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 Table of Contents  
Year : 2018  |  Volume : 46  |  Issue : 4  |  Page : 281-287

Evaluation of the role of mast cell tryptase in the pathogenesis of skin tags

1 Department of Dermatology and Venereology, Faculty of Medicine, Tanta University, Tanta, Egypt
2 Department of Pathology, Faculty of Medicine, Tanta University, Tanta, Egypt

Date of Submission28-Feb-2018
Date of Acceptance14-Nov-2018
Date of Web Publication02-Aug-2019

Correspondence Address:
MD Ghada F.R Hassan
1 Asmaa Bent Abi-Bakr Street, Neseem Street, End of Moheb Street, Al-Mahalla Al-Kobra, El-Gharbia Governorate, 31111
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DOI: 10.4103/tmj.tmj_16_18

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Background Skin tags (STs) are considered as common benign tumors of the skin. They are made of loose fibrous tissue and occur mainly on flexures and neck as protrusions that are soft and pedunculated. The etiopathogenesis of STs is not well understood yet. Mast cells (MCs) have been found to promote fibrosis and collagen deposition through tryptase, which is one of their mediators. So, there may be a link between MCs activation and STs formation.
Aim The aim of this study was to evaluate tryptase from MCs and its possible role in the pathogenesis of STs.
Patients and methods This study was carried out on 40 patients having STs. They were subjected to clinical examination, dermatological examination, and routine investigations. Moreover, skin biopsies were taken from STs from all 40 patients and from normal skin of 20 of these patients to act as a control group. All biopsies were stained by MC tryptase to study the count of MCs in controls as well as STs.
Results STs had significantly higher MC counts compared with control skin. A significant positive correlation was found between MC count and serum triglycerides. A significant positive correlation between number of STs and age of the patients, BMI, and triglycerides was elicited. Obese and overweight patients showed higher MC count than normal weight patients. Thighs, axillae, and neck showed higher MC count compared with other sites, despite the relation between them being not significant.
Conclusion MCs and their product tryptase are overexpressed in STs and may have an essential role in its pathogenesis.

Keywords: mast cell tryptase, pathogenesis, skin tags

How to cite this article:
Hassan GF, Al-Shenawy HA. Evaluation of the role of mast cell tryptase in the pathogenesis of skin tags. Tanta Med J 2018;46:281-7

How to cite this URL:
Hassan GF, Al-Shenawy HA. Evaluation of the role of mast cell tryptase in the pathogenesis of skin tags. Tanta Med J [serial online] 2018 [cited 2020 Jun 6];46:281-7. Available from: http://www.tdj.eg.net/text.asp?2018/46/4/281/263915

  Introduction Top

Skin tags (STs) (acrochordons) are small, sessile, or pedunculated papillomas. They are flesh colored to dark brown. They occur mostly on axilla, neck, and eyelids. They are present with lower incidence in the groin and on the trunk. They manifest equally in both sexes [1]. Histologically, STs are polypoid lesions with loose, edematous fibrovascular core, overlying the mildly acanthotic epidermis [2]. The definite etiology of STs is still unknown. Skin rubbing, aging, and familial predisposition have been reported as contributing factors. STs have common association with many diseases and conditions, including obesity, diabetes mellitus, acromegaly, Crohn’s disease, organ transplantation, and colonic polyps. It has been recorded also with pregnancy and human papillomavirus [1].

Mast cells (MCs) are innate immune cells. They originate from stem cells in the bone marrow (hematopoietic stem cells). They give rise to common myeloid progenitors, which can subsequently differentiate into precursors of MC. MCs, like other inflammatory cells, are essential in mediating the inflammatory process. When activated, MCs rapidly release characteristic granules and various hormonal mediators. These mediators include histamine, proteoglycans, cytokines, MC-specific proteases (tryptase, chymase, and carboxypeptidase A), and other enzymes (cysteine, cathepsins, and matrix metalloproteinase). Moreover, MCs can release and synthesize many growth factors including platelet-derived growth factors and fibroblast growth factor [3]. MCs also release tumor necrosis factor-α, which stimulates the growth of fibroblasts. Tumor necrosis factor-α has been considered as a powerful growth-promoting factor for fibroblasts, as it cause increase in its division and proliferation that lead to formation of STs [2].

Tryptase is an enzyme specific to MC granules [4]. Its serum level increases in patients with systemic anaphylaxis and other inflammatory disorders [5]. MC tryptase affects both the extracellular matrix and the connective tissue cells (which cause fibrosis). It stimulates proliferation of fibroblast, fibroblast chemotaxis, myofibroblast differentiation, and synthesis of collagen (type 1) by fibroblasts through stimulation and activation of the protease activated receptors-2 [3], leading to conditions such as scar, fibrosing alveolitis, and scleroderma [6].

STs are one of the most common disorders of skin that occur in obese patients. They have a direct proportion to high insulin levels and the grade of obesity [7]. Higher free fatty acid levels in obese patients with STs can induce muscle and hepatic insulin resistance, leading to hyperinsulinemia, which results in overexpression of epidermal growth factor receptor as well as endothelial dysfunction and contributes to the etiology of STs [8]. The aim of this study was to evaluate MC tryptase and its possible role in the pathogenesis of STs.

  Patients and methods Top

This study was done on 40 patients with STs after approval by research ethics committee, Faculty of Medicine, Tanta University (approval number2476/03/14). Twenty normal skin biopsies from 20 of the patients served as a control. The diagnosis of STs was based on their typical clinical picture. Exclusion criteria were patients with thyroid function disorders; patients receiving antihyperlipidemic, antihistaminic, or oral hypoglycemic drugs or MC stabilizers; patients with hepatic pathology; and pregnant and lactating women. All patients signed an informed consent after full explanation of the study procedure, purpose, and risks.

All patients were subjected to full history taking and general and dermatological examination, including the site, number, color, consistency, and shape of STs. BMI was evaluated as the ratio of body weight to body height square (kg/m2): underweight: BMI is <20 kg/m2, normal: BMI is 20–25 kg/m2, overweight: BMI is 25 to <30 kg/m2, obese: BMI is 30 to <40 kg/m2, and morbid obese: BMI is ≥40 kg/m2 [9].

Laboratory investigations were done, such as fasting blood glucose (FBG) and postprandial blood glucose (PPBG) and estimation and assessment of lipid profile (cholesterol and triglycerides levels).

Three millimeters punch biopsies under local anesthesia were taken. All tissue specimens were fixed in a 10% formalin solution for 24 h, then washed with graded alcohol for dehydration, and then embedded in paraffin. Sections were subjected to routine hematoxylin and eosin staining to confirm the diagnosis and to assess the histopathological features of STs. Then sections were stained immunohistochemically by MC tryptase antibody to detect tryptase expression in both STs and normal skin specimens.

Reagents and equipment

  1. MC tryptase primary antibody: a monoclonal mouse antibody [MC tryptase Ab-2, clone AA1, isotype: IgG1, immunogen (ready to use for immunohistochemistry staining) Cat.; Thermo Fisher Scientific, Waltham, Massachusetts, USA] was used for staining of paraffin-embedded tissue sections.
  2. The secondary antibody (Universal Kit) is a supersensitive immunodetection system (Ultravision, REF 95-9943B-Lot 546894A; Invitrogen, Waltham, Massachusetts, USA) that contains biotinylated goat antimouse secondary antibody.
  3. The substrate chromogen: 3,3′-Diaminobenzidine mixture was prepared immediately before use.

Staining procedures [10]

Sections were deparaffinized in xylene for 20 min, then transferred the sections to 100% alcohol for 5 min, then hydrated through graded alcohol, each for 5 min, then distilled water for 5 min, and then blocked with 3% hydrogen peroxide/methanol solution to quench endogenous peroxidase activity for 30 min. Then sections were placed in PBS for 20 min, treated with digestion solution (pepsin) at 37°C for 1 h, washed in PBS solution at room temperature, and then treated with tryptase primary antibody for 1 h. Sections were then washed in PBS, and biotinylated secondary antibody was added for 30 min; slides were rewashed in PBS and subsequently incubated for another 30 min with avidin–biotin complex, and then washed again in PBS for 5 min. 3,3′-Diaminobenzidine used as chromogen was added for 30 min, and then the slides were washed thoroughly in running tap water for 5 min. Slides were finally counterstained with Mayer’s hematoxylin, then dehydrated in ascending grades of alcohol, and then the slides were mounted in distyrene, plasticizer, and xylene.

Mast cell counting

As MC is immunopositive for tryptase, we used tryptase expression to detect the number of MCs in STs and normal skin. The number of immunostained cells per field in at least 10 microscopic fields at magnification of ×400 was counted manually. The results were expressed as cell density in 1 mm2, where the high-power fields (×400) of the microscope was 0.159 mm2. The results were repeated three separate times, and the median was taken for statistical analysis. The used microscope was Olympus CH2O microscope (Olympus, Tokyo, Japan) [11].

Statistical analysis

Data were fed to the computer and then analyzed using IBM SPSS software package, version 20.0 (v 16; SPSS Inc., Chicago, Illinois, USA).

  Results Top

Clinical results

The study included 22 (55%) females and 18 (45%) males. Their age ranged from 20 to 63 years with a mean of 40.80±11.75 years and a median of 40 years. A total of 32 (80%) patients had positive family history of STs. Concerning the BMI of the patients, it ranged from 22 to 42.30 kg/m2, with a mean of 30.84±5.44 kg/m2 (median=30.5). Eight (20%) patients were at normal weight, six (15%) patients were overweight, 22 (55%) patients were obese, and four (10%) patients had morbid obesity.

Regarding the site and size of STs, 24 (60%) patients had STs in neck, six (15%) patients in axilla, four (10%) patients in eyelids, four (10%) patients in upper chest, and two (5%) patients in the thigh. Sixteen (40%) patients had small-sized STs that were from 1 to 2 mm (width and length), 20 (50%) patients had medium-sized STs that were ∼2 mm (width) and 5 mm (length), whereas four (10%) patients had large-sized STs that were ∼1 cm in diameter. The number of STs in patients ranged from 1 to 15 STs, with a mean of 5.15±3.63 (median=3.5).

There was a positive relation between STs number and BMI as higher number was found in morbid obese (median=11), obese (median= 6), and overweight (median=3) patients than normal weight (median=2) patients. Moreover, a positive relation was found between the number of STs and age, as the number of STs increased with the age.

Laboratory results

Total serum cholesterol level was normal in 12 (30%) patients and elevated in 28 (70%) patients, as it ranged from 129 to 285 mg/dl, with a mean of 229±45.37 mg/dl (median=245.5). Serum triglycerides level was normal in six (15%) patients and elevated in 34 (85%) patients, as it ranged from 88 to 320 mg/dl, with a mean of 233.20±70.99 mg/dl (median=235.5). A positive significant correlation was found between number of STs and triglycerides level. However, there were no significant correlations between STs number and any of cholesterol, FBG, or PPBG levels ([Table 1]).
Table 1 Correlation between skin tags number and different studied parameters

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Histological results

Sections stained with hematoxylin and eosin revealed that STs consist of central fibrovascular core with epidermal covering. There were hyperplastic epidermis, papillomatosis, hyperkeratosis, and acanthosis, with underlying central fibrovascular core, collagen deposition, and perivascular inflammatory infiltrate ([Figure 1]).
Figure 1 A skin tag shows epidermal covering with central fibrovascular core (hematoxylin and eosin, ×40).

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Immunohistopathological results

Immunohistochemical staining by tryptase antibody showed tryptase-positive MCs in the dermis. Sections from the lesion (STs) showed many MCs present around the blood vessels with increased tryptase expression, which was indicated by positively stained cytoplasmic granules by higher magnification. [Figure 2],[Figure 3],[Figure 4] show a large number of tryptase-positive MCs. However, sections from normal skin revealed a few tryptase-positive MCs in the dermis.
Figure 2 A skin tag stained with tryptase shows many tryptase-positive mast cells around the blood vessels (avidin–biotin complex, ×100).

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Figure 3 A skin tag stained with tryptase shows increased number of tryptase-positive mast cells in the dense collagenous core (avidin–biotin complex, ×200).

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Figure 4 Higher magnification of the previous section shows high number of tryptase-positive mast cells around the blood vessels (avidin–biotin complex, ×400).

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Regarding tryptase-positive MCs, MC count in the STs ranged from 17 to 28, with a mean of 23.55±3.80 MCs (median=24.5). However, in the normal skin, it ranged from 1 to 4, with a mean of 1.50±0.71 MCs (median=1), with statistically significant increase in MC count in STs when compared with control (P=0.002).

According MC count in ST, a positive significant correlation was found between MC count and triglycerides level (P<0.001). However, no significant correlations were observed between MC count in STs and either the age of patients, BMI, cholesterol, FBG, PPBG, or number of STs ([Table 2]).
Table 2 Correlation between mast cell count in skin tags and different studied parameters

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There was no statistically significant relation between MC counts in STs that were taken from different sites, but there was higher MC count in axilla and neck with a mean of 22±2.83 and 23.75±3.82 MCs, respectively. However, in two cases of STs (from the thigh), the highest number of MC count was seen, with a mean of 28 MCs. Moreover, no significant relation between MC count and BMI was elicited, but patients with morbid obesity showed higher MC count with a mean of 26.50±0.71 MCs compared with other body weights. There was no significant relation between MC counts in STs and family history ([Table 3]).
Table 3 Relation between mast cell count in skin tags and different studied parameters

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  Discussion Top

STs are one of the most common fibrous tumors of the skin. They are also called soft fibromas, acrochordons, fibroadenomas, or fibroepithelial polyps. However, the exact cause of STs is not understood. Skin rubbing, hormonal imbalance, and obesity have been reported as contributing factors [12].

MCs are derived from hematopoietic cells. They play an important role in physiological wound healing and contribute in both innate and adaptive immunity, as well as in wound healing [13]. MCs have been found to promote fibrosis by stimulating collagen deposition and fibroblast division and proliferation through their preformed mediators such as tryptase and histamine [14]. In addition, MCs stimulate keratinocytes proliferation and epidermal acanthosis [15]. MC tryptase staining is specific for these cells. It allows them to be seen under microscope even after their degranulation. It may also still stain tryptase even after release in the tissues. MC tryptase is considered as a powerful growth factor for fibroblasts, which may explain the link between MC activation and occurrence of fibrosis [16]. Thus, we studied the MC count and activity in STs using immunohistochemistry for tryptase.

In this study, STs were common in patients older than 30 years. There was a positive significant correlation between number of STs and age of the patients. Banik and Lubach [17] reported that STs were common in the people older than 40 years. This could be attributed to monocyte chemotactic protein-1, which is a chemoattractant for MCs, found to increase with old age [18].

There was a positive family history of STs in 80% of our patients. This was in agreement with Erkek et al. [19], who reported positive family history of STs in 65.5% of their patients. However, Rasi et al. [20] reported positive family history in only 44.23% of their patients. However, there was no significant relation between MC count and positive family history in this study.

Obesity is a factor known to be associated with the formation of STs [21]. In this study, there was a positive significant correlation between the number of STs and BMI. This was in agreement with Akpinar and Dervis [22] who reported that the number of STs increased among the obese patients. They attributed this finding to higher level of insulin growth factor-1 in obese than nonobese patients. Moreover, Shaheen et al. [23] and El Safoury et al. [24] found that the number of STs increased with obesity. Tamega et al. [25] reported the presence of multiple STs is association with overweight. Demir and Demir [26] concluded that the number of STs was significantly higher in patients with large BMI value. However, Sari et al. [27], Rasi et al. [20] and Erdogan et al. [28] disagreed with the result of this study, as they observed no correlation between BMI and the number of STs.

This study showed an increase in the MC count in obese patients than others. This may explain the role of MC and obesity in the pathogenesis of STs even if this result was not significant. Higher MC count was found in morbid obese patients, obese patients, and overweight patients than normal weight patients. Sartipy and Loskutoff [29] had demonstrated that monocyte chemotactic protein-1 is overexpressed in obesity. This illustrates the possible relation between MC and STs. Salem et al. [30] agreed with these results. They reported higher MC count in their obese patients compared with overweight. This could be owing to the presence of more frictional forces in such patients. However, El Safoury et al. [24] found no correlation between MC count and BMI.

In this study, STs were present mostly in the neck, axillae, eyelids, upper chest, and thighs in descending pattern. Rasi et al. [31] reported that the most common site of STs was neck and upper chest, followed by axillae and breast in Iran. Agamia and Gomaa [21] found that STs were mostly present on the neck, axillae, and back and less often on the eyes, face, thighs, and under the breast. Senel et al. [32] found that the most common sites of STs were neck and axillae. This may owing to more liability of the skin in these areas to friction either with clothes or skin itself. In this study, the MC count was higher in thigh, axilla, and neck compared with other sites, in spite of the relation between MC count and site being not significant. El Safoury et al. [24] reported that skin friction may enhance an increase in the number of MCs in the dermis, which release their mediators including tryptase, initiating STs formation. Zaher et al. [33] suggested that high count of MC can only initiate STs formation, but they believed that there are other factors such as friction and viral infections as human papillomavirus.

In this study, there was a significant positive correlation between number of STs and elevated serum triglycerides levels. This was in accordance with Idris and Sunitha [12], El Safoury et al. [34], Senel et al. [32], and Sari et al. [30], who illustrated that triglyceride level was significantly elevated in the patients more than controls. Moreover, Tamega et al. [25] reported higher serum triglycerides levels in the patients than controls, and the presence of multiple STs was associated with hypertriglyceridemia. Moreover, Crook [35] observed multiple STs with increased serum triglycerides. On the contrary, Salem et al. [30] reported that there was no significant correlation between number of ST and triglycerides levels.In this study, no significant correlation between STs number and cholesterol level was found. In agreement with this, Rasi et al. [31] did not detect high cholesterol and triglyceride level in patients with STs. Erdogan et al. [28] found that the number of the STs in patients did not correlate with total serum cholesterol or triglycerides levels.

Diabetes was found in only 15% and prediabetes in 45% of patients in this study. Goyal et al. [36] stated that 40.6% of their patients had STs were diabetics. Mahajan et al. [37] found that STs was the most common skin association with diabetic patients in 33.82% of their cases. Demir and Demir [26] reported that 75% of patients with STs were diabetic. However, we found no correlation between MC count, STs number, and FBG or PPBG.

There was a significant increase in MC count in lesional skin when compared with MC count in normal skin. This significant higher number of MCs expressing tryptase in patients with STs compared with normal skin of same patients explained the possible strong role of MCs and tryptase in the formation of STs, by stimulating fibroblast growth, division, and deposition of collagen. Moreover, MC mediators induce hyperplasia of epidermis, which is considered the main pathological process in STs [38] Abdou et al. [38], El Safoury et al. [13], and Zaher et al. [33] found significant increase of number of MC in ST when compared with normal skin, in agreement with this study.

  Conclusion Top

The presence of MCs in all our patients with high number indicated the possible role of MCs in the etiopathogenesis of STs. Using tryptase as an indicator for MCs is considered a reliable method for accurate MC counting in tissue sections. This could explain the role of tryptase, as one of MC mediators, in ST pathogenesis via its interaction with fibroblasts. Positive correlation of MC count and number of STs with obesity and hypertriglyceridemia may indicate the role of obesity in etiopathogenesis of STs.

Large-scale epidemiological studies are recommended to investigate the possible role of MC tryptase and obesity in the pathogenesis of STs. Reducing body weight and lowering triglycerides level on presence of STs is advised as they may decrease formation of new lesions and help in regression of the present ones.

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Conflicts of interest

There are no conflicts of interest.

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4]

  [Table 1], [Table 2], [Table 3]


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