Prolactin: Does it Have a Role in the Etiopathogenesis of Psoriasis?

Psoriasis is a common inflammatory skin disorder. People with psoriasis typically have sharply demaracated chronic erythematous plaques covered by silvery white scales. The disease is characterized also by hyperproliferation of keratinocytes, which is the hallmark of psoriasis process. Although many theories have been proposed regarding the aetiopathogenesis of psoriasis, it is yet to be fully understood. Recently, it has been reported that prolactin (PRL) which possesses a variety of physiological action including growth promoting activity, exerts a proliferative effect on human keratinocytes. prolactin may therefore , play an important role in the pathogenesis of psoriasis.

The aim of the present study is to detect the role of serum prolactin in the pathogenesis of psoriasis.

Methods: we investigated the serum levels of prolactin in 60 patients with psoriasis vulgaris (30 males and 30 females), their age ranged from 10 and 60 years with mean age 39.83±14.5. Patients had stopped any topical and system one month before taking the sample. Also we investigated the serum levels of prolactin in 20 age and sex matched healthy control subjects for comparison (10males and 10 females), their age ranged from 19 and 60 years with mean age 36.15±13.697. Each patient was subjected to a detailed history taking and they were evaluated clinically according to PASI score. We excluded renal and hepatic patients, pregnant and lactating women, females with history of menstrual irregularities, patients who are receiving any medication affecting prolactin level and males with sexual problems, as these groups may affect prolactin level.

Result: There was statistically significant difference of serum prolactin levels in psortiatic patients in comparing with the controls (p=0.001).

Conclusion: Prolactin may have a role in the aetiopathogenesis of psoriasis. It is not a secondary event to the disease severity as assessed by PASI score.

Prolactin: Does it Have a Role in the Etiopathogenesis of Psoriasis?

Alaa Hassan Maraee, Hanna Mohamed El-Sayed Emam, Mohamed Abdel Wahed and May Mohamed Abdel Monem Shoeib

Department of Dermatology, Venereology & Andrology, Faculty of Medicine, Menoufiya University & National
Research Center

Keyword: Prolactin, Psoriasis, PASI                                                                                                                                                                                                     

Abstract

Psoriasis is a common inflammatory skin disorder. People with psoriasis typically have sharply demaracated chronic erythematous plaques covered by silvery white scales. The disease is characterized also by hyperproliferation of keratinocytes, which is the hallmark of psoriasis process. Although many theories have been proposed regarding the aetiopathogenesis of psoriasis, it is yet to be fully understood. Recently, it has been reported that prolactin (PRL) which possesses a variety of physiological action including growth promoting activity, exerts a proliferative effect on human keratinocytes. prolactin may therefore , play an important role in the pathogenesis of psoriasis.

The aim of the present study is to detect the role of serum prolactin in the pathogenesis of psoriasis.

Methods: we investigated the serum levels of prolactin in 60 patients with psoriasis vulgaris (30 males and 30 females), their age ranged from 10 and 60 years with mean age 39.83±14.5. Patients had stopped any topical and system one month before taking the sample. Also we investigated the serum levels of prolactin in 20 age and sex matched healthy control subjects for comparison (10males and 10 females), their age ranged from 19 and 60 years with mean age 36.15±13.697. Each patient was subjected to a detailed history taking and they were evaluated clinically according to PASI score. We excluded renal and hepatic patients, pregnant and lactating women, females with history of menstrual irregularities, patients who are receiving any medication affecting prolactin level and males with sexual problems, as these groups may affect prolactin level.

Result: There was statistically significant difference of serum prolactin levels in psortiatic patients in comparing with the controls (p=0.001).

Conclusion: Prolactin may have a role in the aetiopathogenesis of psoriasis. It is not a secondary event to the disease severity as assessed by PASI score.

Introduction

Psoriasis is a chronic skin disease that affects about 1.5% of the Caucasian population and is characterized by typical macroscopic and microscopic skin alterations. Psoriatic lesions are sharply demarcated, red and slightly raised lesions with silvery scales⁽²¹⁾.

Although many theories have been proposed regarding the pathogenesis of psoriasis, it is not yet fully understood .Much attention has been directed to the influence of cytokines in psoriasis. It is considered to be an autoimmune disease⁽¹⁾.A defective response of the hypothalamus pituitary adrenal axis to cytokine stimuli was suggested as a possible site of abnormality in inflammatory autoimmune disease⁽¹⁹⁾.

Psoriasis etiopathogenesis is complex and not well known. Lately, besides many different factors that are regarded to play an important role in psoriasis pathology, hormones have been taken into consideration.  The modulation of psoriasis course is studied. The possible role of prolactin (PRL), sex hormones and stress hormones was emphasized in etiology of psoriasis⁽⁴⁾.

Prolactin which is a polypeptide hormone possessing a variety of physiological actions including growth promoting activity in vivo⁽³⁾ and proliferative response to different normal and neoplastic cell types including epithelial cells and lymphocytes in vitro. It has been reported that prolactin exerts a proliferative effect on human keratinocytes⁽⁷⁾.On the other hand, others suggested that prolactin act as a neuroendocrinal modulator of skin immune system by forming a “prolactin –circuit” between the central nervous system and the skin⁽¹⁶⁾.

Prolactin therefore may play an important role in the pathogenesis of psoriasis either through its effect on keratincytes proliferation or its effect on the immune system⁽¹⁵⁾.

Prolactin has been shown to have immunomudolatory like effect. It plays a role in the activity of autoimmune diseases for example systemic lupus erythematosus and rheumatoid arthritis⁽²⁾.

Aim of work

To evaluate serum prolactin level in psoriatic patients and clarify if prolactin has a role in etiopathogenesis of psoriasis or not?

Patients and Methods

This study included 60 patients suffering of psoriasis and 20 age-matched healthy control subjects who presented to the out-patient clinic of dermatology at Menoufiya Faculty of Medicine, Houd El Marsoud hospital and that of the National Research Center between the period of February 2008 and October 2008.

These patients had received no topical or systemic treatment one month prior to sampling. Control group includes 20 age-matched healthy control subjects with no history of skin abnormalities or any chronic debilitating disease.

Methods

All psoriatic patients were subjected to the following:

·      Full medical history taking.

·      Clinical examination.

·      Exclusion criteria.

·      Laboratory investigations.

Full history taking

All patient was subjected to a detailed history including personal history (age, sex, occupation, marital status and special habits), present history (of the disease), past history (history of drug intake, lactation, menstrual irregularities in females, andrological complaints in males and duration of the disease) as well as family history.

Clinical examination

A complete dermatological examination was done for each patient so as to determine the extent and distribution of the disease. The status of the disease in psoriatic patient was scored by means of psoriasis area severity index (PASI score), evaluating erythema, infiltrarion, desquamation and surface area where the degree of affection is evaluated according to the following table (No. 1). The total sum of erythema, infiltration and desquamation is multiplied by the value of area then by 0.1 for head, 0.3 for trunk 0.2 for lower limbs and 0.4 for the upper limbs. The highest potential PASI score is 72; the lowest is 0.

Exclusion criteria

The following patients were excluded from the study:

·      Hepatic and renal patients as both may affect the level of the prolactin hormone (all the included patients should have normal liver and kidney function tests).

·      Pregnant or lactating females (to exclude physiological hyperprolactinemia).

·      Females with history of menstrual irregularities (to exclude pathological hyperprolactinemia).

·      Patients who are receiving any medications affecting prolactin such as phenothiazines (chropromazine), antidopaminergic agents (metaclopramide), antihypertensive agents (calcium channel blokers, methyledopa) and H2 blokers (cimitidine).

Laboratory investigations

All studied patients are subjected to the following laboratory investigations:

·      Complete blood picture (CBC) was done on coulter counter (celtac-5) on the same day.

·      The routine chemical investigations all were done on BMHitachi 911 on the same day and include estimation of: kidney function (serum urea and creatinine), liver functions (serum SGPT and SGOT). Serum prolactin (PRL).

·      Hormonal assay that included serum prolactin measured by ELISA technique.

·      MRI skull in cases with serum PRL more than 100 pg to exclude prolactinoma.

Statistical analysis:

·      Data were analyzed on an IBM compatible computer using statistical package for social sciences (spss) win version 9 statistical package. Numerical data was described in terms of means and standard deviation.

·      Categorical data were described in terms of ratio and percentages.

Results

This study was carried out on 60 patients (30 males and 30 females) suffering from psoriasis and 20 controls, where serum prolactin is measured for patients and controls. Patients presented to the out-patients clinic of dermatology of Menoufiya university hospital, National research center and Hod El-Marsoud hospital. Twenty control subjects were included in this study (9 male and 11 females).

The age of all patient groups ranged from 10 and 60 years with mean age 39.83±14.5 years. The age of control groups ranged from 19 and 60 years with mean age 36.15±13.697 years. By comparing the diseased group and the control group regarding the age, there were no statistically significant differences between means (Table 2).

Serum prolactin level among cases showed statistically significant elevation 80.785±90.05 as compared to control group 8.13± 2.42 (Table 3). The differences between male and female patients regarding serum prolactin level showed no statistical significant differences (Table 4).

No statistically significant differences were detected in serum prolactin level among cases with positive family history compared to those with negative family history (Table 6).

Comparison between serum prolactin level in relation to duration of illness revealed that serum prolactin level is significantly higher among patients with disease duration ≥ 5years compared to those with duration < 5 years (Table 5).

Comparison between patients with disease duration < 5 years and disease duration ≥ 5years as regarding PASI score showed statistically significant difference in Table (7).

PASI score has of no significant difference among patients with –ve family history of psoriasis compared to those with +ve family history as in Table (8).

Relation between PASI score and serum prolactin above 100 ng/ml showed significant relation,but no significant relation in patients with serum prolactin less than 100 ng/ml as in Table (9).

Table 1.    Showing PASI calculation.

Table 2.    Comparison between the diseased group and the control group as regards the age

Table 3.    Comparison between diseased group and the control group as regards the serum prolactin level

Table 4.    Comparison between male and female in the diseased group as regards the serum prolactin level

Table 5.    Comparison between patients with disease duration equal or more than 5 years and those less than 5 years as regards the serum prolactin level

Table 6.    Comparison between patients with +ve family history and those with –ve family as regards the serum prolactin level

Table 7.    Comparison between patients with disease duration equal or more than 5 years and those less than 5 years as regards PASI score

Table 8.    Comparison between patients with +ve family history and those with –ve family as regards PASI score

Table 9.    Comparison between patients with serum Prolactin level more than 100 ng/mland those less than 100 ng/mlas regards PASI score

Discussion

Psoriasis is a common inflammatory skin disease characterized by infiltration of inflammatory cells into the epidermis and altered keratinocytes differentiation. Psoriasis is currently thought of as a T-cell mediated “type-1 autoimmune disease”⁽¹²⁾.

Although many theories have been involved in the pathogenesis of psoriasis, it is yet to be fully understood⁽¹³⁾.

The process begins with an environmental factor, which induces T cell to produce cytokines. The cytokines stimulates keratinocyte proliferation and production of antigenic adhesion molecules in the dermal blood vessels. Much attention has been directed to the influence of cytokines in psoriasis⁽¹⁾.Investigation has now verified that the clinical manifestations of psoriasis follow T cell activation and cytokine production⁽¹⁰⁾.

One of the important hormones produced is prolactin (PRL) which possesses a variety of physiological actions, including growth-promoting activity and proliferation responses of different cell types including epithelial cells and lymphocytes. It has been reported that PRL exerts a proliferative effect on human keratinocytes, PRL may therefore play an important role in the pathogenesis of psoriasis where hyperproliferation of keratinocytes is the hallmark of the disease process⁽⁷⁾.

In the present study, we investigated the serum level of PRL in 60 patients with psoriasis vulgaris, guttate and erythrodermic psoriasis and 20 healthy control subjects for comparison. When the serum prolactin levels in psoriatic patients were correlated with the controls, the differences was statistically significant. P value is significant when it is ≤0.05. Also, we notice that no significant association between the clinical type and level of prolactin hormone.

Our results were supported byGiasuddin et al.⁽⁷⁾who assessed the serum level of PRL in 12 patients with psoriasis vulgaris and the results were compared with 20 normal control subjects. They found that serum prolactin in psoriatic patients is significantly higher than those in control subjects. They suggested that raised serum PRL level may have a role in the hyperproliferation of keratinocytes in vivo, the hallmark of the psoriasis disease process.

However, this finding was against Gorpelioglu et al.⁽⁸⁾ who measured the concentration of PRL in 39 patients with psoriasis and 36 normal control subjects. They found no significant difference between blood PRL levels in patients and control subjects.

Also this finding was against Hedman et al.⁽⁹⁾ who measured the concentration of PRL in 25 patients with psoriasis and 25 normal control subjects using radioimmunoassay. They found no significant differences between blood PRL levels in patients and control subjects.

Priestley et al.⁽¹⁸⁾ did not find a significant difference in PRL and growth hormone levels between patients and controls.

It has long been known that normal PRL levels are required for function of immune-competent T and B lymphocytes. The recent view held is that high serum levels of PRL may help inhibition of natural killer cells in vivo. PRL exerts its effects on humoral and cellular immunity via the PRL receptors on leucocytes, including lymphocytes and causes proliferation and differentiation. CD 4(+) T lymphocytes secrete their cytokines in stimulated keratinocytes; thus inflammation increases⁽⁸⁾.

Misery⁽¹⁴⁾, has found that neurohormones such as prolactin are expressed in the skin and secreted by cutaneous cells which also express prolactin receptors. These neurohormones affect epidermal and dermal cells during the course of skin diseases especially inflammatory reactions. This is particularly true in psoriasis as prolactin was found to be responsible for induction and maintenance of the inflammatory process in the diseases.

Paus⁽¹⁶⁾,has also suggested that the potential significance of prolactin for human biology and pathology is due to the fact the prolactin acts as a neuroendocrine modulator of skin epithelial cell proliferation especially in psoriasis.

As regard the bromocriptine which is the inhibitor for PRL hormone secretion in psoriatic patients, Valentino et al.⁽²⁰⁾ tested the activity of bromocriptine in 18 untreated psoriatic patients. Bromocriptine was shown to be effective in 13 of the 18 psoriatic patients.

Eurly et al.⁽⁶⁾have found that adding bromocriptine to gold salts was followed by a efficacy with improvement in clinical, biological and occupational status in cases with psoriatic. Because none of cases had hyperprolactinaemia, the bromocriptine probably had an intrinsic anti-inflammatory effect.

It has been hypothesized that PRL may modulate skin immune system and may be involved in the pathogenesis of psoriasis; psoriatic patients are often associated with hyperprolactinemia or bromocriptine which inhibits PRL release is therapeutically effective for psoriatic. Functional PRL receptors (PRLRs) are detected on epidermal keratinocytes, and PRL effectively increased the in vitro growth of keratinocytes. Prolactin may enhance IFN-Y-induced chemokines (CXC : chemokin, L : ligand ) CXCL9, CXCL10, and CXCL11 production in keratinocytes. Prolactin may promote type 1 T cell infiltration into psoriatic lsions via these chemokines⁽¹¹⁾.

One anti-psoriatic drug, cyclosporine A (CyA) is known to suppress PRL binding to the PRLR. This agent may thus suppress PRL-induced CXCL9, CXCL10, or CXCL11 production in keratinocytes, indicating one possible mechanism of its therapeutic efficacy for psoriasis⁽¹¹⁾.

Cyclosporine A (CYA) is an effective treatment for psoriasis with known effects on several cell types implicated in its pathogenesis. Among its many actions, CyA has been shown to inhibit prolactin binding to the prolactin receptors on human T and B lymphocytes. CyA also significantly inhibits the prolactin-stimulated increase in ornithine decarboxylase activity in lymphocytes. Thus, the antiproliferative effects of CyA in psoriasis may be in part mediated by its ability to displace prolactin from its receptors⁽²⁰⁾.

Regana and Millet⁽²⁰⁾ reported 3 cases of women whose worsening in psoriasis with hyperprolactinemia due to prolactinomas. All three were treated with bromocriptine and had normalization of PRL levels and concurrent improvement of psoriatic lesions. All three incurred relapses in psoriasis when they discontinued bromocriptine.

Multiple case reports have also suggested the potential efficacy of bromocriptine in the treatment of psoriatic arthritis. In one open label study, 35 patients with psoriatic arthritis resistant to conventional therapy were treated with bromocriptine (started at 2.5 mg and titrated up to 30 mg day). Significant improvement was seen in 77%, with 34% showing complete remission and 43% with 50% improvement in articular symptoms, elevated levels of prolactin have been found in patients with psoriasis, leading to hypothesized causal relationships and a possible therapeutic target⁽⁵⁾.

The inhibitor of prolactin synthesis bromocriptine was shown to improve the skin and joint manifestations of hyperprolactinaemic patients who had Psoriatic arthritis (PsA) concomitantly; however, because a similar improvement has been observed in patients without hyperprolactinaemia, it may be that bromocriptine has an intrinsic direct anti-inflammatory action⁽¹⁷⁾.

Both the prolactin gene and the human leucocyte antigen (HLA) complex are present on chromosome 6 and some of the antigen of the HLA Complex, particulary Cw6 and DR7, are implicated in the etiopathogenesis of psoriasis as a probable explanation for genetic predisposition to the disease. It is considered likely that the actual psoriasis genes lie on chromosome 6 and near the HLA Complex⁽¹⁾.

In the current study: By Comparison between serum prolactin level and PASI score in relation to duration of illness revealed that serum prolactin level and PASI score are significantly higher among patients with disease duration ≥ 5years compared to those with duration <5 years. This may be due to, whenever the time of disease is prolonged the stress is more and as a result more prolactin secretion with more increase of PASI score. Also, PASI score is significantly higher among patients with serum prolactin more than 100 ngml – to the best of our knowledge – there is no previous researches describe these relations. This may be attributed to, whenever serum prolactin increasees more, PASI score increases.

Conclusion

From the data of this study we could conclude that prolactin may have a role in the aetiopathogenesis of psoriasis, it is not a secondary event to the disease severity as assessed by PASI score.

Recommendations

1.    Studies of prolactin receptors of the skin are highly recommended.

2.    Controlled therapeutic trials of bromocriptine are indicated in psoriatic patients especially over sever cases even if prolactin levels are normal.

3.    Further studies should also develop more specific therapy using antibodies against PRL.

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هرمون البرولاكتين : هل له دور في النشوء المرضي لمرض الصدفية !!

علاء حسن مرعى؛هناء محمد السيد امام؛محمد عبد الواحد جابر؛مى محمد عبد النمعم شعيب

قسم الجلدية والتناسلية كلية الطب جامعة المنوفية*والمعهد القومى للبحوث

تعرف الصدفية بأنها مرض جلدي مزمن يتصف إكلينيكياً بحدوث حليمات صغيرة تتجمع في شكل صحائف جلدية مغطاة بقشور فضية سميكة.ويرجع ذلك إلى التكاثر السريع لخلايا الطبقة العلوية للجلد.وحتى الأن وعلى الرغم من تحديد العديد من النظريات الافتراضية عن أسباب حدوث مرض الصدفية إلا أن العلم لم يصل إلى السبب الحقيقي وإن كانت النظرية الوراثية تحتل الصدارة في هذا المجال .. حيث أن تلك النظرية تعلل سبب حدوث  مرض الصدفية بأنه ينتج عن عيوب وراثية في الجهاز المناعي والتي تظهر نتيجة التفاعل مع العوامل البيئة المحيطة المختلفة .وحديثاً بدأت نظرية التغيرات الهرمونية والتغيرات المناعية تظهر في الاعتبار حيث ثبت أن حدوث الزيادة في الاعراض والتحور في التاريخ المرضي للصدفية يتوافق مع بعض التغيرات الهرمونية والتغيرات المناعية الأمر الذي هدا بالعلماء إلي التفكير هل هذه التغيرات مؤثر (سبب) أم أثر (نتيجة) في مرض الصدفية  .هذا وقد تدارس العلماء مدي تأثير هرمون البرولاكتين على مرض الصدفية سواء في حدوث المرض أو في تطور الحالة الإكلينيكية تفسيراًُ وتأويلاً ومدي إرتباط هذه الزيادة في هرمون البرولاكتين بالتفاعلات المناعية التي تؤثر على خلايا الطبقة السطحية للجلد.وقد أجريت هذه الدراسة بهدف توضيح دور هرمون البرولاكتين في النشؤ لمرضي الصدفية .. علي ستون حالة مرضية بالصدفية وعشرة حالات مجموعة ضابطة وتم تجميع الحالات من عيادة الجلدية بالمستشفي الجامعي بكلية الطب جامعة المنوفية ومستشفي الحوض المرصود وعيادة الأمراض الجلدية بالمركز القومي للبحوث وتم إنتقاء حالات الصدفية بعد إستيبعاد السيدات الحوامل وفي فترة الرضاعة وفي حالات إضطراب الدورة الشهرية والمرضي تحت تأثير الأدوية التي ترفع من نسبة البرولاكتين في الدم. وقد تعرض المرضي والمجموعة الضابطة لأستيفاء التاريخ المرضي والفحص الأكلينيكي وتحديد درجة شدة الحالة المرضية للصدفية وإجراء التحاليل الطبية الروتينية منها صورة دم كاملة ووظائف الكلي ووظائف الكبد وقياس هرمون البيرولاكتين في الدم.وقد أظهرت ت النتائج أنه يوجد أرتفاع ذو دلالة إحصائية في مستوي هرمون البرولاكتين في مرضي الصدفية مقارنة بالمجموعة الضابطة .. وهذا الأرتفاع قد وجد أنه لا يرتبط بالعمر ولا الجنس ولا بدرجة شدة الإصابة بالمرض . والنتائج التي أنتهت إليها الدراسة تتطابق مع العديد من المراجع العلمية التي أكدت هذه الظاهرة في حدوث تغير في نسبة هرمون البرولاكتين في الدم في مرضي الصدفية . وبالتالي يمكن أن يكون لهرمون البرولاكتين دور في العوامل الهرمونية والمناعية المسببة لمرضي الصدفية .. وهذا يفتح باب جديد لبريق امل قد يساعد فى الحصول علي بعض الشفاء لمرضي الصدفية وإن كان يحتاج إلي المزيد من الدراسات المناعية والدراسات العلاجية المقارنة بأستخدام الأجسام والمضادات للدوبابين أو بأستخدام الأجسام المضادات للهيرمون ذاته.