Avijit Mondal

Secondary syphilis: An unusual presentation

A 35‐year‐old male presented with multiple, itchy, violaceous papules and plaques on medial thighs bilaterally and on scrotum for 2 months [Figure 1a]. He had few similar lesions elsewhere too. There was a history of repeated unprotected sexual exposure with commercial sex workers in recent past. There was no history of any urethral discharge and burning micturition, rash on the body, or any constitutional symptom; however, there was a history of a painless ulcer on glans penis 4 months before presentation and the ulcer had healed in 4–5 weeks with self‐medication with topical and systemic antibiotics. On examination, there were multiple, firm, moist, nontender, flat‐topped papules and plaques on the scrotum and medial thighs. Few similar lesions were noted in the left axilla too. Of note, axillary lesions

A young boy with brownish papules and plaque

Indian Journal of Paediatric Dermatology | Volume 18 | Issue 2 | April-June 2017 144 develops in increasing numbers throughout childhood and early adulthood (particularly at puberty) and then slowly involutes. Genetic and environmental factors (especially sunlight) influence the development of these melanocytic nevi.[1] Acquired nevi are further classified into junctional (flat, uniformly pigmented, dark brown to black color), compound (elevated, lighter shade of brown), and intradermal (more elevated, pale brown, or even skin‐colored) types.[2] The interest in these benign lesions lies in their relationship with melanoma as there is a small but definitive risk of development of melanoma in these lesions and hence, such cases should remain under follow‐up and/or perform the regular self‐examination. Immunohistochemical stains can be of great value in the diagnosis of a melanocytic neoplasm. S‐100, MelanA/Mart‐1 (A103), tyrosinase (T311), and microphthalmia transcription factor typically stain both the junctional and the dermal components of common acquired nevi, with sensitivities approaching 100%.[3] The clinical differentials in our case were dermatofibroma (painful nodule, dimple sign positive, histology showing nodular dermal proliferation of spindle‐shaped fibroblasts and myofibroblasts), trichofolliculoma (wisp of hairs coming out of lesion, histology showing central patulous follicular infundibulum, from which fully formed follicles radiate) and leiomyoma (painful tumor and histology showing collection of fusiform myocytes).[4] These lesions do not require any treatment and can be smartly left over but a changing lesion suspicious of melanoma warrants surgical excision and histological workup.

Pyogenic granuloma–like basal cell carcinoma on the abdomen: A deceptive presentation

1. Kashyap S, Shanker V, Sharma N. Amniotic band: A rare presentation. Indian J Dermatol 2015;60:200‐2. 2. Adeosun OO, James O, Akinmoladun VI, Owobu T. Amniotic band syndrome associated with orofacial clefts: A report of two cases. Oral Surg 2012;5:185‐9. 3. Kroes HY, Pals G, van Essen AJ. Ehlers‐Danlos syndrome type IV: Unusual congenital anomalies in a mother and son with a COL3A1 mutation and a normal collagen III protein profile. Clin Genet 2003;63:224‐7. 4. Ross MG. Pathogenesis of amniotic band syndrome. Am J Obstet Gynecol 2007;197:219‐20. 5. Bouguila J, Ben Khoud N, Ghrissi A, Bellalah Z, Belghith A, Landolsi E, et al. Amniotic band syndrome and facial malformations. Rev Stomatol Chir Maxillofac 2007;108:526‐9. 6. Das D, Das G, Gayen S, Konar A. Median facial cleft in amniotic band syndrome. Middle East Afr J Ophthalmol 2011;18:192‐4. 7. Akadiri OA, Eigbobo JO, Otaigbe BE. Amniotic band syndrome in a Nigerian cleft patient: A case report. Niger J Plast Surg 2014;10:15‐7. 8. Karaman A, Kahveci H, Öztürk C. Amniotic band sequence associated with fronto‐ethmoidal meningo‐encephalocele. New J Med 2012;29:187‐8. 9. Halder A. Amniotic band syndrome and/or limb body wall complex: Split or lump. Appl Clin Genet 2010;3:7‐15. 10. Nardozza LM, Araujo Júnior E, Caetano AC, Moron AF. Prenatal diagnosis of amniotic band syndrome in the third trimester of pregnancy using 3D ultrasound. J Clin Imaging Sci 2012;2:22.

Porokeratotic eccrine ostial and dermal duct nevus: A noteworthy presentation.

We herein present a case of PEODDN that had unique clinical and histopathological findings. Our patient was a 30-year-old healthy lady who presented with multiple, asymptomatic, elevated skin lesions over her left upper limb. Small lesions appeared three years ago over her left index finger and gradually extended to the forearm. There was no seasonal variation. Cutaneous examination demonstrated multiple well-circumscribed, hyperpigmented, verrucous papules on the dorsum of the left index finger extending up to the extensor aspect of mid forearm. Some of the lesions were discrete while others coalesced to form plaques in a linear configuration. Of note, many of these papules showed a central pit [Figure 1]. Hair, nails, and mucosae were within normal limits; however, the nail of the index finger showed multiple shallow pits and a single longitudinal groove. Family history and systemic examination were not contributory. Linear porokeratosis, linear lichen planus, linear verrucous epidermal nevus, and linear Darier’s disease were considered in the list of clinical differentials. A complete blood cell count with differential analysis and a comprehensive biochemistry panel did not reveal any abnormality. Histopathology of a representative skin lesion from the forearm showed hyperkeratosis, acanthosis, and papillomatosis. Cornoid lamella overlying a dilated eccrine duct ostium was visualized. An interesting finding was the presence of focal lichenoid infiltrate in the upper dermis [Figure 2a and b]. Based on the clinical and histopathological findings, our case was diagnosed as PEODDN along with a unique histological finding of a lichenoid infiltrate.

Grouped vesicular lesions in an infant

An 8-month-old female infant presented with vesicular lesions on the right lower extremity for 2 days. There were grouped vesicles on an erythematous base over right leg, dorsum of right foot and sole, distributed in the L5 and S1 dermatomes (Fig 1). The baby was irritable, but afebrile. The baby was born at term and by normal vaginal delivery and her birth weight was 2.5 kg. Postnatal period was uneventful. Her developmental milestones were within normal range. There was history of maternal varicella infection during 3rd months of pregnancy. Tzanck smear from the lesions showed mononuclear and multinucleated acantholytic cells with ground glass nuclei, consistent with Tzanck cells. Based on history and clinical findings, diagnosis of Herpes zoster was made. The infant was treated symptomatically with topical calamine lotion and oral antipyretic. The lesions crusted in 1 week and resolved completely in 2 weeks, without any sequelae.

Multiple annular erythematous lesions with trailing scale.

A 6-year-old boy presented with recurrent pruritic scaly lesions all over trunk for last 2 years. These lesions appeared spontaneously and resolved in 4-8 weeks without any sequale. Rest of the history was non-contributory and no other family member was having similar lesions. On examination, multiple, annular erythematous lesions with trailing scale at the inner border were present on trunk (Fig. 1). Few annular lesions were found on tongue too. On enquiry, tongue lesions used to appear and disappear simultaneously with trunk lesions. Palm, sole, nail, scalp and other mucosa were unremarkable. Routine investigations and KOH mount did not reveal any abnormality. Clinically, the child was diagnosed as Erythema annulare centrifugum (EAC). Histopathological findings were consistent with the diagnosis. Involvement of tongue is very rare. The incidence of disease peaks in the fifth decade.