponsor of 4,901 studies on the registry; 2,098 are open to participants now.

Of its 13 completed or terminated interventional studies of FDA-regulated products, 0 (0%) have results posted.

Counted across the registry records on this site, refreshed daily.

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Who can participate

Ages eligible
12 Years to 40 Years
Sexes eligible
All
Accepts healthy volunteers
Yes
Sampling method
Non-probability sample

Study population

A group of 100 patients with acne vulgaris and another control group of 100 age and sex matched healthy volunteers

Eligibility 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.
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Study design

Observational model
Case-control
Time perspective
Prospective
Enrollment
200 participants (estimated)
Patient registry
No

Groups and cohorts

  • cases with acne vulgaris

    A group of 100 patients with acne vulgaris. blood sample are taken in the morning hours, between 08:00 and 10:00 am.

    Diagnostic Test: blood sample

  • control group

    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.

    Diagnostic Test: blood sample

Interventions

  • Diagnostic testblood sample

    Serum PRL levels are measured using ELISA assay kit in both groups and correlated with severity of acne in acne group. The genomic DNA from peripheral leukocytes is extracted. Genotyping of 1149G/T single nucleotide polymorphism (SNP) PRL extrapituitary promoter is done in acne patients and healthy individuals (control group) using PCR-RFLP method.

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What researchers measure

Primary outcomes

  1. polymorphism of extrapituitary promoter of PRL gene in acne cases and controls

    The blood samples are taken in the morning hours, between 08:00 and 10:00 am The genomic DNA from peripheral leukocytes is extracted. Genotyping of 1149G/T single nucleotide polymorphism (SNP) PRL extrapituitary promoter is done in acne patients and healthy individuals (control group) using PCR-RFLP method. The genomic DNA from peripheral leukocytes is extracted. Genotyping of 1149G/T single nucleotide polymorphism (SNP) PRL extrapituitary promoter is done in acne patients and healthy individuals (control group) using PCR-RFLP method.

    Time frame: 1 year

Secondary outcomes

  1. serum prolactin levels in acne patients and controls and among different acne severity grades

    The blood samples are taken in the morning hours, between 08:00 and 10:00 am. Serum PRL levels are measured using ELISA assay kit in both groups and correlated with severity of acne in acne group.

    Time frame: 1 year

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Study locations

No study locations are listed for this record.

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References and documents

Publications

  • Zouboulis CC, Eady A, Philpott M, Goldsmith LA, Orfanos C, Cunliffe WC, Rosenfield R. What is the pathogenesis of acne? Exp Dermatol. 2005 Feb;14(2):143-52. doi: 10.1111/j.0906-6705.2005.0285a.x. PubMed 15679586 ↗
  • Ganceviciene R, Graziene V, Bohm M, Zouboulis CC. Increased in situ expression of melanocortin-1 receptor in sebaceous glands of lesional skin of patients with acne vulgaris. Exp Dermatol. 2007 Jul;16(7):547-52. doi: 10.1111/j.1600-0625.2007.00565.x. PubMed 17576233 ↗
  • Arck PC, Slominski A, Theoharides TC, Peters EM, Paus R. Neuroimmunology of stress: skin takes center stage. J Invest Dermatol. 2006 Aug;126(8):1697-704. doi: 10.1038/sj.jid.5700104. PubMed 16845409 ↗
  • Oakes SR, Rogers RL, Naylor MJ, Ormandy CJ. Prolactin regulation of mammary gland development. J Mammary Gland Biol Neoplasia. 2008 Mar;13(1):13-28. doi: 10.1007/s10911-008-9069-5. Epub 2008 Jan 25. PubMed 18219564 ↗
  • Zouboulis CC, Schagen S, Alestas T. The sebocyte culture: a model to study the pathophysiology of the sebaceous gland in sebostasis, seborrhoea and acne. Arch Dermatol Res. 2008 Sep;300(8):397-413. doi: 10.1007/s00403-008-0879-5. Epub 2008 Aug 9. PubMed 18690467 ↗
  • Langan EA, Ramot Y, Goffin V, Griffiths CE, Foitzik K, Paus R. Mind the (gender) gap: does prolactin exert gender and/or site-specific effects on the human hair follicle? J Invest Dermatol. 2010 Mar;130(3):886-91. doi: 10.1038/jid.2009.340. Epub 2009 Nov 5. No abstract available. PubMed 19890346 ↗
  • Reem GH, Ray DW, Davis JR. The human prolactin gene upstream promoter is regulated in lymphoid cells by activators of T-cells and by cAMP. J Mol Endocrinol. 1999 Jun;22(3):285-92. doi: 10.1677/jme.0.0220285. PubMed 10343287 ↗
  • Paus R. Does prolactin play a role in skin biology and pathology? Med Hypotheses. 1991 Sep;36(1):33-42. doi: 10.1016/0306-9877(91)90161-q. PubMed 1766412 ↗

Individual participant data

Plan to share: No

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Updates

Tracking since Sep 25, 2026
No changes since tracking began. The registry record was last updated on Jun 14, 2017, before this site started recording changes on Sep 25, 2026. Its history is on ClinicalTrials.gov ↗
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Registry details

Key details

Study ID
NCT03186222
Lead sponsor
Assiut University
Responsible party
Yasmin Mostafa Tawfik (principal investigator, Assiut University) — Principal investigator
First posted
Jun 14, 2017
Start date
Jan 2018 (estimated)
Primary completion
Jan 2019 (estimated)
Completion
Jun 2019 (estimated)
Last update
Jun 14, 2017

Study contacts

Sara Awad, MD
Contact
saramawad@gmail.com
+201023102094
Yasmin Tawfik, MD
Contact
dr.yasminmostawfik@yahoo.com
01006033331
Sara Awad, MD
principal investigator · Assiut University

Oversight

Data monitoring committee
No
FDA-regulated drug
No
FDA-regulated device
No
View the source record on ClinicalTrials.gov ↗

Not currently enrolling

This study is status unknown, as verified in Jun 2017. You cannot join it, but the record below documents what was studied.

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