Letters to the Editor
The most common patterns in mucosal melanoma of lips were structureless (100%), lines (54%) especially reticular (27%) and parallel (9%).[1] According to Blum et al. only the presence of structureless zones was significantly associated with malignant lesions.[1] Structureless patterns were found in all malignant lesions but only in 53.2% of benign lesions.[1] Dots were detectable in 28.6% of the malignant mucosal lesions and in 7.9% of the benign lesions.[1] According to Blum et al. multiple colors are a better clue to malignant lesions than multiple patterns.[1] Lin et al. stated that mucosal melanomas mainly presented with the multicomponent and homogeneous patterns.[2] In the differential diagnosis of benign melanosis of the lip, three major dermatoscopic patterns were identified: a “structureless” pattern with a blue hue, a “parallel pattern”, often found in clinically typical melanocytic macules of the lips and the “reticular‑like” pattern associated with melanosis, rather rarely occurring on the lips.[3] If a benign lesion was structureless, its color was usually brown but did not include blue, gray, or white.[1] The significant difference between benign and malignant lesions included not only the occurrence of blue, gray and white colors, but their number as well.[1] According to Stante et al. a recognition of early signs of lentigo maligna on dermatoscopy, before the lesion is associated with the ABCD signs of melanoma, is a clue to early diagnosis.[4] The early dermatoscopic indicators of lentigo maligna are asymmetrical pigmented follicular openings, slate‑grey short streaks and rhomboidal structures.[3,4] Classic dermatoscopic features of extra‑facial melanoma (an atypical pigment network, irregularly distributed dots, globules, streaks and pseudo‑pods) and dermatoscopic criteria of vertical growth (ulceration, black structureless areas) have rarely been observed in cases of lentigo maligna.[5] In the case of lentigo maligna of the auricle presented above, a large number of colors, an atypical pigment network and a number of black, structureless areas were also noted. Furthermore, the features typical for melanoma in situ such as those described previously by Seidnari et al., were all seen in the present case.[6]
Grazyna Kaminska‑Winciorek1, Jacek Calik2, Jerzy Wydmanski1,3, Robert A Schwartz4, Rafal Czajkowski5 Dermato‑Oncology Unit, The Center for Cancer Prevention and Treatment, Katowice, 2Department of Oncology, Lower Silesian Oncology Center, Wroclaw, 3Department of Conventional and
1
Intraoperative Radiotherapy, Maria Skłodowska‑Curie Memorial Cancer Center and Institute of Oncology Gliwice Branch, Gliwice, Poland, 4Dermatology, Preventive Medicine and Pathology, Rutgers New Jersey Medical School, Rutgers University, Newark, New Jersey, USA, 5Department of Dermatology, Sexually Transmitted Diseases and Immunodermatology, Ludwik Rydygier Medical College in Bydgoszcz, Nicolaus Copernicus University, Torun, Poland Address for correspondence: Dr. Grazyna Kaminska‑Winciorek, Dermato‑Oncology Unit, The Center for Cancer Prevention and Treatment, 16 Fliegera Street, 40‑060 Katowice, Poland. E‑mail: [email protected]
REFERENCES 1. Blum A, Simionescu O, Argenziano G, Braun R, Cabo H, Eichhorn A, et al. Dermoscopy of pigmented lesions of the mucosa and the mucocutaneous junction: Results of a multicenter study by the International Dermoscopy Society (IDS). Arch Dermatol 2011;147:1181‑7. 2. Lin J, Koga H, Takata M, Saida T. Dermoscopy of pigmented lesions on mucocutaneous junction and mucous membrane. Br J Dermatol 2009;161:1255‑61. 3. Mannone F, De Giorgi V, Cattaneo A, Massi D, De Magnis A, Carli P. Dermoscopic features of mucosal melanosis. Dermatol Surg 2004;30:1118‑23. 4. Stante M, Giorgi V, Stanganelli I, Alfaioli B, Carli P. Dermoscopy for early detection of facial lentigo maligna. Br J Dermatol 2005;152:361‑4. 5. Pralong P, Bathelier E, Dalle S, Poulalhon N, Debarbieux S, Thomas L. Dermoscopy of lentigo maligna melanoma: Report of 125 cases. Br J Dermatol 2012;167:280‑7. 6. Seidenari S, Bassoli S, Borsari S, Ferrari C, Giusti F, Ponti G, et al. Variegated dermoscopy of in situ melanoma. Dermatology 2012;224:262‑70. Access this article online Quick Response Code:
Website: www.ijdvl.com DOI: 10.4103/0378-6323.136976 PMID: *****
Dermoscopy in tungiasis Sir, A 24‑year‑old Chilean male complained of a painful white papule with a brownish central area on the lateral aspect of his left foot [Figure 1]. He noticed it immediately after returning from a 1‑week trip to Paraguay. On dermoscopic examination, we observed a round lesion with a dark central pore, an incomplete radiated crown and a pigmented peripheral ring, arranged from the inner to outer aspect [Figure 2]. Additionally, blue‑black blotches and whitish oval structures linked together forming chain like structures were noted [Figure 2]. A clinical diagnosis of tungiasis
Indian Journal of Dermatology, Venereology, and Leprology | July-August 2014 | Vol 80 | Issue 4
371
Letters to the Editor
was made, and we shaved the lesion with evacuation of the eggs and fecal material [Figure 3]. This was followed by cryotherapy and tetanus vaccination. Tungiasis is a cutaneous infestation, originally from Central and South America, which then spread to sub‑Saharan Africa and Asia up to the west coast of India.[1] It is caused by the female flea Tunga penetrans. The flea inhabits dry, sandy soils. The prevalence in endemic areas may reach up to 50%,[2] whereas in non‑endemic areas a few cases may be observed among tourists. Skin infections and infestations are the most frequent morbidity encountered among tourists, with tungiasis in the list of top ten dermatological diagnoses among them.[1]
Figure 1: White papule with a brownish central area on the lateral aspect of the left foot
The infestation cycle of the flea lasts for about a month. The fertilized flea introduces itself into the epidermis of the host. It affects humans, dogs, pigs, birds, and other species. The flea fixes its mouth to the blood vessels in the superficial dermis and feeds on blood. Four to five days later, a white papule or nodule appears with a central black dot (the abdominal and genital opening), and the eggs start to develop. The flea grows to about 1 cm in length and from the 8th to 10th day onwards, it expels 150 to 200 eggs per day for about 7 to 10 days through the genital opening along with feces, after which it dies. White papules or nodules with a central black dot can be seen especially over the feet, but any site can be affected. The most common symptom is pruritus, but foreign body sensation has also been reported.[1] Diagnosis in endemic areas is usually clinical. Dermoscopy, which allows visualization of the submacroscopic epidermal and superficial dermal structures, can be a valuable diagnostic tool in non‑endemic areas and in cases with an atypical distribution. A black central pore can be seen, which corresponds to the genital opening of the flea, with a peripheral pigmented ring that corresponds to the posterior abdomen.[3] A radial crown has been described between the pore and the peripheral ring, which is a zone of columnar hemorrhagic parakeratosis in a radial arrangement.[4] Blue‑black blotches have also been reported, which are presumed to be the eggs[4] or hematin in the gastrointestinal tract.[3] In some specimens, whitish oval structures linked together forming chain‑like structures can be noted, which correspond to the eggs in the flea’s abdomen.[5] 372
Figure 2: Round lesion with a dark central pore (discontinued arrow), an incomplete radiated crown (single arrow) and a pigmented peripheral ring (double arrow). Within the papule, blue-black blotches (arrow heads) and whitish oval structures linked together forming chain-like structures (demarcated area) can be seen
Figure 3: Dermoscopic view of the evacuated eggs and feces
Indian Journal of Dermatology, Venereology, and Leprology | July-August 2014 | Vol 80 | Issue 4
Letters to the Editor
Álvaro Abarzúa, Karina Cataldo, Sergio Álvarez Department of Dermatology, Pontificia Universidad Católica de Chile, Santiago, Chile Address for correspondence: Dr. Karina Cataldo, Vicuña Mackenna 4686, Santiago, Chile. E-mail: [email protected]
REFERENCES 1. O’Brien BM. A practical approach to common skin problems in returning travellers. Travel Med Infect Dis 2009;7:125‑46. 2. Lefebvre M, Capito C, Durant C, Hervier B, Grossi O. Tungiasis: A poorly documented tropical dermatosis. Med Mal Infect 2011;41:465‑8. 3. Bauer J, Forschner A, Garbe C, Röcken M. Viariability of dermoscopic features of tungiasis. Arch Dermatol 2005;141:643‑4. 4. Marazza G, Campanelli A, Kaya G, Braun RP, Saurat JH, Piguet V. Tunga penetrans: Description of a new dermoscopic sign‑the radial crown. Arch Dermatol 2009;145:348‑9. 5. Bakos RM, Bakos L. ‘Whitish chains’: A remarkable in vivo dermoscopic finding of tungiasis. Br J Dermatol 2008;159:991‑2. Access this article online Quick Response Code:
Website: www.ijdvl.com DOI: 10.4103/0378-6323.136980 PMID: *****
Calcipotriol and adapalene therapy for disseminated superficial actinic porokeratosis Sir, Disseminated superficial actinic porokeratosis (DSAP) is a chronic disorder of keratinization characterized by numerous papules and plaques distributed on sun‑exposed sites. Although various therapeutic options are available, an ideal and standardized treatment protocol for DSAP is lacking. Here, we report a case of DSAP in an otherwise healthy 63‑year‑old Japanese man who was successfully treated with calcipotriol and adapalene. A 63‑year‑old Japanese male carpenter was referred to our department with a 10‑year history of multiple, brown, occasionally itchy lesions over the extremities
in a photodistributed pattern. The lesions, diagnosed as eczema by a local doctor, had not responded to topical corticosteroids. There was worsening after sun exposure and during summer and the patient used to wear long‑sleeved clothes to prevent exacerbation. He was otherwise healthy and denied any history of immunosuppression, radiation therapy, or arsenic intake. His family history was negative for DSAP and other relevant dermatological diseases. On physical examination, multiple, red‑brown, annular keratotic lesions measuring up to 1 cm in diameter were symmetrically distributed on sun‑exposed areas of the extremities [Figure 1a]. Some scaly plaques were observed on the face but the trunk was not involved. Close inspection revealed that individual lesions had central atrophy and an elevated hyperkeratotic ridge. Dermoscopic examination revealed open pores with plugs and a whitish peripheral rim [Figure 1b]. The results of routine laboratory investigations were within normal limits. A punch biopsy taken from the keratotic border of a lesion on the right lower arm revealed a characteristic keratin‑filled invagination with a cornoid lamella and absence of granular layer beneath the cornoid lamella [Figure 1c]. A diagnosis of disseminated superficial actinic porokeratosis (DSAP) was made and topical treatment with 0.005% calcipotriol ointment twice daily was started. However, after the first 3 months, only a slight improvement was observed and treatment was changed to calcipotriol once daily in the morning and topical adapalene (0.1%) gel every night. After 3 months of treatment with both calcipotriol and adapalene, the skin lesions improved substantially leaving only slight hyperpigmentation [Figure 1d]. The treatment was well tolerated without significant adverse effects and no recurrence was seen after reducing the frequency of topical application to every other day. DSAP was first described by Chernosky and Freeman.[1] Since then, various treatment options for this condition including topical diclofenac, vitamin D3 analogs, 5‑fluorouracil, retinoids, 5% imiquimod, photodynamic therapy, carbon dioxide laser and oral retinoids have been reported with varying degrees of success.[2] However, reports of DSAP treated with vitamin D3 analogs are rare.[3] Vitamin D3 analogs are thought to induce the transcription of genes necessary for keratinocyte differentiation such as transglutaminase and involucrin. They may also inhibit keratinocyte proliferation by inducing sphingomyelin hydrolysis and modulation of protein kinase C activity. Harrison and Stollery reported a
Indian Journal of Dermatology, Venereology, and Leprology | July-August 2014 | Vol 80 | Issue 4
373
Copyright of Indian Journal of Dermatology, Venereology & Leprology is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
The most common patterns in mucosal melanoma of lips were structureless (100%), lines (54%) especially reticular (27%) and parallel (9%).[1] According to Blum et al. only the presence of structureless zones was significantly associated with malignant lesions.[1] Structureless patterns were found in all malignant lesions but only in 53.2% of benign lesions.[1] Dots were detectable in 28.6% of the malignant mucosal lesions and in 7.9% of the benign lesions.[1] According to Blum et al. multiple colors are a better clue to malignant lesions than multiple patterns.[1] Lin et al. stated that mucosal melanomas mainly presented with the multicomponent and homogeneous patterns.[2] In the differential diagnosis of benign melanosis of the lip, three major dermatoscopic patterns were identified: a “structureless” pattern with a blue hue, a “parallel pattern”, often found in clinically typical melanocytic macules of the lips and the “reticular‑like” pattern associated with melanosis, rather rarely occurring on the lips.[3] If a benign lesion was structureless, its color was usually brown but did not include blue, gray, or white.[1] The significant difference between benign and malignant lesions included not only the occurrence of blue, gray and white colors, but their number as well.[1] According to Stante et al. a recognition of early signs of lentigo maligna on dermatoscopy, before the lesion is associated with the ABCD signs of melanoma, is a clue to early diagnosis.[4] The early dermatoscopic indicators of lentigo maligna are asymmetrical pigmented follicular openings, slate‑grey short streaks and rhomboidal structures.[3,4] Classic dermatoscopic features of extra‑facial melanoma (an atypical pigment network, irregularly distributed dots, globules, streaks and pseudo‑pods) and dermatoscopic criteria of vertical growth (ulceration, black structureless areas) have rarely been observed in cases of lentigo maligna.[5] In the case of lentigo maligna of the auricle presented above, a large number of colors, an atypical pigment network and a number of black, structureless areas were also noted. Furthermore, the features typical for melanoma in situ such as those described previously by Seidnari et al., were all seen in the present case.[6]
Grazyna Kaminska‑Winciorek1, Jacek Calik2, Jerzy Wydmanski1,3, Robert A Schwartz4, Rafal Czajkowski5 Dermato‑Oncology Unit, The Center for Cancer Prevention and Treatment, Katowice, 2Department of Oncology, Lower Silesian Oncology Center, Wroclaw, 3Department of Conventional and
1
Intraoperative Radiotherapy, Maria Skłodowska‑Curie Memorial Cancer Center and Institute of Oncology Gliwice Branch, Gliwice, Poland, 4Dermatology, Preventive Medicine and Pathology, Rutgers New Jersey Medical School, Rutgers University, Newark, New Jersey, USA, 5Department of Dermatology, Sexually Transmitted Diseases and Immunodermatology, Ludwik Rydygier Medical College in Bydgoszcz, Nicolaus Copernicus University, Torun, Poland Address for correspondence: Dr. Grazyna Kaminska‑Winciorek, Dermato‑Oncology Unit, The Center for Cancer Prevention and Treatment, 16 Fliegera Street, 40‑060 Katowice, Poland. E‑mail: [email protected]
REFERENCES 1. Blum A, Simionescu O, Argenziano G, Braun R, Cabo H, Eichhorn A, et al. Dermoscopy of pigmented lesions of the mucosa and the mucocutaneous junction: Results of a multicenter study by the International Dermoscopy Society (IDS). Arch Dermatol 2011;147:1181‑7. 2. Lin J, Koga H, Takata M, Saida T. Dermoscopy of pigmented lesions on mucocutaneous junction and mucous membrane. Br J Dermatol 2009;161:1255‑61. 3. Mannone F, De Giorgi V, Cattaneo A, Massi D, De Magnis A, Carli P. Dermoscopic features of mucosal melanosis. Dermatol Surg 2004;30:1118‑23. 4. Stante M, Giorgi V, Stanganelli I, Alfaioli B, Carli P. Dermoscopy for early detection of facial lentigo maligna. Br J Dermatol 2005;152:361‑4. 5. Pralong P, Bathelier E, Dalle S, Poulalhon N, Debarbieux S, Thomas L. Dermoscopy of lentigo maligna melanoma: Report of 125 cases. Br J Dermatol 2012;167:280‑7. 6. Seidenari S, Bassoli S, Borsari S, Ferrari C, Giusti F, Ponti G, et al. Variegated dermoscopy of in situ melanoma. Dermatology 2012;224:262‑70. Access this article online Quick Response Code:
Website: www.ijdvl.com DOI: 10.4103/0378-6323.136976 PMID: *****
Dermoscopy in tungiasis Sir, A 24‑year‑old Chilean male complained of a painful white papule with a brownish central area on the lateral aspect of his left foot [Figure 1]. He noticed it immediately after returning from a 1‑week trip to Paraguay. On dermoscopic examination, we observed a round lesion with a dark central pore, an incomplete radiated crown and a pigmented peripheral ring, arranged from the inner to outer aspect [Figure 2]. Additionally, blue‑black blotches and whitish oval structures linked together forming chain like structures were noted [Figure 2]. A clinical diagnosis of tungiasis
Indian Journal of Dermatology, Venereology, and Leprology | July-August 2014 | Vol 80 | Issue 4
371
Letters to the Editor
was made, and we shaved the lesion with evacuation of the eggs and fecal material [Figure 3]. This was followed by cryotherapy and tetanus vaccination. Tungiasis is a cutaneous infestation, originally from Central and South America, which then spread to sub‑Saharan Africa and Asia up to the west coast of India.[1] It is caused by the female flea Tunga penetrans. The flea inhabits dry, sandy soils. The prevalence in endemic areas may reach up to 50%,[2] whereas in non‑endemic areas a few cases may be observed among tourists. Skin infections and infestations are the most frequent morbidity encountered among tourists, with tungiasis in the list of top ten dermatological diagnoses among them.[1]
Figure 1: White papule with a brownish central area on the lateral aspect of the left foot
The infestation cycle of the flea lasts for about a month. The fertilized flea introduces itself into the epidermis of the host. It affects humans, dogs, pigs, birds, and other species. The flea fixes its mouth to the blood vessels in the superficial dermis and feeds on blood. Four to five days later, a white papule or nodule appears with a central black dot (the abdominal and genital opening), and the eggs start to develop. The flea grows to about 1 cm in length and from the 8th to 10th day onwards, it expels 150 to 200 eggs per day for about 7 to 10 days through the genital opening along with feces, after which it dies. White papules or nodules with a central black dot can be seen especially over the feet, but any site can be affected. The most common symptom is pruritus, but foreign body sensation has also been reported.[1] Diagnosis in endemic areas is usually clinical. Dermoscopy, which allows visualization of the submacroscopic epidermal and superficial dermal structures, can be a valuable diagnostic tool in non‑endemic areas and in cases with an atypical distribution. A black central pore can be seen, which corresponds to the genital opening of the flea, with a peripheral pigmented ring that corresponds to the posterior abdomen.[3] A radial crown has been described between the pore and the peripheral ring, which is a zone of columnar hemorrhagic parakeratosis in a radial arrangement.[4] Blue‑black blotches have also been reported, which are presumed to be the eggs[4] or hematin in the gastrointestinal tract.[3] In some specimens, whitish oval structures linked together forming chain‑like structures can be noted, which correspond to the eggs in the flea’s abdomen.[5] 372
Figure 2: Round lesion with a dark central pore (discontinued arrow), an incomplete radiated crown (single arrow) and a pigmented peripheral ring (double arrow). Within the papule, blue-black blotches (arrow heads) and whitish oval structures linked together forming chain-like structures (demarcated area) can be seen
Figure 3: Dermoscopic view of the evacuated eggs and feces
Indian Journal of Dermatology, Venereology, and Leprology | July-August 2014 | Vol 80 | Issue 4
Letters to the Editor
Álvaro Abarzúa, Karina Cataldo, Sergio Álvarez Department of Dermatology, Pontificia Universidad Católica de Chile, Santiago, Chile Address for correspondence: Dr. Karina Cataldo, Vicuña Mackenna 4686, Santiago, Chile. E-mail: [email protected]
REFERENCES 1. O’Brien BM. A practical approach to common skin problems in returning travellers. Travel Med Infect Dis 2009;7:125‑46. 2. Lefebvre M, Capito C, Durant C, Hervier B, Grossi O. Tungiasis: A poorly documented tropical dermatosis. Med Mal Infect 2011;41:465‑8. 3. Bauer J, Forschner A, Garbe C, Röcken M. Viariability of dermoscopic features of tungiasis. Arch Dermatol 2005;141:643‑4. 4. Marazza G, Campanelli A, Kaya G, Braun RP, Saurat JH, Piguet V. Tunga penetrans: Description of a new dermoscopic sign‑the radial crown. Arch Dermatol 2009;145:348‑9. 5. Bakos RM, Bakos L. ‘Whitish chains’: A remarkable in vivo dermoscopic finding of tungiasis. Br J Dermatol 2008;159:991‑2. Access this article online Quick Response Code:
Website: www.ijdvl.com DOI: 10.4103/0378-6323.136980 PMID: *****
Calcipotriol and adapalene therapy for disseminated superficial actinic porokeratosis Sir, Disseminated superficial actinic porokeratosis (DSAP) is a chronic disorder of keratinization characterized by numerous papules and plaques distributed on sun‑exposed sites. Although various therapeutic options are available, an ideal and standardized treatment protocol for DSAP is lacking. Here, we report a case of DSAP in an otherwise healthy 63‑year‑old Japanese man who was successfully treated with calcipotriol and adapalene. A 63‑year‑old Japanese male carpenter was referred to our department with a 10‑year history of multiple, brown, occasionally itchy lesions over the extremities
in a photodistributed pattern. The lesions, diagnosed as eczema by a local doctor, had not responded to topical corticosteroids. There was worsening after sun exposure and during summer and the patient used to wear long‑sleeved clothes to prevent exacerbation. He was otherwise healthy and denied any history of immunosuppression, radiation therapy, or arsenic intake. His family history was negative for DSAP and other relevant dermatological diseases. On physical examination, multiple, red‑brown, annular keratotic lesions measuring up to 1 cm in diameter were symmetrically distributed on sun‑exposed areas of the extremities [Figure 1a]. Some scaly plaques were observed on the face but the trunk was not involved. Close inspection revealed that individual lesions had central atrophy and an elevated hyperkeratotic ridge. Dermoscopic examination revealed open pores with plugs and a whitish peripheral rim [Figure 1b]. The results of routine laboratory investigations were within normal limits. A punch biopsy taken from the keratotic border of a lesion on the right lower arm revealed a characteristic keratin‑filled invagination with a cornoid lamella and absence of granular layer beneath the cornoid lamella [Figure 1c]. A diagnosis of disseminated superficial actinic porokeratosis (DSAP) was made and topical treatment with 0.005% calcipotriol ointment twice daily was started. However, after the first 3 months, only a slight improvement was observed and treatment was changed to calcipotriol once daily in the morning and topical adapalene (0.1%) gel every night. After 3 months of treatment with both calcipotriol and adapalene, the skin lesions improved substantially leaving only slight hyperpigmentation [Figure 1d]. The treatment was well tolerated without significant adverse effects and no recurrence was seen after reducing the frequency of topical application to every other day. DSAP was first described by Chernosky and Freeman.[1] Since then, various treatment options for this condition including topical diclofenac, vitamin D3 analogs, 5‑fluorouracil, retinoids, 5% imiquimod, photodynamic therapy, carbon dioxide laser and oral retinoids have been reported with varying degrees of success.[2] However, reports of DSAP treated with vitamin D3 analogs are rare.[3] Vitamin D3 analogs are thought to induce the transcription of genes necessary for keratinocyte differentiation such as transglutaminase and involucrin. They may also inhibit keratinocyte proliferation by inducing sphingomyelin hydrolysis and modulation of protein kinase C activity. Harrison and Stollery reported a
Indian Journal of Dermatology, Venereology, and Leprology | July-August 2014 | Vol 80 | Issue 4
373
Copyright of Indian Journal of Dermatology, Venereology & Leprology is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
