Correspondence
(a)
(b)
(c)
Figure 2 (a) Histopathology shows epidermal atrophy with marked basal hydropic degeneration accompanied by a lymphocytic infiltrate. (b) The blood vessel wall shows a fibrinoid change and a surrounding neutrophilic infiltrate. (c) The eccrine gland shows necrotic epithelial cells. [Hematoxylin and eosin stain; original magnification (a) 9400, (b) 9200, (c) 9400]
sequelae presenting as non-infectious, hemorrhagic bullae developing only over striae in a patient with recently diagnosed SLE and lupus nephritis.
Natalie C. Yin, BS Sonal Choudhary, MD Joshua R. Freedman, MD, MS Francisco A. Kerdel, MD Department of Dermatology and Cutaneous Surgery University of Miami Miller School of Medicine Miami FL, USA E-mail: [email protected] Clara Milikowski, MD Department of Pathology University of Miami Miller School of Medicine Miami FL USA
References 1 Tuffanelli DL, Dubois EL. Cutaneous manifestations of systemic lupus erythematosus. Arch Dermatol 1964; 90: 377–386. 2 Callen JP. Cutaneous bullae following acute steroid withdrawal in systemic lupus erythematosus. Br J Dermatol 1981; 105: 603–606. 3 Kumar V, Binder WL, Schotland E, et al. Coexistence of bullous pemphigoid and systemic lupus erythematosus. Arch Dermatol 1978; 114: 1187–1190. 4 Penneys NS, Wiley HE III. Herpetiform blisters in systemic lupus erythematosus. Arch Dermatol 1979; 115: 1427–1428. 5 Yell JA, Wojnarowska F. Bullous skin disease in lupus erythematosus. Lupus 1997; 6: 112–121. ª 2014 The International Society of Dermatology
6 Scholtz M. Lupus erythematosus acutus disseminatus hemorrhagicus. Arch Derm Syphilol 1922; 6: 466–475. 7 Vitali C, Bencivelli W, Isenberg DA, et al. Disease activity in systemic lupus erythematosus: report of the Consensus Study Group of the European Workshop for Rheumatology Research. II. Identification of the variables indicative of disease activity and their use in the development of an activity score. The European Consensus Study Group for Disease Activity in SLE. Clin Exp Rheumatol 1992; 10: 541–547. 8 Laman SD, Provost TT. Cutaneous manifestations of lupus erythematosus. Rheum Dis Clin North Am 1994; 20: 195–212. 9 Calamia KT, Balabanova M. Vasculitis in systemic lupus erythematosus. Clin Dermatol 2004; 22: 148–156. 10 Belmont HM, Abramson SB, Lie JT. Pathology and pathogenesis of vascular injury in systemic lupus erythematosus. Interactions of inflammatory cells and activated endothelium. Arthritis Rheum 1996; 39: 9–22. 11 Cid MC. Endothelial cell biology, perivascular inflammation, and vasculitis. Cleve Clin J Med 2002; 69 (Suppl. 2): 45–49. 12 Watson RE, Parry EJ, Humphries JD, et al. Fibrillin microfibrils are reduced in skin exhibiting striae distensae. Br J Dermatol 1998; 138: 931–937. 13 Kwon CW, Lee CW, Kim YT, et al. Urticarial vasculitis developed on the striae distensae during pregnancy. Int J Dermatol 1993; 32: 751–752.
Flagellate erythema in parvovirus B19 infection
Editor, Human parvovirus B19 (PVB19) is a single-stranded DNA virus of the family Parvoviridae and the etiologic agent of erythema infectiosum or fifth disease. Other clinical manifestations of this virus are papular purpuric gloves and socks syndrome, purpuric exanthemas, arthropathy, hydrops fetalis, and aplastic crisis.1–3 We report an International Journal of Dermatology 2014, 53, e578–e596
e583
e584
Correspondence
(a)
(b)
immunocompetent child with PVB19 infection who presented with a febrile purpuric–petechial rash and a striking flagellate erythema not previously described in this infection. A 4-year-old girl, otherwise healthy, was admitted to hospital with a fever of 39 °C that had been present over the previous three days and an erythematous rash present during the previous two days. Generalized moderate pruritus was observed. On physical examination, the child was found to have a hyperemic pharynx, purpuric papules on the chin and ears (with no erythema of the cheeks), and a maculopapular erythematous rash over the trunk and limbs. Her legs, forearms, and the dorsa of her hands and feet were edematous and covered with small petechial papules (Fig. 1a), and her back exhibited erythematous papules and plaques in a linear pattern (Fig. 1b). There was no involvement of the mucous membranes. Cardiopulmonary auscultation was normal. Laboratory studies revealed pancytopenia and increased C-reactive protein. Blood and urine cultures were negative. Echocardiography showed a minimal pericardial effusion with no ventricular dysfunction. An enzymelinked immunosorbent assay (ELISA) for anti-PVB19 immunoglobulin M (IgM) antibodies in serum was positive. Acute PVB19 infection was diagnosed, and the patient was treated with supportive therapy, antihistamines, and IV immunoglobulin. The clinical course was favorable, and the blood abnormalities recovered. The cutaneous rash progressively disappeared without recurrence, and the linear lesions on the patient’s back resolved with no pigmentation. Infection with PVB19 may cause a wide range of dermatologic manifestations.1–3 Erythema infectiosum and papular purpuric gloves and socks syndrome are the most International Journal of Dermatology 2014, 53, e578–e596
Figure 1 Skin lesions in a 4-year-old girl admitted to hospital with fever of 39 °C, manifesting as (a) a generalized erythematous maculopapular rash with purpuric– petechial lesions, edema and small petechial papules on the limbs, and (b) flagellate erythema on the back
characteristic. Other nonspecific findings include reticular erythema, maculopapular eruptions, petechiae, and purpura. In addition, a purpuric–petechial eruption with a generalized involvement has been reported in association with PVB19, and our patient’s presentation was compatible with this form of infection.3 In immunocompetent children, the disease is usually self-limiting, but hematologic abnormalities and other serious complications such as myocarditis have been reported. Flagellate erythema is a dermatologic lesion that presents with pruriginous or painful red linear streaks, which are found most commonly on the back and flanks.4 It has been reported mainly in association with chemotherapeutic agents (bleomycin, docetaxel, and bendamustine), shiitake mushroom intake, and dermatomyositis, but its pathogenesis is generally uncertain.4–7 Scratching in patients receiving cytostatic drugs would cause vasodilatation and a higher flow of these toxic drugs to the skin. In instances of shiitake mushroom intake, an allergic mechanism has been suggested, most likely related to the polysaccharide lentinan. In dermatomyositis, flagellate erythema is favored by the autoimmune disorder and is more inflammatory and persistent, but its pathogenesis is unknown. Flagellate erythema commonly disappears without pigmentation, as occurred in our patient, although a persistent pigmentation lasting for months is possible. In summary, our patient demonstrated a febrile purpuric–petechial eruption associated with flagellate erythema during the course of PVB19 infection. In this case, flagellate erythema might be explained by the combination of scratching and dermal endothelial damage caused by PVB19.8 We present this case because this association has not been reported previously as far as we know. ª 2014 The International Society of Dermatology
Correspondence
Ana Miguelez, MD Department of Dermatology University Hospital of La Princesa Madrid Spain Joaquın Due~ nas, MD Department of Pediatrics Son Espases University Hospital Palma de Mallorca Spain Daniel Hervas, MD Juan A. Hervas, MD, PhD University Institute of Health Sciences (IUNICS) University of the Balearic Islands Palma de Mallorca Spain E-mail: [email protected] Francisco Salva, PhD Department of Microbiology Son Espases University Hospital Palma de Mallorca Spain Ana Martın-Santiago, MD Department of Dermatology Son Espases University Hospital Palma de Mallorca Spain
References 1 Heegaard ED, Brown KE. Human parvovirus B19. Clin Microbiol Rev 2002; 15: 485–505. 2 Katta R. Parvovirus B19: a review. Dermatol Clin 2002; 20: 333–342. 3 Hashimoto H, Yuno T. Parvovirus B19-associated purpuric–petechial eruption. J Clin Virol 2011; 52: 269–271. 4 Yamamoto T, Nishioka K. Flagellate erythema. Int J Dermatol 2006; 45: 627–631. 5 Ziemer M, Goetze S, Juhasz K, et al. Flagellate dermatitis as a bleomycin-specific adverse effect of cytostatic therapy. Am J Clin Dermatol 2011; 12: 68–76. 6 Poppe LM, Anders D, Kneitz H, et al. Flagellate dermatitis caused by shiitake mushrooms. An Bras Dermatol 2012; 87: 463–465. 7 Watanabe T, Tsuchida T. Flagellate erythema in dermatomyositis. Dermatology 1995; 190: 230–231. et al. 8 Santonja C, Nieto-Gonz alez G, Santos-Briz A, Immunohistochemical detection of parvovirus B19 in
ª 2014 The International Society of Dermatology
gloves and socks papular purpuric syndrome: direct evidence for viral endothelial involvement. Report of three cases and review of the literature. Am J Dermatopathol 2011; 33: 790–795.
Intensification therapy with golimumab: a new treatment strategy for moderate–severe refractory psoriasis
Moderate–severe psoriasis is a disabling entity that requires treatment with systemic drugs and in some cases with biological products. Unfortunately, these regimens can lose efficacy with time. Several options can be utilized to obtain the best result for the patient.1 A 55-year-old man with hypertension and obesity, who was a chronic smoker and drinker, presented with moderate–severe plaque psoriasis with psoriatic arthritis (PsA). He had been treated with acitretin, methotrexate (MTX), psoralen and ultraviolet A therapy (PUVA), cyclosporine A, mycophenolate mofetil, efalizumab, infliximab, etanercept, adalimumab, and ustekinumab with and without MTX. All of these treatments had been withdrawn for adverse effects or the loss of efficacy at the cutaneous and/or joint level. The subject had last been treated with golimumab at a dose of 50 mg s.c. per month, along with weekly s.c. injections of MTX 10 mg and had achieved a Disease Activity Score-28 (DAS28) index of 0, but had maintained a Psoriasis Area and Severity Index (PASI) score of 24 (Fig. 1a). We decided to increase this subject’s therapy with golimumab to 50 mg s.c. administered every 15 days and achieved a PASI score of 0 after two months, with no adverse effects (Fig. 1b). The patient remained clear of symptoms until September 2012, when the efficacy of the treatment was observed to decrease. The patient reported a PASI score of 7 at six months after the increase in golimumab therapy, which he has maintained to the present. A 61-year-old overweight woman with type 1 diabetes mellitus, hypertension, and dyslipidemia presented with moderate–severe plaque psoriasis with PsA. She was treated with narrowband ultraviolet B (UVB) phototherapy, PUVA therapy, MTX, etanercept, adalimumab, infliximab, and ustekinumab with and without MTX, all of which were withdrawn as a result of adverse effects or loss of efficacy at the cutaneous and/or joint level. The subject’s last treatment had been golimumab administered s.c. at a dose of 50 mg per month, along with associated with weekly s.c. injections of MTX 15 mg. She reported a DAS28 score of 0 and a PASI score of 11. This patient’s therapy was intensified so that golimumab, associated with MTX, was administered at a dose of 15 mg s.c. every week (Fig. 2a). After two months of treatment with this regimen, the patient achieved a PASI score of 0 (Fig. 2b). At six months, a slight loss of efficacy was International Journal of Dermatology 2014, 53, e578–e596
e585
This document is a scanned copy of a printed document. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material.
(a)
(b)
(c)
Figure 2 (a) Histopathology shows epidermal atrophy with marked basal hydropic degeneration accompanied by a lymphocytic infiltrate. (b) The blood vessel wall shows a fibrinoid change and a surrounding neutrophilic infiltrate. (c) The eccrine gland shows necrotic epithelial cells. [Hematoxylin and eosin stain; original magnification (a) 9400, (b) 9200, (c) 9400]
sequelae presenting as non-infectious, hemorrhagic bullae developing only over striae in a patient with recently diagnosed SLE and lupus nephritis.
Natalie C. Yin, BS Sonal Choudhary, MD Joshua R. Freedman, MD, MS Francisco A. Kerdel, MD Department of Dermatology and Cutaneous Surgery University of Miami Miller School of Medicine Miami FL, USA E-mail: [email protected] Clara Milikowski, MD Department of Pathology University of Miami Miller School of Medicine Miami FL USA
References 1 Tuffanelli DL, Dubois EL. Cutaneous manifestations of systemic lupus erythematosus. Arch Dermatol 1964; 90: 377–386. 2 Callen JP. Cutaneous bullae following acute steroid withdrawal in systemic lupus erythematosus. Br J Dermatol 1981; 105: 603–606. 3 Kumar V, Binder WL, Schotland E, et al. Coexistence of bullous pemphigoid and systemic lupus erythematosus. Arch Dermatol 1978; 114: 1187–1190. 4 Penneys NS, Wiley HE III. Herpetiform blisters in systemic lupus erythematosus. Arch Dermatol 1979; 115: 1427–1428. 5 Yell JA, Wojnarowska F. Bullous skin disease in lupus erythematosus. Lupus 1997; 6: 112–121. ª 2014 The International Society of Dermatology
6 Scholtz M. Lupus erythematosus acutus disseminatus hemorrhagicus. Arch Derm Syphilol 1922; 6: 466–475. 7 Vitali C, Bencivelli W, Isenberg DA, et al. Disease activity in systemic lupus erythematosus: report of the Consensus Study Group of the European Workshop for Rheumatology Research. II. Identification of the variables indicative of disease activity and their use in the development of an activity score. The European Consensus Study Group for Disease Activity in SLE. Clin Exp Rheumatol 1992; 10: 541–547. 8 Laman SD, Provost TT. Cutaneous manifestations of lupus erythematosus. Rheum Dis Clin North Am 1994; 20: 195–212. 9 Calamia KT, Balabanova M. Vasculitis in systemic lupus erythematosus. Clin Dermatol 2004; 22: 148–156. 10 Belmont HM, Abramson SB, Lie JT. Pathology and pathogenesis of vascular injury in systemic lupus erythematosus. Interactions of inflammatory cells and activated endothelium. Arthritis Rheum 1996; 39: 9–22. 11 Cid MC. Endothelial cell biology, perivascular inflammation, and vasculitis. Cleve Clin J Med 2002; 69 (Suppl. 2): 45–49. 12 Watson RE, Parry EJ, Humphries JD, et al. Fibrillin microfibrils are reduced in skin exhibiting striae distensae. Br J Dermatol 1998; 138: 931–937. 13 Kwon CW, Lee CW, Kim YT, et al. Urticarial vasculitis developed on the striae distensae during pregnancy. Int J Dermatol 1993; 32: 751–752.
Flagellate erythema in parvovirus B19 infection
Editor, Human parvovirus B19 (PVB19) is a single-stranded DNA virus of the family Parvoviridae and the etiologic agent of erythema infectiosum or fifth disease. Other clinical manifestations of this virus are papular purpuric gloves and socks syndrome, purpuric exanthemas, arthropathy, hydrops fetalis, and aplastic crisis.1–3 We report an International Journal of Dermatology 2014, 53, e578–e596
e583
e584
Correspondence
(a)
(b)
immunocompetent child with PVB19 infection who presented with a febrile purpuric–petechial rash and a striking flagellate erythema not previously described in this infection. A 4-year-old girl, otherwise healthy, was admitted to hospital with a fever of 39 °C that had been present over the previous three days and an erythematous rash present during the previous two days. Generalized moderate pruritus was observed. On physical examination, the child was found to have a hyperemic pharynx, purpuric papules on the chin and ears (with no erythema of the cheeks), and a maculopapular erythematous rash over the trunk and limbs. Her legs, forearms, and the dorsa of her hands and feet were edematous and covered with small petechial papules (Fig. 1a), and her back exhibited erythematous papules and plaques in a linear pattern (Fig. 1b). There was no involvement of the mucous membranes. Cardiopulmonary auscultation was normal. Laboratory studies revealed pancytopenia and increased C-reactive protein. Blood and urine cultures were negative. Echocardiography showed a minimal pericardial effusion with no ventricular dysfunction. An enzymelinked immunosorbent assay (ELISA) for anti-PVB19 immunoglobulin M (IgM) antibodies in serum was positive. Acute PVB19 infection was diagnosed, and the patient was treated with supportive therapy, antihistamines, and IV immunoglobulin. The clinical course was favorable, and the blood abnormalities recovered. The cutaneous rash progressively disappeared without recurrence, and the linear lesions on the patient’s back resolved with no pigmentation. Infection with PVB19 may cause a wide range of dermatologic manifestations.1–3 Erythema infectiosum and papular purpuric gloves and socks syndrome are the most International Journal of Dermatology 2014, 53, e578–e596
Figure 1 Skin lesions in a 4-year-old girl admitted to hospital with fever of 39 °C, manifesting as (a) a generalized erythematous maculopapular rash with purpuric– petechial lesions, edema and small petechial papules on the limbs, and (b) flagellate erythema on the back
characteristic. Other nonspecific findings include reticular erythema, maculopapular eruptions, petechiae, and purpura. In addition, a purpuric–petechial eruption with a generalized involvement has been reported in association with PVB19, and our patient’s presentation was compatible with this form of infection.3 In immunocompetent children, the disease is usually self-limiting, but hematologic abnormalities and other serious complications such as myocarditis have been reported. Flagellate erythema is a dermatologic lesion that presents with pruriginous or painful red linear streaks, which are found most commonly on the back and flanks.4 It has been reported mainly in association with chemotherapeutic agents (bleomycin, docetaxel, and bendamustine), shiitake mushroom intake, and dermatomyositis, but its pathogenesis is generally uncertain.4–7 Scratching in patients receiving cytostatic drugs would cause vasodilatation and a higher flow of these toxic drugs to the skin. In instances of shiitake mushroom intake, an allergic mechanism has been suggested, most likely related to the polysaccharide lentinan. In dermatomyositis, flagellate erythema is favored by the autoimmune disorder and is more inflammatory and persistent, but its pathogenesis is unknown. Flagellate erythema commonly disappears without pigmentation, as occurred in our patient, although a persistent pigmentation lasting for months is possible. In summary, our patient demonstrated a febrile purpuric–petechial eruption associated with flagellate erythema during the course of PVB19 infection. In this case, flagellate erythema might be explained by the combination of scratching and dermal endothelial damage caused by PVB19.8 We present this case because this association has not been reported previously as far as we know. ª 2014 The International Society of Dermatology
Correspondence
Ana Miguelez, MD Department of Dermatology University Hospital of La Princesa Madrid Spain Joaquın Due~ nas, MD Department of Pediatrics Son Espases University Hospital Palma de Mallorca Spain Daniel Hervas, MD Juan A. Hervas, MD, PhD University Institute of Health Sciences (IUNICS) University of the Balearic Islands Palma de Mallorca Spain E-mail: [email protected] Francisco Salva, PhD Department of Microbiology Son Espases University Hospital Palma de Mallorca Spain Ana Martın-Santiago, MD Department of Dermatology Son Espases University Hospital Palma de Mallorca Spain
References 1 Heegaard ED, Brown KE. Human parvovirus B19. Clin Microbiol Rev 2002; 15: 485–505. 2 Katta R. Parvovirus B19: a review. Dermatol Clin 2002; 20: 333–342. 3 Hashimoto H, Yuno T. Parvovirus B19-associated purpuric–petechial eruption. J Clin Virol 2011; 52: 269–271. 4 Yamamoto T, Nishioka K. Flagellate erythema. Int J Dermatol 2006; 45: 627–631. 5 Ziemer M, Goetze S, Juhasz K, et al. Flagellate dermatitis as a bleomycin-specific adverse effect of cytostatic therapy. Am J Clin Dermatol 2011; 12: 68–76. 6 Poppe LM, Anders D, Kneitz H, et al. Flagellate dermatitis caused by shiitake mushrooms. An Bras Dermatol 2012; 87: 463–465. 7 Watanabe T, Tsuchida T. Flagellate erythema in dermatomyositis. Dermatology 1995; 190: 230–231. et al. 8 Santonja C, Nieto-Gonz alez G, Santos-Briz A, Immunohistochemical detection of parvovirus B19 in
ª 2014 The International Society of Dermatology
gloves and socks papular purpuric syndrome: direct evidence for viral endothelial involvement. Report of three cases and review of the literature. Am J Dermatopathol 2011; 33: 790–795.
Intensification therapy with golimumab: a new treatment strategy for moderate–severe refractory psoriasis
Moderate–severe psoriasis is a disabling entity that requires treatment with systemic drugs and in some cases with biological products. Unfortunately, these regimens can lose efficacy with time. Several options can be utilized to obtain the best result for the patient.1 A 55-year-old man with hypertension and obesity, who was a chronic smoker and drinker, presented with moderate–severe plaque psoriasis with psoriatic arthritis (PsA). He had been treated with acitretin, methotrexate (MTX), psoralen and ultraviolet A therapy (PUVA), cyclosporine A, mycophenolate mofetil, efalizumab, infliximab, etanercept, adalimumab, and ustekinumab with and without MTX. All of these treatments had been withdrawn for adverse effects or the loss of efficacy at the cutaneous and/or joint level. The subject had last been treated with golimumab at a dose of 50 mg s.c. per month, along with weekly s.c. injections of MTX 10 mg and had achieved a Disease Activity Score-28 (DAS28) index of 0, but had maintained a Psoriasis Area and Severity Index (PASI) score of 24 (Fig. 1a). We decided to increase this subject’s therapy with golimumab to 50 mg s.c. administered every 15 days and achieved a PASI score of 0 after two months, with no adverse effects (Fig. 1b). The patient remained clear of symptoms until September 2012, when the efficacy of the treatment was observed to decrease. The patient reported a PASI score of 7 at six months after the increase in golimumab therapy, which he has maintained to the present. A 61-year-old overweight woman with type 1 diabetes mellitus, hypertension, and dyslipidemia presented with moderate–severe plaque psoriasis with PsA. She was treated with narrowband ultraviolet B (UVB) phototherapy, PUVA therapy, MTX, etanercept, adalimumab, infliximab, and ustekinumab with and without MTX, all of which were withdrawn as a result of adverse effects or loss of efficacy at the cutaneous and/or joint level. The subject’s last treatment had been golimumab administered s.c. at a dose of 50 mg per month, along with associated with weekly s.c. injections of MTX 15 mg. She reported a DAS28 score of 0 and a PASI score of 11. This patient’s therapy was intensified so that golimumab, associated with MTX, was administered at a dose of 15 mg s.c. every week (Fig. 2a). After two months of treatment with this regimen, the patient achieved a PASI score of 0 (Fig. 2b). At six months, a slight loss of efficacy was International Journal of Dermatology 2014, 53, e578–e596
e585
This document is a scanned copy of a printed document. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material.
