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Year : 2020  |  Volume : 6  |  Issue : 2  |  Page : 99-101

Dramatic response to metronidazole in a patient with pemphigus foliaceus

1 Department of Dermatology, Ankara Bilkent City Hospital, Ankara, Turkey
2 Department of Pathology, Ankara Bilkent City Hospital, Ankara, Turkey

Date of Submission23-Dec-2019
Date of Decision20-Apr-2020
Date of Acceptance06-Oct-2020
Date of Web Publication28-Dec-2020

Correspondence Address:
Ahu Yorulmaz
Department of Dermatology, The Bilkent City Hospital, Bilkent Integrated Healthcare Campus, Cankaya, Ankara
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijdd.ijdd_69_19

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How to cite this article:
Yorulmaz A, Yalcin B, Tamer E, Kaya MC, Koca B. Dramatic response to metronidazole in a patient with pemphigus foliaceus. Indian J Drugs Dermatol 2020;6:99-101

How to cite this URL:
Yorulmaz A, Yalcin B, Tamer E, Kaya MC, Koca B. Dramatic response to metronidazole in a patient with pemphigus foliaceus. Indian J Drugs Dermatol [serial online] 2020 [cited 2023 Feb 2];6:99-101. Available from: https://www.ijdd.in/text.asp?2020/6/2/99/305130


Pemphigus foliaceus (PF) is a relatively benign form of pemphigus, which is characterized by transient flaccid superficial vesicles scattered on seborrheic areas. These evanescent primary lesions are generally replaced by secondary lesions, which eventually leads to scaly crusted erosions arising on an erythematous background.[1] Demodicosis is a disease of pilosebaceous units associated with human Demodex mites. According to clinical aspects of the patients, demodicosis can be classified as primary or secondary demodicosis. Secondary demodicosis occurs in patients with other known dermatological or systemic diseases, mainly immunosuppressive conditions.[2] Here, we report a case of demodicosis, of whom the main diagnosis of PF was markedly exacerbated by demodicosis, but also alleviated with systemic metronidazole.

  Case Report Top

One of our follow-up patients (50, male) visited our outpatient clinic with several weeks' history of itching and redness on his face. He declared frequent application of medium potent topical corticosteroids on his face without any improvement in itching and redness. He was diagnosed with PF 9 years ago, for which he had been under methylprednisolone (96 mg daily) and azathioprine (150 mg daily) treatment for the first 3 years of his diagnosis. We excluded systemic corticosteroids from the treatment of the patient since the time when bilateral avascular necrosis of the femoral head had developed 6 years ago. He was receiving azathioprine (50 mg twice daily), ramipril/hydrochlorothiazide (5/25 mg twice daily), lansoprazole (30 mg daily), iron, calcium, and vitamin D replacement when he presented presented to our clinic [Figure 1]. A dermatological examination revealed scaly erosions on the parieto-occipital region of the head, crusted erosions all over the body, and few vesicles scattered over the trunk. In addition, scaly indurated erythematous plaques were observed on the seborrheic areas of the face [Figure 2]. Laboratory investigations including complete blood count and differential, erythrocyte sedimentation rate, serum chemistry profile, and urinalysis were within normal limits. Serological tests revealed that antinuclear antibodies were weakly positive, desmoglein-1 was positive, and desmoglein-3 was negative. Since the patient had a history of frequent application of topical corticosteroids, we suspected a diagnosis of demodicosis and performed standardized skin surface biopsy (SSSB), which yielded a positive result. For SSSB, a drop of cyanoacrylate glue was placed on a 1 cm2 area marked on a slide glass. The slide was pressed against the right cheek of the patient for 1 min and then lifted gently. A coverslip was placed over the sample and one drop of immersion oil was applied. The sample was examined under the light microscopy, which demonstrated more than five parasites confirming the diagnosis of demodicosis. Thus, based on the history and clinical and laboratory findings, a diagnosis of demodicosis masquerading as PF was established. The patient was prescribed topical permethrin cream and systemic metronidazole, although topical permethrin was discontinued on day 3 because of skin irritation. The patient showed a dramatic response to metronidazole (500 mg twice daily for 21 days) in terms of facial lesions [Figure 3]. At the 30th day follow-up, SSSB was repeated, which demonstrated a negative result. However, at the 30th day follow-up, he exhibited new crops of lesions consist of crusted erosions over the trunk, which were refractory to topical corticosteroids. Hence, intravenous immunoglobulin therapy was initiated as a complementary treatment for the patient. For facial skin care, the patient was instructed to use tea tree oil facial wash twice daily and apply topical emollients and sunscreens generously. At 3rd month follow-up visit, it was detected that the patient was almost free of facial lesions [Figure 3].
Figure 1: Pathology sample retrieved from pathology archive and reexamined; acantholysis and dyskeratotic cells within stratum granulosum (H and E, ×10). Positive direct immunofluorescence; intraepidermal immunoglobulin G deposits

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Figure 2: Scaly indurated erythematous plaques on the seborrheic areas of the face. Scaly erosions on the scalp, widespread crusted erosions on the trunk and extremities

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Figure 3: (a) 10th day of metronidazole therapy. (b) 30th day follow-up, 9 days off metronidazole. (c) 90th day follow-up

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  Discussion Top

Demodicosis has been classified according to the presence or absence of any preexisting dermatological or systemic diseases.[2],[3],[4] It has been suggested that in primary demodicosis, symptoms are directly caused by excessive Demodex population, whereas in secondary demodicosis, although symptoms are initially linked to local or systemic immunosuppression, secondarily influenced by the subsequently increased number of mites because of immunosuppression.[3] The pathogenic role of Demodex mites in the pathogenesis of inflammatory dermatoses remains to be controversial.[2],[3],[4] It is known that Demodex infestations are generally asymptomatic but may play a pathogenic role only when present in high densities and accompanied by an imbalance of host immune responses.[5] Demodex mites have evolved mechanisms to avoid detection by the host immune system.[6] However, when the immune system is suppressed, the number of mites increases and they may become pathogenic parasites, triggering a host immune reaction by activation of the toll-like receptor 2 immune response pathway, which eventually leads to inflammatory skin changes.[6]

The biological function of Demodex mites as a constituent of normal human skin flora and their exact pathogenic potential in humans remain to be elucidated.[2],[6] It is not clear whether Demodex mites cause inflammatory skin diseases or immunosuppression induced by inflammation of skin disease causes Demodex mites to become pathogenic. Here, we have reported a case of demodicosis, of whom the main diagnosis of PF was markedly exacerbated by demodicosis, moreover alleviated with systemic metronidazole. Up to now, only one case of demodicosis of arms in a patient with PF has been described.[7] We have identified similarities of the patients, such as receiving systemic immunosuppressives and topical corticosteroids. However, we highlight a noteworthy feature of our patient that is inflammatory reaction induced with demodicosis. Demodicosis caused infiltrated erythematous plaques on the seborrheic areas of the face, which is completely different than scaly crusted erosion that is normally expected in PF. Moreover, a dramatic resolution of lesions was observed with metronidazole, which further proves the pathogenic role of demodicosis in our patient.

On the other hand, one of the limitations of our case report was that we could not include images of SSSB, which were performed both before and after metronidazole treatment. We suggest that the resolution of facial lesions in our patient was due to the effect of metronidazole in reducing the Demodex population, since repeated SSSB demonstrated negative result. However, we cannot ignore the anti-inflammatory effect of metronidazole, which may, in turn, affect the host's immune responses. Further case reports are needed to document the effect of metronidazole in demodicosis accompanied by inflammatory facial disorders.

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Conflicts of interest

There are no conflicts of interest.

  References Top

James KA, Culton DA, Diaz LA. Diagnosis and clinical features of pemphigus foliaceus. Dermatol Clin 2011;29:405-12, viii.  Back to cited text no. 1
Chen W, Plewig G. Human demodicosis: Revisit and a proposed classification. Br J Dermatol 2014;170:1219-25.  Back to cited text no. 2
Litwin D, Chen W, Dzika E, Korycińska J. Human permanent ectoparasites; recent advances on biology and clinical significance of demodex mites: Narrative review article. Iran J Parasitol 2017;12:12-21.  Back to cited text no. 3
Gazi U, Taylan-Ozkan A, Mumcuoglu KY. Immune mechanisms in human and canine demodicosis: A review. Parasite Immunol 2019;41:e12673.  Back to cited text no. 4
Rather PA, Hassan I. Human demodex mite: The versatile mite of dermatological importance. Indian J Dermatol 2014;59:60-6.  Back to cited text no. 5
[PUBMED]  [Full text]  
Lacey N, Russell-Hallinan A, Zouboulis CC, Powell FC. Demodex mites modulate sebocyte immune reaction: Possible role in the pathogenesis of rosacea. Br J Dermatol 2018;179:420-30.  Back to cited text no. 6
Kim BR, Park HS, Yoon HS, Cho S. Demodicidosis on the arms of a patient with pemphigus foliaceus. J Am Acad Dermatol 2014;71:e92-3.  Back to cited text no. 7


  [Figure 1], [Figure 2], [Figure 3]

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