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 Table of Contents  
Year : 2016  |  Volume : 3  |  Issue : 2  |  Page : 83-89

Stubborn facial hypermelanosis in females: A clinicopathologic evaluation

Department of Dermatology, Sri Ramachandra University, Chennai, Tamil Nadu, India

Date of Web Publication27-Dec-2016

Correspondence Address:
Dr. Aditya Kumar Bubna
Assistant Professor, Department of Dermatology, Sri Ramachandra University, Porur, Chennai - 600 116, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2349-5847.196299

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Background: Disorders of increased facial pigmentation constitute a major group of disorders in all dermatology clinics. Apart from cosmetic disfigurement, these disorders could significantly affect patient psychology. Therefore, it becomes imperative on the part of clinician to arrive at a conclusive diagnosis so that appropriate therapy could be administered.
Aim: To correlate the clinical and histology findings in 70 females 30–50 years of age with persistent facial hypermelanosis.
Methods: Following a written, informed consent, a 2 mm punch biopsy was performed from the lesional skin, succeeded by microscopic evaluation and clinical correlation.
Results: Out of the 70 patients studied, 31 had melasma, 14 with seborrhoeic melanosis (SM) and lichenoid dermatitis each, four with acanthosis nigricans (AN) and ashy dermatoses, and the remaining three with Riehl’s melanosis. Out of these patients studied, all patients with melasma and AN demonstrated 100% clinicopathologic concordance. Koilocytes were identified in two patients with persistent facial hypermelanosis, and in 17 patients, the histology findings were undecided.
Conclusion: Melasma appears to be the most common cause of facial hypermelanosis in females and has demonstrated a 100% clinicopathologic correlation. Subclinical infection with human papilloma virus (HPV) could be a cause of increased facial pigmentation which, if not carefully evaluated, could go undetected. SM still remains a disputable entity. Majority of these disorders are chronic and highly recalcitrant to all conventional therapeutic modalities.

Keywords: Discoid lupus erythematosus, human papilloma virus, melasma, seborrhoeic melanosis

How to cite this article:
Bhatia V, Bubna AK, Subramanyam S, Veeraraghavan M, Rangarajan S, Sankarasubramanian A. Stubborn facial hypermelanosis in females: A clinicopathologic evaluation. Pigment Int 2016;3:83-9

How to cite this URL:
Bhatia V, Bubna AK, Subramanyam S, Veeraraghavan M, Rangarajan S, Sankarasubramanian A. Stubborn facial hypermelanosis in females: A clinicopathologic evaluation. Pigment Int [serial online] 2016 [cited 2023 Mar 26];3:83-9. Available from: https://www.pigmentinternational.com/text.asp?2016/3/2/83/196299

  Introduction Top

Patients with disorders, characterised by increased facial pigmentation, constitute a major group, presenting to all dermatology clinics. Pigmented races, particularly Indians, are predisposed for the same. Apart from the aesthetic concern, the impact these disorders have on a patient’s social life cannot be underestimated. Most of these disorders are resistant to conventional therapeutic dermatologist to carefully evaluate the patient further in order to detect any new finding that could have got overlooked in the event of clinical mimicry of diseases. Our study was, therefore, conducted to correlate the clinical and histology findings of stubborn facial hypermelanosis in our participants with the purpose of getting a conclusive diagnosis for the same based on both clinical and microscopic parameters.

  Methods Top

This was a cross sectional study done over a period of 6 months. Only females 30–50 years of age, who had persistent facial hyperpigmentation, were included in our study. The term ‘persistent’ in our study was defined as those patients in whom pigmentation remained for a period of 1 year or more, and did not respond to conventional lines of management. As a small 2 mm punch biopsy was going to be taken from the facial lesion each patient was thoroughly counselled for the same, and only after obtaining a written, informed consent, the biopsy was performed. Any patient with unrealistic expectations were excluded from the study. Out of the 200 patients with facial hypermelanosis who attended our department during the study period of 6 months, only 70 patients agreed to participate in the study. After clinical evaluation, a 2 mm punch biopsy was performed in all 70 patients from the lesional facial skin; following which, the microscopic properties of each biopsy were studied, and correlation between the clinical and histology findings was designated into three categories as depicted in [Table 1].
Table 1: Categories designated by our findings on clinicopathologic correlation

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  Results Top

Out of the 70 patients evaluated, six clinical entities were identified. 31 patients were diagnosed with melasma, 14 patients with seborrhoeic melanosis (SM) and lichenoid dermatitis (LD) each, four patients with ashy dermatoses (AD) and acanthosis nigricans (AN) each, and the remaining three with Riehl’s melanosis (RM). A graphical representation for the same is available in [Figure 1]. Similarly, the number of patients in our study depicting clinical and histologic concordant, discordant and undecided findings have been elaborated in [Figure 2]. The clinical and histologic diagnoses of these entities were concluded based on features enumerated in [Table 2].
Figure 1: Bar diagram depicting the values obtained for all the clinical entities diagnosed in our study

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Figure 2: Pie diagram representing the values of clinical and histological concordance, discordance and undecided findings of the various entities in our study

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Table 2: Salient clinical features and histopathology findings of the six hypermelanotic conditions identified in our patients

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On correlating the clinical and microscopic findings, all 31 patients diagnosed with melasma had concordant findings. Interestingly all our 31 melasma patients demonstrated epidermal melasma on histology [Figure 3]a and [Figure 3]b.
Figure 3: (a) Clinical presentation of melasma with blotchy pigmentation over bilateral cheeks. (b) Histology of melasma depicting increased pigmentation of the basal cell layer with the formation of pigmentary caps over the nuclei of the basilar keratinocytes (H&E ×200)

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Our next clinical entity was SM. Out of the 14 patients, an undecided microscopy finding was identified in 12 patients, demonstrating a sparse dermal lymphocytic infiltrate as the characteristic finding. In one patient, the biopsy specimen was suggestive of discoid lupus erythematosus (DLE) with hyperkeratosis, thinning of the stratum malpighii and follicular plugging observed in the epidermis along with a perivascular and periadnexal infiltrate of lymphocytes in the dermis. In another patient, koilocytes were the hallmark finding witnessed without any clinical lesion suggestive of warts [Figure 4]a–[Figure 4]d.
Figure 4: (a) Seborrhoeic melanosis (SM) as seen clinically in our participants. (b) Histology of majority patients diagnosed with SM demonstrating superficial dermal infiltrates of lymphocytes (H&E ×100). (c) Histology of one patient diagnosed clinically as SM with microscopic features suggestive of DLE (H&E ×100). (d) Histology of one patient diagnosed with SM depicting koilocytes in the epidermis on microscopy (H&E ×200)

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Of the 14 clinically diagnosed cases of LD, 12 demonstrated the classical lichenoid tissue reaction pattern on histology [Figure 5]a and [Figure 5]b. Features suggestive of DLE were identified in one patient, and koilocytes were observed in another patient.
Figure 5: (a) Clinical presentation of lichenoid dermatitis (LD). (b) Histology of LD with a superficial dermal lymphocytic infiltrate (H&E ×200)

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AD was our fourth clinical entity. Only in one patient the microscopic findings were suggestive of AD. The remaining three patients depicted a non-specific finding of chronic inflammatory cells in the superficial part of the dermis [Figure 6]a–[Figure 6]c.
Figure 6: (a) Clinical presentation of ashy dermatoses (AD). (b) Microscopic findings as seen in one patient of AD (H&E ×200). (c) Vague histology of superficial dermal lymphocytes in the remaining three diagnosed cases of AD (H&E ×200)

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A clinicopathologic concordance was observed in all patients diagnosed with AN [Figure 7]a and [Figure 7]b.
Figure 7: (a) Clinical findings in acanthosis nigricans (AN). (b) Histology findings in AN (H&E ×200)

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In RM, apart from a single patient demonstrating the characteristic findings on histopathology, the remaining patients only showcased lymphocytes in the upper corium something very similar as seen in patients with AD [Figure 8]a–[Figure 8]c.
Figure 8: (a) Clinical findings of Riehl’s melanosis (RM). (b) Histology findings diagnostic of RM in one of our participants (H&E ×200). (c) Undecided histology of chronic inflammatory infiltrates in the dermis in the remaining two patients (H&E ×200)

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  Discussion Top

Disorders of facial hypermelanosis are a class of dermatoses which could genuinely test the patience and fortitude of a clinician owing to its highly stubborn character. It, therefore, becomes mandatory for clinicians to meticulously evaluate all such patients. Our study was, therefore, taken up with the view of correlating the clinical and microscopic findings of facial hypermelanosis. This kind of a study taking these parameters into consideration to the best of our knowledge has not been conducted before and, thus, warrants mention.

Melasma is a disorder of acquired hypermelanosis affecting 0.25–4% of patients seen in southeast Asian countries.[1] It has been considered to be the most common facial pigmentary condition in females. Melasma also was seen to be the most common clinical diagnosis in all patients evaluated by us. It was observed in 44.3% of our patients. A clinical study of facial pigmentation done from Kashmir[2] also depicted melasma to constitute the maximum case load of 54.4% which was slightly higher than our value. Though the clinical findings of melasma were characteristic, histologic sections maybe required in certain cases considered to be melasma mimickers. Increased epidermal melanin, usually confined to the basal and suprabasal cells, is the hallmark finding witnessed in melasma.[3],[4] However, in one study done by Kang et al.,[5] melanisation was also deciphered to extend throughout all the epidermal layers. In the dermis melanophages, collagen degeneration and telangiectasia are some of the findings observed. In our patients, all the skin specimens depicted basilar cell melanisation with no dermal changes evident, thereby making the authors to speculate the recalcitrant nature of even the epidermal variant of melasma.

SM is a clinical condition characterised by brownish discoloration involving the seborrhoeic body parts along with presence of seborrhoea and pityriasis capitis.[6] All our patients with SM needed to fulfil these characteristics to get labelled as SM. As there are no clear histologic parameters to define SM, the authors decided to consider histologic findings of seborrhoeic dermatitis to be concordant with clinical cases of SM. Apart from an undecided microscopy observed in majority of the participants, DLE was diagnosed in one patient, and in another koilocytes were identified on histology.

DLE arising de novo as melanotic macules without the classical phenotype may not be as uncommon as suspected. In a clinical study from India, this morphology of DLE was detected in 25% of the participants.[7] Similarly, Aberer,[8] has also highlighted upon this macular hyperpigmented variant of DLE. Therefore, in cases of unresponsive hypermelanotic macules of the face, this differential diagnosis certainly cannot be ignored. Whether this constitutes a stage in the evolution of the disease to finally result in the classical presentation of DLE or could this be a phenotype of the disease persisting throughout the course of the disease needs more clinical studies to clearly determine owing to paucity of literature for the same.

Koilocytes are vacuolated cells seen in the epidermis which are characteristic of human papilloma virus (HPV).[9] In a case report published by Jacobs et al.,[10] spotted hyperpigmentation of the face secondary to HPV 29 has been reported. However, there has not been further mention with regard to HPV as a cause of facial melanosis in medical literature. Though there remains a paucity of data depicting the relationship of HPV and facial hyperpigmentation, association of the two could be much more than actually considered.

LD is derived from the term lichen meaning symbiotic growth of algae and fungi. According to a clinician, lichenoid is defined as a plaque resembling a lichen stuck onto the skin.[11] There are many conditions coming under the armamentarium of LD with lichen planus being the prototype. Though there are specific disorders grouped under LD, on a number of occasions the clinician may not be able to clearly specify these disorders owing to the vague clinical presentation, and, therefore, in these instances the term LD is applied. Here, a histologic examination becomes mandatory. LD is characterised by a band of chronic inflammatory cells embedded in the superficial corium which has been designated as lichenoid tissue reaction pattern. In our 14 patients clinically diagnosed with LD, 12 had conclusive findings of classical interface dermatitis with lymphocytes. In one patient, specific findings of DLE were witnessed, a dermatoses included under the subset of lichenoid tissue reaction patterns. Though there appear to be many clinical variants of DLE, resemblance of DLE to SM and LD has not been reported in medical literature before to the best of our knowledge. The other finding of koilocytes again alerts the concerned clinician on this rare presentation of subclinical HPV infection.

AD of Ramirez is a highly recalcitrant dermatosis with its aetiology being highly undecided. Clinically, it presents as ash coloured to bluish brown macules in a symmetric distribution and is histologically characterised by upper dermal perivascular mononuclear cells, dermal melanophages and increased melanisation of the epidermis.[12] Out of the four patients, only one had concordant findings. The remaining three demonstrated sparse superficial dermal lymphocytic infiltrates. Whether this discrepancy signifies disease evolution needs further elucidation as there have not been any prior studies commenting in this regard.

AN presents clinically as velvety brown patches with a corrugated texture. Microscopic features of AN are characterised by hyperkeratosis, papillomatosis and very slight irregular acanthosis.[13] All our patients had 100% concordance, thereby helping us conclude on the reliability of clinical diagnosis for AN.

RM is also referred to as pigment contact dermatitis. It is a variant of contact dermatitis which is non-eczematous and is characterised by macular hyperpigmentation usually with ill-defined borders and usually occupying the lateral aspect of the face.[14] Histologically, the characteristic findings witnessed in RM include basal cell vacuolisation, dermal melanophages and superficial dermal infiltrate of lymphocytes mainly having a perivascular distribution with absence of spongiosis.[15] In only one patient, these findings were demonstrable. In the remaining two patients, a sparse superficial dermal lymphocytic infiltrate was the hallmark finding. Again the authors relate these findings to stages in disease progression.

  Conclusion Top

To conclude, the authors would like to state that melasma appears to be the most common disorder of facial hyperpigmentation in females with the epidermal variant also, being highly resistant to treatment. SM still remains a disputable entity that requires further elucidation and the need for a skin biopsy in these cases to further throw light on the exact diagnosis. The presence of subclinical infection with HPV may be responsible for facial hypermelanosis, and this could prove to be more common than actually thought of. The macular pigmentary variant of DLE needs careful evaluation, and owing to paucity of literature for the same, may not attract the attention of many clinicians. Nevertheless its possibility should be kept in mind. AN and melasma demonstrated 100% clinicopathologic concordance in our study. We reiterate the fact that AD is a highly recalcitrant dermatosis, and we also speculate that sparse lymphocytic infiltrates in the dermis to actually depict an early stage of disease histogenesis. RM may not demonstrate characteristic findings on microscopy always. However, the concerned clinician should not be deterred in making this diagnosis if other supporting clues from history and clinical examination are available. Disorders of facial hyperpigmentation could significantly affect the quality of life of patients, and therefore the need for supportive counselling.


Dr. Leena Dennis Joseph and Dr. J. Thanka, Professors, Department of Pathology, Sri Ramachandra University, Porur, Chennai.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

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Grimes PE, Yamada N, Bhawan J. Light microscopic, immunohistochemical, and ultrastructural alterations in patients with melasma. Am J Dermatopathol 2005;27:96-101.  Back to cited text no. 4
Kang WH, Yoon KH, Lee ES, Kim J, Lee KB, Yim H et al. Melasma: Histopathological characteristics in 56 Korean patients. Br J Dermatol 2002;146:228-37.  Back to cited text no. 5
Dhar S, Dutta P, Malakar R. Pigmentary disorders. In: Valia RG, Valia AR, editors. IADVL Textbook of Dermatology. 3rd ed. Mumbai: Bhalani Publishing House; 2010. p. 736-98.  Back to cited text no. 6
George R, Mathai R, Kurian S. Cutaneous lupus erythematosus in India: Immunofluorescence profile. Int J Dermatol 1992;31:265-9.  Back to cited text no. 7
Aberer E. Lupus erythematosus. Wide range of symptoms through clinical variation, associated diseases and imitators. Hautarzt 2010;61:676-82.  Back to cited text no. 8
Xu X, Erickson L, Chen L, Elder DE. Diseases caused by viruses. In: Elder DE, Elenitsas R, Johnson BL Jr, Murphy GF, Xu X, editors. Lever’s Histopathology of Skin. 10th ed. Philadelphia: Lippincott Williams and Wilkins; 2009.p. 637-65.  Back to cited text no. 9
Jacobs S, Baron JM, Rübben A, Grussendorf Conen EI. HPV 29 associated hyperpigmentation of the face. Eur J Dermatol 2002;12:189-90.  Back to cited text no. 10
Rapini RP. Clinical and pathologic differential diagnosis. In: Bolognis JL, Jorizzo JL, Rapini R, editors. Dermatology. 2nd ed. London: Mosby Elsevier; 2009.p. 1-22.  Back to cited text no. 11
Wang WL, Lazar A. Lichenoid and interface dermatitis. In: Calonje E, Brenn T, Lazar A, Mckee PH, editors. Mckeee’s Pathology of Skin. 4th ed. London: Elsevier Saunders; 2012.p. 219-58.  Back to cited text no. 12
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  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8]

  [Table 1], [Table 2]


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