Letters to the Editor
Plasma tryptase and histamine concentrations reflect the increased proliferation of mast cells and/or their activation.[4] Bone marrow biopsy in those with childhood‑onset cutaneous disease is not recommended unless there is evidence of systemic disease such as unexplained peripheral blood abnormalities, hepatosplenomegaly, and lymphadenopathy.[5] It has been suggested that a serum tryptase level exceeding 100 ng/ml or more is an indication for bone marrow examination regardless of age.[2] Due to monetary constraints, the plasma tryptase levels could not be done in our patient. As he had frequent flushing episodes, appearance of new skin lesions and multiple mastocytomas, bone marrow examination was carried out, which turned out to be normal. The therapy for mastocytosis is focused on providing symptomatic relief and avoidance of triggering factors. H1 antihistamines control pruritus, flushing and urticaria. In spite of receiving antihistamines, our patient had, an initial, increase in the duration of flushing episodes. We assume that this was because triggering factors like friction could not be avoided due to the multiplicity of lesions.The other reason could be an inadequate dose of antihistamines due to lack of sufficient data on dosage in the very young. Sometimes, flushing can be caused by chemical mediators other than histamine.To add to the problem, the safety profile of drugs with mast cell stabilizing properties like ketotifen and azelastine in infants and the very young has not been established.[6] Surgical excision of solitary mastocytoma, topical calcineurin inhibitors and topical corticosteroids are among the other modalities of treatment. The course of the disease in children is often benign and there is usually no progression to systemic disease. The occurence of multiple mastocytomas with bullous lesions as a presenting feature is unusual. The control of flushing in such an instance may be difficult. There is need for more therapeutic options and guidelines for the treatment of pediatric mastocytosis, especially in very young infants.
Taru Garg, Ram Chander, Niti Gaur, Aashim Singh, Anita Nangia1 Departments of Dermatology, Venereology and Leprology, and 1Pathology, Lady Hardinge Medical College and Associated Hospitals, New Delhi, India
Address for correspondence: Dr. Taru Garg, Department of Dermatology, Venereology and Leprology, Lady Hardinge Medical College and Associated Hospitals, New Delhi ‑ 110 001, India. E‑mail: [email protected]
REFERENCES 1. Lange M, Nedoszytko B, Górska A, Zawrocki A, Sobjanek M, Kozlowski D. Mastocytosis in children and adults: Clinical disease heterogeneity. Arch Med Sci 2012;8:533‑41. 2. Ben‑Amitai D, Metzker A, Cohen HA. Paediatric cutaneous mastocytosis: A review of 180 Patients. Isr Med Assoc J 2005;7:320‑2. 3. Murphy M, Walsh D, Drumm B, Watson R. Bullous mastocytosis: A fatal outcome. Pediatr Dermatol 1999;16:452‑5. 4. Schwartz LB, Sakai K, Bradford TR, Ren SL, Zweiman B, Worobec AS, et al. The alpha form of human tryptase is the predominant type present in blood at baseline in normal subjects and is elevated in those with systemic mastocytosis. J Clin Invest 1995;96:2702‑10. 5. Kettelhut BV, Metcalfe DD. Plasma histamine concentrations in evaluation of pediatric mastocytosis. J Pediatr 1987;111:419‑21. 6. Carter MC, Metcalfe DD. Pediatric mastocytosis. Arch Dis Child 2002;86:315‑9. Access this article online Quick Response Code:
Website: www.ijdvl.com DOI: 10.4103/0378-6323.144189 PMID: *****
Dyschromatosis symmetrica hereditaria with neurological abnormalities Sir, Dyschromatosis symmetrica hereditaria (DSH) is a pigmentary genodermatosis of autosomal dominant inheritance which is characterized by a combination of hyperpigmented and hypopigmented macules on the face, back of the hands, and feet.[1] The condition primarily affects the skin and has rarely been associated with neurologic manifestations. A 2‑year old boy, born to non‑consanguineous parents presented with hyperpigmented and hypopigmented spots on his hands and feet that began at 3 months of age. Till 18 months of age, he achieved normal developmental milestones but 6 months prior to presenting to us, the parents noted regression in language development and
Indian Journal of Dermatology, Venereology, and Leprology | November-December 2014 | Vol 80 | Issue 6
549
Letters to the Editor
behavioral problems like unaccustomed laughing and crying. There was no history of associated seizures or jaundice and his perinatal history was uneventful. No one else in the family had similar skin lesions or any neurological abnormality. Examination revealed freckle‑like pigmented macules on his face. In addition, hyperpigmented and hypopigmented macules arranged in a reticulate pattern were present over the dorsa of hands and feet [Figure 1]. The surface of skin lesions did not show telangiectasia, atrophy, or scaling. Palms, soles, and mucosa were spared. There were no similar lesions elsewhere on his body. He was able to stand without support and walked with an abnormal gait with inverted feet. A dystonic (hypertonic) posture was observed in both upper and lower limbs (right more than left) along with brisk deep tendon reflexes. Rest of the systemic examination including ophthalmological examination was normal. Laboratory investigations, including routine blood and metabolic screening, calcium, phosphorus, magnesium, serum lactate, thyroid and parathyroid function, hepatic function, and serum ceruloplasmin level, TORCH screening [Toxoplasmosis, Other (syphilis, varicella‑zoster, parvovirus B19), Rubella, Cytomegalovirus (CMV), and Herpes infections], and urine examination was normal. Histopathological examination of a 4 mm punch biopsy specimen of a hyperpigmented area showed increased pigmentation of the basal layer. Based on the clinical features and the histopathological findings, a diagnosis of dyschromatosis symmetrica hereditaria was made. Computed tomographic (CT) scan of the brain showed bilaterally symmetrical calcifications in the region of basal ganglia [Figure 2]. No other structural change of brain was identified. Electroencephalography (EEG) was normal. Clinical and radiological (CT scan of brain) evaluation of his parents showed no abnormality. We
could not perform any genetic analysis to confirm the mutation in the involved gene in the present case due to non‑availability of required facilities and financial constraints. Dyschromatosis symmetrica hereditaria, synonymously known as reticulate acropigmentation of Dohi, has been reported mainly in the Japanese and Chinese population. It occurs due to a mutation in the adenosine deaminase, RNA specific gene ADAR1 which catalyzes the hydrolytic deamination of adenosine to inosine in double‑stranded RNA.[2] To date, more than 100 mutations of ADAR1 have been reported in patients with this condition, and the catalytic domain deaminase is believed to be crucial to the activities of this gene.[3‑5] The disease is usually restricted to the skin and only a limited number of cases have been reported in association with extra‑cutaneous abnormality.[3,6] An extensive search of the English language literature in PubMed, Medline, and Google Scholar database revealed only a few cases showing an association with neurological abnormalities. Pigmentation begins in infancy or childhood and gradually increases in depth and extent. Once these hypopigmented and hyperpigmented lesions are fully established, they persist life long without any change in color or distribution. Biopsy of hyperpigmented and hypopigmented macules shows basal layer melanosis and hypomelanosis, respectively.[11] Family history is present in 56-77.6% of patients with DSH.[3,7] There is no definitive treatment for this condition. The disease needs to be differentiated from dyschromatosis universalis hereditaria (DUH), which is characterized by more extensive lesions including the non‑acral and covered areas of the skin. Some other differential diagnoses include
a Figure 1: Pigmentary changes on dorsum of feet 550
b
Figure 2: (a and b) Computed tomographic scan of brain showing bilateral basal ganglia calcification (marked by arrows)
Indian Journal of Dermatology, Venereology, and Leprology | November-December 2014 | Vol 80 | Issue 6
Letters to the Editor
reticulate acropigmentation of Kitamura, mild variants of xeroderma pigmentosum, dyschromic amyloidosis, dyskeratosis congenita, and disorders due to exposure to chemicals or radiation, amongst others.[11] Neurological abnormalities in the form of seizure, dystonia and developmental regression, autistic disorder, and depression have been reported to be associated with dyschromatosis symmetrica hereditaria.[3,4] In 1994, Patrizi et al., reported a 9‑year‑old Caucasian girl who developed cutaneous changes at the age of 2 years and torsion dystonia at the age of 7 years.[12] Kondo et al., reported a case which had similar neurologic and imaging findings as in our patient.[2] Tojo et al., described a familial case of this disease with dystonia, metal deterioration, brain calcification along with aortic root sclerosis.[13] Kaliyadan et al., described a case of dyschromatosis symmetrica hereditaria in a 9‑year‑old Indian girl who had progressive regression of developmental milestones, feeble vocalization, difficulty in walking, and dystonic posturing.[10] In 2013, Peng et al. reported a retrospective series of dyschromatosis symmetrica hereditaria, three of whom had neuro‑psychiatric manifestations.[3] Although a few cases of this condition have been reported from India,[7‑9] we found only one previous report with associated neurological anomalies.[10] The exact etiology of the association with neurological manifestations in general and bilateral basal ganglia calcification and dystonia in particular is not known.
3. Peng AC, Chen AY, Chao SC. Dyschromatosis symmetrica hereditaria: A retrospective case series and literature review. Dermatol Sin 2013;31:19‑24. 4. Hayashi M, Suzuki T. Dyschromatosis symmetrica hereditaria. J Dermatol 2013;40:336‑43. 5. Chen YA, Chao SC, Lee JY. A novel deletion mutation in the adenosine deaminase RNA‑specific gene in a Taiwanese patient with dyschromatosis symmetrica hereditary. Dermatol Sin 2011;29:109‑10. 6. Miyamura Y, Suzuki T, Kono M, Inagaki K, Ito S, Suzuki N, et al. Mutations of the RNA‑specific adenosine deaminase gene (DSRAD) are involved in dyschromatosis symmetrica hereditaria. Am J Hum Genet 2003;73:693‑9. 7. Sharma R, Chandra M. Reticulate acropigmentation of dohi‑a report of two unrelated families. Indian J Dermatol Venereol Leprol 2000;66:139‑40. 8. Mohana D, Verma U, Amar AJ, Choudhary RK. Reticulate acropigmentation of dohi: A case report with insight into genodermatoses with mottled pigmentation. Indian J Dermatol 2012;57:42‑4. 9. Rao KS, Shetty JN. Acropigmentation of dohi. Indian J Dermatol Venereol Leprol 1998;64:128‑9. 10. Kaliyadan F, Vinayan KP, Fernandes B, Jayasree MG. Acral dyschromatosis with developmental regression and dystonia in a seven‑year‑old child: Dyschromatosis symmetrica hereditaria variant or a new syndrome?. Indian J Dermatol Venereol Leprol 2009;75:412‑4. 11. James WD, Berger TG, Elston DM. Andrew’s Diseases of the Skin. 10th ed. Philadelphia: Saunders Elsevier; 2011. 12. Patrizi A, Manneschi V, Pini A, Baioni E, Ghetti P. Dyschromatosis symmetrica hereditaria associated with idiopathic torsion dystonia. A case report. Acta Derm Venereol 1994;74:135‑7. 13. Tojo K, Sekijima Y, Suzuki T, Suzuki N, Tomita Y, Yoshida K, et al. Dystonia, mental deterioration, and dyschromatosis symmetrica hereditaria in a family with ADAR1 mutation. Mov Disord 2006;21:1510‑3.
Access this article online Quick Response Code:
DOI: 10.4103/0378-6323.144191
Abhijit Dutta, Sudip Kumar Ghosh1, Rajesh Kumar Mandal 2 Department of Pediatric Medicine, North Bengal Medical College, Darjeeling, 1Department of Dermatology, Venereology, and Leprosy, RG Kar Medical College, Kolkata, West Bengal, India, 2 Department of Dermatology, Venereology, and Leprosy, North Bengal Medical College, Darjeeling, India Address for correspondence: Dr. Sudip Kumar Ghosh, Department of Dermatology, Venereology, and Leprosy, RG Kar Medical College, 1, Khudiram Bose Sarani, Kolkata - 700 004, West Bengal, India. E-mail: [email protected]
REFERENCES 1. Oyama M, Shimizu H, Ohata Y, Tajima S, Nishikawa T. Dyschromatosis symmetrica hereditaria (reticulate acropigmentation of Dohi): Report of a Japanese family with the condition and a literature review of 185 cases. Br J Dermatol 1999;140:491‑6. 2. Kondo T, Suzuki T, Ito S, Kono M, Negoro T, Tomita Y. Dyschromatosis symmetrica hereditaria associated with neurological disorders. J Dermatol 2008;35:662‑6.
Website: www.ijdvl.com
PMID: *****
Localized purpuric lesions in a case of classical pityriasis rosea Sir, Pityriasis rosea is an acute inflammatory self‑limiting dermatosis characterized by oval papulo-squamous lesions on the trunk and extremities. Its typical presentation is easily recognized. Many atypical forms are known which may be challenging to diagnose. Purpuric pityriasis rosea is an unusual variant with less than 15 cases reported in English literature.[1] We report a patient with typical pityriasis
Indian Journal of Dermatology, Venereology, and Leprology | November-December 2014 | Vol 80 | Issue 6
551
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.
Plasma tryptase and histamine concentrations reflect the increased proliferation of mast cells and/or their activation.[4] Bone marrow biopsy in those with childhood‑onset cutaneous disease is not recommended unless there is evidence of systemic disease such as unexplained peripheral blood abnormalities, hepatosplenomegaly, and lymphadenopathy.[5] It has been suggested that a serum tryptase level exceeding 100 ng/ml or more is an indication for bone marrow examination regardless of age.[2] Due to monetary constraints, the plasma tryptase levels could not be done in our patient. As he had frequent flushing episodes, appearance of new skin lesions and multiple mastocytomas, bone marrow examination was carried out, which turned out to be normal. The therapy for mastocytosis is focused on providing symptomatic relief and avoidance of triggering factors. H1 antihistamines control pruritus, flushing and urticaria. In spite of receiving antihistamines, our patient had, an initial, increase in the duration of flushing episodes. We assume that this was because triggering factors like friction could not be avoided due to the multiplicity of lesions.The other reason could be an inadequate dose of antihistamines due to lack of sufficient data on dosage in the very young. Sometimes, flushing can be caused by chemical mediators other than histamine.To add to the problem, the safety profile of drugs with mast cell stabilizing properties like ketotifen and azelastine in infants and the very young has not been established.[6] Surgical excision of solitary mastocytoma, topical calcineurin inhibitors and topical corticosteroids are among the other modalities of treatment. The course of the disease in children is often benign and there is usually no progression to systemic disease. The occurence of multiple mastocytomas with bullous lesions as a presenting feature is unusual. The control of flushing in such an instance may be difficult. There is need for more therapeutic options and guidelines for the treatment of pediatric mastocytosis, especially in very young infants.
Taru Garg, Ram Chander, Niti Gaur, Aashim Singh, Anita Nangia1 Departments of Dermatology, Venereology and Leprology, and 1Pathology, Lady Hardinge Medical College and Associated Hospitals, New Delhi, India
Address for correspondence: Dr. Taru Garg, Department of Dermatology, Venereology and Leprology, Lady Hardinge Medical College and Associated Hospitals, New Delhi ‑ 110 001, India. E‑mail: [email protected]
REFERENCES 1. Lange M, Nedoszytko B, Górska A, Zawrocki A, Sobjanek M, Kozlowski D. Mastocytosis in children and adults: Clinical disease heterogeneity. Arch Med Sci 2012;8:533‑41. 2. Ben‑Amitai D, Metzker A, Cohen HA. Paediatric cutaneous mastocytosis: A review of 180 Patients. Isr Med Assoc J 2005;7:320‑2. 3. Murphy M, Walsh D, Drumm B, Watson R. Bullous mastocytosis: A fatal outcome. Pediatr Dermatol 1999;16:452‑5. 4. Schwartz LB, Sakai K, Bradford TR, Ren SL, Zweiman B, Worobec AS, et al. The alpha form of human tryptase is the predominant type present in blood at baseline in normal subjects and is elevated in those with systemic mastocytosis. J Clin Invest 1995;96:2702‑10. 5. Kettelhut BV, Metcalfe DD. Plasma histamine concentrations in evaluation of pediatric mastocytosis. J Pediatr 1987;111:419‑21. 6. Carter MC, Metcalfe DD. Pediatric mastocytosis. Arch Dis Child 2002;86:315‑9. Access this article online Quick Response Code:
Website: www.ijdvl.com DOI: 10.4103/0378-6323.144189 PMID: *****
Dyschromatosis symmetrica hereditaria with neurological abnormalities Sir, Dyschromatosis symmetrica hereditaria (DSH) is a pigmentary genodermatosis of autosomal dominant inheritance which is characterized by a combination of hyperpigmented and hypopigmented macules on the face, back of the hands, and feet.[1] The condition primarily affects the skin and has rarely been associated with neurologic manifestations. A 2‑year old boy, born to non‑consanguineous parents presented with hyperpigmented and hypopigmented spots on his hands and feet that began at 3 months of age. Till 18 months of age, he achieved normal developmental milestones but 6 months prior to presenting to us, the parents noted regression in language development and
Indian Journal of Dermatology, Venereology, and Leprology | November-December 2014 | Vol 80 | Issue 6
549
Letters to the Editor
behavioral problems like unaccustomed laughing and crying. There was no history of associated seizures or jaundice and his perinatal history was uneventful. No one else in the family had similar skin lesions or any neurological abnormality. Examination revealed freckle‑like pigmented macules on his face. In addition, hyperpigmented and hypopigmented macules arranged in a reticulate pattern were present over the dorsa of hands and feet [Figure 1]. The surface of skin lesions did not show telangiectasia, atrophy, or scaling. Palms, soles, and mucosa were spared. There were no similar lesions elsewhere on his body. He was able to stand without support and walked with an abnormal gait with inverted feet. A dystonic (hypertonic) posture was observed in both upper and lower limbs (right more than left) along with brisk deep tendon reflexes. Rest of the systemic examination including ophthalmological examination was normal. Laboratory investigations, including routine blood and metabolic screening, calcium, phosphorus, magnesium, serum lactate, thyroid and parathyroid function, hepatic function, and serum ceruloplasmin level, TORCH screening [Toxoplasmosis, Other (syphilis, varicella‑zoster, parvovirus B19), Rubella, Cytomegalovirus (CMV), and Herpes infections], and urine examination was normal. Histopathological examination of a 4 mm punch biopsy specimen of a hyperpigmented area showed increased pigmentation of the basal layer. Based on the clinical features and the histopathological findings, a diagnosis of dyschromatosis symmetrica hereditaria was made. Computed tomographic (CT) scan of the brain showed bilaterally symmetrical calcifications in the region of basal ganglia [Figure 2]. No other structural change of brain was identified. Electroencephalography (EEG) was normal. Clinical and radiological (CT scan of brain) evaluation of his parents showed no abnormality. We
could not perform any genetic analysis to confirm the mutation in the involved gene in the present case due to non‑availability of required facilities and financial constraints. Dyschromatosis symmetrica hereditaria, synonymously known as reticulate acropigmentation of Dohi, has been reported mainly in the Japanese and Chinese population. It occurs due to a mutation in the adenosine deaminase, RNA specific gene ADAR1 which catalyzes the hydrolytic deamination of adenosine to inosine in double‑stranded RNA.[2] To date, more than 100 mutations of ADAR1 have been reported in patients with this condition, and the catalytic domain deaminase is believed to be crucial to the activities of this gene.[3‑5] The disease is usually restricted to the skin and only a limited number of cases have been reported in association with extra‑cutaneous abnormality.[3,6] An extensive search of the English language literature in PubMed, Medline, and Google Scholar database revealed only a few cases showing an association with neurological abnormalities. Pigmentation begins in infancy or childhood and gradually increases in depth and extent. Once these hypopigmented and hyperpigmented lesions are fully established, they persist life long without any change in color or distribution. Biopsy of hyperpigmented and hypopigmented macules shows basal layer melanosis and hypomelanosis, respectively.[11] Family history is present in 56-77.6% of patients with DSH.[3,7] There is no definitive treatment for this condition. The disease needs to be differentiated from dyschromatosis universalis hereditaria (DUH), which is characterized by more extensive lesions including the non‑acral and covered areas of the skin. Some other differential diagnoses include
a Figure 1: Pigmentary changes on dorsum of feet 550
b
Figure 2: (a and b) Computed tomographic scan of brain showing bilateral basal ganglia calcification (marked by arrows)
Indian Journal of Dermatology, Venereology, and Leprology | November-December 2014 | Vol 80 | Issue 6
Letters to the Editor
reticulate acropigmentation of Kitamura, mild variants of xeroderma pigmentosum, dyschromic amyloidosis, dyskeratosis congenita, and disorders due to exposure to chemicals or radiation, amongst others.[11] Neurological abnormalities in the form of seizure, dystonia and developmental regression, autistic disorder, and depression have been reported to be associated with dyschromatosis symmetrica hereditaria.[3,4] In 1994, Patrizi et al., reported a 9‑year‑old Caucasian girl who developed cutaneous changes at the age of 2 years and torsion dystonia at the age of 7 years.[12] Kondo et al., reported a case which had similar neurologic and imaging findings as in our patient.[2] Tojo et al., described a familial case of this disease with dystonia, metal deterioration, brain calcification along with aortic root sclerosis.[13] Kaliyadan et al., described a case of dyschromatosis symmetrica hereditaria in a 9‑year‑old Indian girl who had progressive regression of developmental milestones, feeble vocalization, difficulty in walking, and dystonic posturing.[10] In 2013, Peng et al. reported a retrospective series of dyschromatosis symmetrica hereditaria, three of whom had neuro‑psychiatric manifestations.[3] Although a few cases of this condition have been reported from India,[7‑9] we found only one previous report with associated neurological anomalies.[10] The exact etiology of the association with neurological manifestations in general and bilateral basal ganglia calcification and dystonia in particular is not known.
3. Peng AC, Chen AY, Chao SC. Dyschromatosis symmetrica hereditaria: A retrospective case series and literature review. Dermatol Sin 2013;31:19‑24. 4. Hayashi M, Suzuki T. Dyschromatosis symmetrica hereditaria. J Dermatol 2013;40:336‑43. 5. Chen YA, Chao SC, Lee JY. A novel deletion mutation in the adenosine deaminase RNA‑specific gene in a Taiwanese patient with dyschromatosis symmetrica hereditary. Dermatol Sin 2011;29:109‑10. 6. Miyamura Y, Suzuki T, Kono M, Inagaki K, Ito S, Suzuki N, et al. Mutations of the RNA‑specific adenosine deaminase gene (DSRAD) are involved in dyschromatosis symmetrica hereditaria. Am J Hum Genet 2003;73:693‑9. 7. Sharma R, Chandra M. Reticulate acropigmentation of dohi‑a report of two unrelated families. Indian J Dermatol Venereol Leprol 2000;66:139‑40. 8. Mohana D, Verma U, Amar AJ, Choudhary RK. Reticulate acropigmentation of dohi: A case report with insight into genodermatoses with mottled pigmentation. Indian J Dermatol 2012;57:42‑4. 9. Rao KS, Shetty JN. Acropigmentation of dohi. Indian J Dermatol Venereol Leprol 1998;64:128‑9. 10. Kaliyadan F, Vinayan KP, Fernandes B, Jayasree MG. Acral dyschromatosis with developmental regression and dystonia in a seven‑year‑old child: Dyschromatosis symmetrica hereditaria variant or a new syndrome?. Indian J Dermatol Venereol Leprol 2009;75:412‑4. 11. James WD, Berger TG, Elston DM. Andrew’s Diseases of the Skin. 10th ed. Philadelphia: Saunders Elsevier; 2011. 12. Patrizi A, Manneschi V, Pini A, Baioni E, Ghetti P. Dyschromatosis symmetrica hereditaria associated with idiopathic torsion dystonia. A case report. Acta Derm Venereol 1994;74:135‑7. 13. Tojo K, Sekijima Y, Suzuki T, Suzuki N, Tomita Y, Yoshida K, et al. Dystonia, mental deterioration, and dyschromatosis symmetrica hereditaria in a family with ADAR1 mutation. Mov Disord 2006;21:1510‑3.
Access this article online Quick Response Code:
DOI: 10.4103/0378-6323.144191
Abhijit Dutta, Sudip Kumar Ghosh1, Rajesh Kumar Mandal 2 Department of Pediatric Medicine, North Bengal Medical College, Darjeeling, 1Department of Dermatology, Venereology, and Leprosy, RG Kar Medical College, Kolkata, West Bengal, India, 2 Department of Dermatology, Venereology, and Leprosy, North Bengal Medical College, Darjeeling, India Address for correspondence: Dr. Sudip Kumar Ghosh, Department of Dermatology, Venereology, and Leprosy, RG Kar Medical College, 1, Khudiram Bose Sarani, Kolkata - 700 004, West Bengal, India. E-mail: [email protected]
REFERENCES 1. Oyama M, Shimizu H, Ohata Y, Tajima S, Nishikawa T. Dyschromatosis symmetrica hereditaria (reticulate acropigmentation of Dohi): Report of a Japanese family with the condition and a literature review of 185 cases. Br J Dermatol 1999;140:491‑6. 2. Kondo T, Suzuki T, Ito S, Kono M, Negoro T, Tomita Y. Dyschromatosis symmetrica hereditaria associated with neurological disorders. J Dermatol 2008;35:662‑6.
Website: www.ijdvl.com
PMID: *****
Localized purpuric lesions in a case of classical pityriasis rosea Sir, Pityriasis rosea is an acute inflammatory self‑limiting dermatosis characterized by oval papulo-squamous lesions on the trunk and extremities. Its typical presentation is easily recognized. Many atypical forms are known which may be challenging to diagnose. Purpuric pityriasis rosea is an unusual variant with less than 15 cases reported in English literature.[1] We report a patient with typical pityriasis
Indian Journal of Dermatology, Venereology, and Leprology | November-December 2014 | Vol 80 | Issue 6
551
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.
