Nonpruritic Papular Facial Eruption

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Nonpruritic Papular Facial Eruption

The Diagnosis: Granulomatous Periorificial Dermatitis

Review of the prior biopsy from the lower cutaneous lip revealed granulomatous perifolliculitis. The patient’s age combined with the morphology, distribution, and histopathologic features (Figure) of his eruption were characteristic of granulomatous periorificial dermatitis (GPD) of childhood. The patient was treated with oral erythromycin and topical metronidazole with immediate improvement, particularly with resolution of the erythema.

An attenuated epidermis overlying noncaseating dermal granulomas (A)(H&E, original magnification ×10). Granulomatous perifollicular inflammation with infiltration of the follicular epithelium by neutrophils and lymphocytes (B)(H&E, original magnification ×20).

Granulomatous periorificial dermatitis is a benign, self-limited eruption in healthy prepubertal children that is characterized by coalescent, asymptomatic, dome-shaped, yellow-brown to erythematous papules.1,2 The monomorphous lesions are firm, measure 1 to 3 mm in diameter, and are most commonly located around the mouth.2,3 Other areas of involvement include the nostrils and alar creases as well as the periocular skin.4 Less commonly, GPD has been described on the scalp, ears, neck, trunk, extremities, and genital region.5 Slight peripheral scaling or erythema and small pitted scarring are variable.4,5 There may be a history of failed topical corticosteroid treatment that either caused no change or a flare in the rash.1-5 Patients have no systemic findings.3,5

Biopsy of GPD shows characteristic noncaseating granulomas in the dermis, typified by perifollicular localization.5 The granulomatous infiltrate consists of epithelioid histiocytes and multinucleated giant cells surrounded by lymphocytes, with focal collections of neutrophils and occasionally overlying parakeratosis.2,3

The nomenclature of GPD has varied since the 1970s and has included Gianotti-type perioral dermatitis,6 GPD of childhood,7 rosacealike eruption in children,8 FACE (facial Afro-Caribbean childhood eruption),9 and sarcoidlike granulomatous dermatitis.10

The etiology of GPD is unknown, though it has been associated with use of topical, inhaled, or systemic steroids; a personal history of skin problems; a family history of atopy; vaccination; and local reactions to allergens such as cosmetic preparations, antiseptic solutions, tartar control toothpaste, and bubble gum.4,5,11-13 Granulomatous periorificial dermatitis may represent a pediatric variant of granulomatous rosacea or a granulomatous variant of perioral dermatitis, but importantly, it is not related to sarcoidosis.1,4,5 Granulomatous periorificial dermatitis typically affects children of dark-skinned, African Caribbean ancestry, though it has been described in both white and Asian populations.1,2,5 Genders are equally affected.

Although generally a benign condition that spontaneously remits within a few months to 3 years,5 GPD can be quite disruptive to a patient’s self-image, necessitating therapy to hasten resolution. Prior to initiation of treatment, any topical corticosteroids being applied to the affected region should be discontinued. For children older than 9 years, a suggested regimen is oral tetracycline 250 mg twice daily; for those younger than 9 years, erythromycin 30 to 40 mg/kg daily in 2 divided doses is advised.14 Metronidazole 0.75% cream and gel also have shown efficacy in GPD and represent a topical adjunct or alternative to oral therapy.1,14,15

References
  1. Knautz MA, Lesher JL. Childhood granulomatous periorificial dermatitis. Pediatr Dermatol. 1996;13:131-134.
  2. Choi YL, Lee KJ, Cho HJ, et al. Case of childhood granulomatous periorificial dermatitis in a Korean boy treated by oral erythromycin. J Dermatol. 2006;33:806-808.
  3. Tarm K, Creel NB, Krivda SJ, et al. Granulomatous periorificial dermatitis. Cutis. 2004;73:399-402.
  4. Nguyen V, Eichenfield LF. Periorificial dermatitis in children and adolescents. J Am Acad Dermatol. 2006;55:781-785.
  5. Urbatsch AJ, Frieden I, Williams ML, et al. Extrafacial and generalized granulomatous periorificial dermatitis. Arch Dermatol. 2002;138:1354-1358.
  6. Gianotti F, Ermacora E, Bennelli MG, et al. Particuliere dermatite peri-orale infantile: observations sur cinq cas. Bull Soc Fr Dermatol Syph. 1970;77:341.
  7. Frieden IJ, Prose NS, Fletcher V, et al. Granulomatous perioral dermatitis in children. Arch Dermatol. 1989;125:369-373.
  8. Savin JA, Alexander S, Marks R. A rosacea-like eruption of children. Br J Dermatol. 1972;87:425-429.
  9. Marten RH, Presbury DG, Adamson JE, et al. An unusual popular and acneiform facial eruption in the Negro child. Br J Dermatol. 1974;91:435-438.
  10. Falk ES. Sarcoid-like granulomatous periocular dermatitis treated with tetracycline. Acta Derm Venereol. 1985;65:270-272.
  11. Hafeez ZH. Perioral dermatitis: an update. Int J Dermatol. 2003;42:514-517.
  12. Ferlito TA. Tartar-control toothpaste and perioral dermatitis. J Clin Oncol. 1992;27:43-44.
  13. Georgouras K, Kocsard E. Micropapular sarcoidal facial eruption in a child. Acta Derm Venereol. 1978;48:433-436.
  14. Laude TA, Salvemini JN. Perioral dermatitis in children. Semin Cutan Med Surg. 1999;18:206-209.
  15. Miller SR, Shalita AR. Topical metronidazole gel (0.75%) for the treatment of perioral dermatitis in children. J Am Acad Dermatol. 1994;31:847-848.
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Dr. Schmitt is from the Dermatology Division, Dean Health System, Madison, Wisconsin. Dr. Toth-Manikowski is from Johns Hopkins University, Baltimore, Maryland. Dr. Fishman is from Illinois Dermatology Institute, Northbrook. Dr. Bain is from the Dermatology Department, University of Illinois, Chicago.

The authors report no conflict of interest.

Correspondence: Caroline E. Schmitt, MD, Dean Clinic, 1821 S Stoughton Rd, Madison, WI 53716 ([email protected]).

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The authors report no conflict of interest.

Correspondence: Caroline E. Schmitt, MD, Dean Clinic, 1821 S Stoughton Rd, Madison, WI 53716 ([email protected]).

Author and Disclosure Information

Dr. Schmitt is from the Dermatology Division, Dean Health System, Madison, Wisconsin. Dr. Toth-Manikowski is from Johns Hopkins University, Baltimore, Maryland. Dr. Fishman is from Illinois Dermatology Institute, Northbrook. Dr. Bain is from the Dermatology Department, University of Illinois, Chicago.

The authors report no conflict of interest.

Correspondence: Caroline E. Schmitt, MD, Dean Clinic, 1821 S Stoughton Rd, Madison, WI 53716 ([email protected]).

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The Diagnosis: Granulomatous Periorificial Dermatitis

Review of the prior biopsy from the lower cutaneous lip revealed granulomatous perifolliculitis. The patient’s age combined with the morphology, distribution, and histopathologic features (Figure) of his eruption were characteristic of granulomatous periorificial dermatitis (GPD) of childhood. The patient was treated with oral erythromycin and topical metronidazole with immediate improvement, particularly with resolution of the erythema.

An attenuated epidermis overlying noncaseating dermal granulomas (A)(H&E, original magnification ×10). Granulomatous perifollicular inflammation with infiltration of the follicular epithelium by neutrophils and lymphocytes (B)(H&E, original magnification ×20).

Granulomatous periorificial dermatitis is a benign, self-limited eruption in healthy prepubertal children that is characterized by coalescent, asymptomatic, dome-shaped, yellow-brown to erythematous papules.1,2 The monomorphous lesions are firm, measure 1 to 3 mm in diameter, and are most commonly located around the mouth.2,3 Other areas of involvement include the nostrils and alar creases as well as the periocular skin.4 Less commonly, GPD has been described on the scalp, ears, neck, trunk, extremities, and genital region.5 Slight peripheral scaling or erythema and small pitted scarring are variable.4,5 There may be a history of failed topical corticosteroid treatment that either caused no change or a flare in the rash.1-5 Patients have no systemic findings.3,5

Biopsy of GPD shows characteristic noncaseating granulomas in the dermis, typified by perifollicular localization.5 The granulomatous infiltrate consists of epithelioid histiocytes and multinucleated giant cells surrounded by lymphocytes, with focal collections of neutrophils and occasionally overlying parakeratosis.2,3

The nomenclature of GPD has varied since the 1970s and has included Gianotti-type perioral dermatitis,6 GPD of childhood,7 rosacealike eruption in children,8 FACE (facial Afro-Caribbean childhood eruption),9 and sarcoidlike granulomatous dermatitis.10

The etiology of GPD is unknown, though it has been associated with use of topical, inhaled, or systemic steroids; a personal history of skin problems; a family history of atopy; vaccination; and local reactions to allergens such as cosmetic preparations, antiseptic solutions, tartar control toothpaste, and bubble gum.4,5,11-13 Granulomatous periorificial dermatitis may represent a pediatric variant of granulomatous rosacea or a granulomatous variant of perioral dermatitis, but importantly, it is not related to sarcoidosis.1,4,5 Granulomatous periorificial dermatitis typically affects children of dark-skinned, African Caribbean ancestry, though it has been described in both white and Asian populations.1,2,5 Genders are equally affected.

Although generally a benign condition that spontaneously remits within a few months to 3 years,5 GPD can be quite disruptive to a patient’s self-image, necessitating therapy to hasten resolution. Prior to initiation of treatment, any topical corticosteroids being applied to the affected region should be discontinued. For children older than 9 years, a suggested regimen is oral tetracycline 250 mg twice daily; for those younger than 9 years, erythromycin 30 to 40 mg/kg daily in 2 divided doses is advised.14 Metronidazole 0.75% cream and gel also have shown efficacy in GPD and represent a topical adjunct or alternative to oral therapy.1,14,15

The Diagnosis: Granulomatous Periorificial Dermatitis

Review of the prior biopsy from the lower cutaneous lip revealed granulomatous perifolliculitis. The patient’s age combined with the morphology, distribution, and histopathologic features (Figure) of his eruption were characteristic of granulomatous periorificial dermatitis (GPD) of childhood. The patient was treated with oral erythromycin and topical metronidazole with immediate improvement, particularly with resolution of the erythema.

An attenuated epidermis overlying noncaseating dermal granulomas (A)(H&E, original magnification ×10). Granulomatous perifollicular inflammation with infiltration of the follicular epithelium by neutrophils and lymphocytes (B)(H&E, original magnification ×20).

Granulomatous periorificial dermatitis is a benign, self-limited eruption in healthy prepubertal children that is characterized by coalescent, asymptomatic, dome-shaped, yellow-brown to erythematous papules.1,2 The monomorphous lesions are firm, measure 1 to 3 mm in diameter, and are most commonly located around the mouth.2,3 Other areas of involvement include the nostrils and alar creases as well as the periocular skin.4 Less commonly, GPD has been described on the scalp, ears, neck, trunk, extremities, and genital region.5 Slight peripheral scaling or erythema and small pitted scarring are variable.4,5 There may be a history of failed topical corticosteroid treatment that either caused no change or a flare in the rash.1-5 Patients have no systemic findings.3,5

Biopsy of GPD shows characteristic noncaseating granulomas in the dermis, typified by perifollicular localization.5 The granulomatous infiltrate consists of epithelioid histiocytes and multinucleated giant cells surrounded by lymphocytes, with focal collections of neutrophils and occasionally overlying parakeratosis.2,3

The nomenclature of GPD has varied since the 1970s and has included Gianotti-type perioral dermatitis,6 GPD of childhood,7 rosacealike eruption in children,8 FACE (facial Afro-Caribbean childhood eruption),9 and sarcoidlike granulomatous dermatitis.10

The etiology of GPD is unknown, though it has been associated with use of topical, inhaled, or systemic steroids; a personal history of skin problems; a family history of atopy; vaccination; and local reactions to allergens such as cosmetic preparations, antiseptic solutions, tartar control toothpaste, and bubble gum.4,5,11-13 Granulomatous periorificial dermatitis may represent a pediatric variant of granulomatous rosacea or a granulomatous variant of perioral dermatitis, but importantly, it is not related to sarcoidosis.1,4,5 Granulomatous periorificial dermatitis typically affects children of dark-skinned, African Caribbean ancestry, though it has been described in both white and Asian populations.1,2,5 Genders are equally affected.

Although generally a benign condition that spontaneously remits within a few months to 3 years,5 GPD can be quite disruptive to a patient’s self-image, necessitating therapy to hasten resolution. Prior to initiation of treatment, any topical corticosteroids being applied to the affected region should be discontinued. For children older than 9 years, a suggested regimen is oral tetracycline 250 mg twice daily; for those younger than 9 years, erythromycin 30 to 40 mg/kg daily in 2 divided doses is advised.14 Metronidazole 0.75% cream and gel also have shown efficacy in GPD and represent a topical adjunct or alternative to oral therapy.1,14,15

References
  1. Knautz MA, Lesher JL. Childhood granulomatous periorificial dermatitis. Pediatr Dermatol. 1996;13:131-134.
  2. Choi YL, Lee KJ, Cho HJ, et al. Case of childhood granulomatous periorificial dermatitis in a Korean boy treated by oral erythromycin. J Dermatol. 2006;33:806-808.
  3. Tarm K, Creel NB, Krivda SJ, et al. Granulomatous periorificial dermatitis. Cutis. 2004;73:399-402.
  4. Nguyen V, Eichenfield LF. Periorificial dermatitis in children and adolescents. J Am Acad Dermatol. 2006;55:781-785.
  5. Urbatsch AJ, Frieden I, Williams ML, et al. Extrafacial and generalized granulomatous periorificial dermatitis. Arch Dermatol. 2002;138:1354-1358.
  6. Gianotti F, Ermacora E, Bennelli MG, et al. Particuliere dermatite peri-orale infantile: observations sur cinq cas. Bull Soc Fr Dermatol Syph. 1970;77:341.
  7. Frieden IJ, Prose NS, Fletcher V, et al. Granulomatous perioral dermatitis in children. Arch Dermatol. 1989;125:369-373.
  8. Savin JA, Alexander S, Marks R. A rosacea-like eruption of children. Br J Dermatol. 1972;87:425-429.
  9. Marten RH, Presbury DG, Adamson JE, et al. An unusual popular and acneiform facial eruption in the Negro child. Br J Dermatol. 1974;91:435-438.
  10. Falk ES. Sarcoid-like granulomatous periocular dermatitis treated with tetracycline. Acta Derm Venereol. 1985;65:270-272.
  11. Hafeez ZH. Perioral dermatitis: an update. Int J Dermatol. 2003;42:514-517.
  12. Ferlito TA. Tartar-control toothpaste and perioral dermatitis. J Clin Oncol. 1992;27:43-44.
  13. Georgouras K, Kocsard E. Micropapular sarcoidal facial eruption in a child. Acta Derm Venereol. 1978;48:433-436.
  14. Laude TA, Salvemini JN. Perioral dermatitis in children. Semin Cutan Med Surg. 1999;18:206-209.
  15. Miller SR, Shalita AR. Topical metronidazole gel (0.75%) for the treatment of perioral dermatitis in children. J Am Acad Dermatol. 1994;31:847-848.
References
  1. Knautz MA, Lesher JL. Childhood granulomatous periorificial dermatitis. Pediatr Dermatol. 1996;13:131-134.
  2. Choi YL, Lee KJ, Cho HJ, et al. Case of childhood granulomatous periorificial dermatitis in a Korean boy treated by oral erythromycin. J Dermatol. 2006;33:806-808.
  3. Tarm K, Creel NB, Krivda SJ, et al. Granulomatous periorificial dermatitis. Cutis. 2004;73:399-402.
  4. Nguyen V, Eichenfield LF. Periorificial dermatitis in children and adolescents. J Am Acad Dermatol. 2006;55:781-785.
  5. Urbatsch AJ, Frieden I, Williams ML, et al. Extrafacial and generalized granulomatous periorificial dermatitis. Arch Dermatol. 2002;138:1354-1358.
  6. Gianotti F, Ermacora E, Bennelli MG, et al. Particuliere dermatite peri-orale infantile: observations sur cinq cas. Bull Soc Fr Dermatol Syph. 1970;77:341.
  7. Frieden IJ, Prose NS, Fletcher V, et al. Granulomatous perioral dermatitis in children. Arch Dermatol. 1989;125:369-373.
  8. Savin JA, Alexander S, Marks R. A rosacea-like eruption of children. Br J Dermatol. 1972;87:425-429.
  9. Marten RH, Presbury DG, Adamson JE, et al. An unusual popular and acneiform facial eruption in the Negro child. Br J Dermatol. 1974;91:435-438.
  10. Falk ES. Sarcoid-like granulomatous periocular dermatitis treated with tetracycline. Acta Derm Venereol. 1985;65:270-272.
  11. Hafeez ZH. Perioral dermatitis: an update. Int J Dermatol. 2003;42:514-517.
  12. Ferlito TA. Tartar-control toothpaste and perioral dermatitis. J Clin Oncol. 1992;27:43-44.
  13. Georgouras K, Kocsard E. Micropapular sarcoidal facial eruption in a child. Acta Derm Venereol. 1978;48:433-436.
  14. Laude TA, Salvemini JN. Perioral dermatitis in children. Semin Cutan Med Surg. 1999;18:206-209.
  15. Miller SR, Shalita AR. Topical metronidazole gel (0.75%) for the treatment of perioral dermatitis in children. J Am Acad Dermatol. 1994;31:847-848.
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Nonpruritic Papular Facial Eruption
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A 7-year-old boy was referred to the dermatology department with a red, bumpy, nonpruritic facial rash of 6 months’ duration. There was no identifiable trigger. The lesions were grouped around the nose and mouth with some extension onto the neck. He was treated with pimecrolimus cream 1% for presumed atopic dermatitis with good response, but the rash recurred soon thereafter. A biopsy performed at an outside institution shortly after rash onset showed dermal granulomas, leading to a diagnosis of cutaneous sarcoidosis (lupus pernio). Prior to presenting to our clinic, treatment with topical and oral corticosteroids failed. He had a normal chest radiograph, ophthalmologic examination, and angiotensin-converting enzyme level to exclude extracutaneous sarcoidosis. On physical examination the patient had innumerable, monomorphic, flesh-colored to erythematous papules confluent over the medial eyelids and canthi, perinasal skin, cutaneous lips, and preauricular skin extending onto the lateral aspect of the neck. There was superimposed scale around the mouth.

 

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Verrucous Cobblestonelike Papules and Nodules of the Right Lower Limb

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Verrucous Cobblestonelike Papules and Nodules of the Right Lower Limb

The Diagnosis: Elephantiasis Nostras Verrucosa

Elephantiasis nostras verrucosa (ENV) is a chronic deforming disorder characterized by hyperkeratosis and papillomatosis of the epidermis with underlying woody fibrosis of the dermis and the subcutaneous tissue in the setting of chronic nonfilarial lymphedema. Mossy papules, plaques, and cobblestonelike nodules are classic clinical features of ENV (Figure). The cobblestone lesion often is foul smelling and may be colonized with multiple bacteria and fungi.1

Verrucous cobblestonelike papules and nodules on the right lower limb.

The differential diagnosis includes filariasis, chromoblastomycosis, and venous stasis dermatitis. Filariasis is infection with the filarial worms Wuchereria bancrofti, Brugia malayi, or Brugia timori. These parasites are transmitted to humans through the bite of an infected mosquito and develop into adult worms in the lymphatic vessels, causing lymphedema. Elephantiasis, the classic sign of late-stage disease, also causes swelling of the legs and genital organs that can be disfiguring. Thus travel history to Southeast Asia and Africa regions is particularly important.

Chromoblastomycosis is a chronic fungal infection of the skin and subcutaneous tissue caused by traumatic inoculation of a specific group of dematiaceous fungi, usually Fonsecaea pedrosoi, Phialophora verrucosa, Cladosporium carrionii, or Fonsecaea compacta. Chromoblastomycosis-induced lymphedema may mimic elephantiasis. Thus it is important to perform fungal culture and fungal scraping, which will show typical thick-walled, cigar-colored, sclerotic cells (known as Medlar bodies).

The skin changes of venous stasis dermatitis include edema, varicosities, hyperpigmentation, atrophie blanche, diffuse red-brown discoloration representing deep dermal deposits of hemosiderin, and lipodermatosclerosis. Venous stasis dermatitis is caused by chronic venous insufficiency. It is one of the predispositions to ENV, as it can cause repeated infections and cellulitis leading to blockage of lymphatic drainage and secondary lymphedema. A study of 21 cases highlighted that chronic venous insufficiency may be an underappreciated risk factor in the pathogenesis of ENV.2

The development of verrucous cobblestonelike plaques in ENV occurs with chronic lymphedema. Chronic lymphedema can be caused by a variety of etiologies including infection, chronic venous stasis, congestive heart failure, obesity, trauma, tumor obstruction, and radiation. Our patient was obese with chronic venous stasis, congestive heart failure, and recurrent cellulitis that can lead to secondary lymphatic obstruction and edema, all contributing to the picture of ENV. Because of the unilateral presentation in our patient, we believe that recurrent infections and inflammation are the important risk factors that lead to fibrosis of the dermis and lymph channels, ultimately resulting in ENV.

The diagnosis of ENV is based on the patient’s history and characteristic skin changes. However, a biopsy should be performed if the diagnosis is not clinically apparent, if the lesion looks suspicious for malignancy, or if areas of chronic ulceration exist. Histologic findings include hyperkeratosis as well as a collarette of acanthotic epidermis extending around dilated lymph vessels in the upper dermis. Sometimes a few dilated lymph vessels present in the deeper or subcutaneous tissue. Bacterial and fungal culture should be done to exclude concomitant infection. Ultrasonography can be used to evaluate the lymphatic and venous systems.

Treatment of ENV aims at improving lymphedema and preventing infection. Physical therapy to improve lymphedema includes manual lymphatic drainage, massage, compression stockings, elastic bandages, and leg elevation. In cases associated with obesity, weight loss is recommended. In cases of recurrent cellulitis or lymphangitis, long-term antibiotic therapy with agents such as penicillins or cephalosporins is sometimes used.3 Success has been reported with the use of oral and topical retinoids, such as acitretin and tazarotene, which are thought to decrease epidermal proliferation, fibrogenesis, and inflammation.4,5 Our patient was started on tretinoin cream. Surgery is reserved for cases of lymphedema resistant to medical therapies, including debridement,6 lymphatic and lymphovenous anastomosis,7 lymphatic transplantation, and amputation for severe cases.

Malignancies can develop in areas of chronic lymphedema such as lymphangiosarcoma, squamous cell carcinoma, Kaposi sarcoma, B-cell lymphoma, and malignant fibrous histiocytoma. The morbidity and mortality usually are from the underlying medical problems rather than ENV itself. Our patient died 1 month after the diagnosis of ENV from his poorly controlled heart failure.

References
  1. Schissel DJ, Hivnor C, Elston DM. Elephantiasis nostras verrucosa. Cutis. 1998;62:77-80.
  2. Dean SM, Zirwas MJ, Horst AV. Elephantiasis nostras verrucosa: an institutional analysis of 21 cases. J Am Acad Dermatol. 2011;64:1104-1110.
  3. Olszewski WL, Jamal S, Manokaran G, et al. The effectiveness of long-acting penicillin (penidur) in preventing recurrences of dermatolymphangioadenitis (DLA) and controlling skin, deep tissues, and lymph bacterial flora in patients with “filarial” lymphedema. Lymphology. 2005;38:66-80.
  4. Feind-Koopmans A, van de Kerkhof PC. Successful treatment of papillomatosis cutis lymphostatica with acitretin. Acta Derm Venereol. 1995;75:411.
  5. Boyd J, Sloan S, Meffert J. Elephantiasis nostrum verrucosa of the abdomen: clinical results with tazarotene. J Drugs Dermatol. 2004;3:446-448.
  6. Iwao F, Sato-Matsumura KC, Sawamura D, et al. Elephantiasis nostras verrucosa successfully treated by surgical debridement. Dermatol Surg. 2004;30:939-41.
  7. Motegi S, Tamura A, Okada E, et al. Successful treatment with lymphaticovenular anastomosis for secondary skin lesions of chronic lymphedema. Dermatology. 2007;215:147-151.
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The Diagnosis: Elephantiasis Nostras Verrucosa

Elephantiasis nostras verrucosa (ENV) is a chronic deforming disorder characterized by hyperkeratosis and papillomatosis of the epidermis with underlying woody fibrosis of the dermis and the subcutaneous tissue in the setting of chronic nonfilarial lymphedema. Mossy papules, plaques, and cobblestonelike nodules are classic clinical features of ENV (Figure). The cobblestone lesion often is foul smelling and may be colonized with multiple bacteria and fungi.1

Verrucous cobblestonelike papules and nodules on the right lower limb.

The differential diagnosis includes filariasis, chromoblastomycosis, and venous stasis dermatitis. Filariasis is infection with the filarial worms Wuchereria bancrofti, Brugia malayi, or Brugia timori. These parasites are transmitted to humans through the bite of an infected mosquito and develop into adult worms in the lymphatic vessels, causing lymphedema. Elephantiasis, the classic sign of late-stage disease, also causes swelling of the legs and genital organs that can be disfiguring. Thus travel history to Southeast Asia and Africa regions is particularly important.

Chromoblastomycosis is a chronic fungal infection of the skin and subcutaneous tissue caused by traumatic inoculation of a specific group of dematiaceous fungi, usually Fonsecaea pedrosoi, Phialophora verrucosa, Cladosporium carrionii, or Fonsecaea compacta. Chromoblastomycosis-induced lymphedema may mimic elephantiasis. Thus it is important to perform fungal culture and fungal scraping, which will show typical thick-walled, cigar-colored, sclerotic cells (known as Medlar bodies).

The skin changes of venous stasis dermatitis include edema, varicosities, hyperpigmentation, atrophie blanche, diffuse red-brown discoloration representing deep dermal deposits of hemosiderin, and lipodermatosclerosis. Venous stasis dermatitis is caused by chronic venous insufficiency. It is one of the predispositions to ENV, as it can cause repeated infections and cellulitis leading to blockage of lymphatic drainage and secondary lymphedema. A study of 21 cases highlighted that chronic venous insufficiency may be an underappreciated risk factor in the pathogenesis of ENV.2

The development of verrucous cobblestonelike plaques in ENV occurs with chronic lymphedema. Chronic lymphedema can be caused by a variety of etiologies including infection, chronic venous stasis, congestive heart failure, obesity, trauma, tumor obstruction, and radiation. Our patient was obese with chronic venous stasis, congestive heart failure, and recurrent cellulitis that can lead to secondary lymphatic obstruction and edema, all contributing to the picture of ENV. Because of the unilateral presentation in our patient, we believe that recurrent infections and inflammation are the important risk factors that lead to fibrosis of the dermis and lymph channels, ultimately resulting in ENV.

The diagnosis of ENV is based on the patient’s history and characteristic skin changes. However, a biopsy should be performed if the diagnosis is not clinically apparent, if the lesion looks suspicious for malignancy, or if areas of chronic ulceration exist. Histologic findings include hyperkeratosis as well as a collarette of acanthotic epidermis extending around dilated lymph vessels in the upper dermis. Sometimes a few dilated lymph vessels present in the deeper or subcutaneous tissue. Bacterial and fungal culture should be done to exclude concomitant infection. Ultrasonography can be used to evaluate the lymphatic and venous systems.

Treatment of ENV aims at improving lymphedema and preventing infection. Physical therapy to improve lymphedema includes manual lymphatic drainage, massage, compression stockings, elastic bandages, and leg elevation. In cases associated with obesity, weight loss is recommended. In cases of recurrent cellulitis or lymphangitis, long-term antibiotic therapy with agents such as penicillins or cephalosporins is sometimes used.3 Success has been reported with the use of oral and topical retinoids, such as acitretin and tazarotene, which are thought to decrease epidermal proliferation, fibrogenesis, and inflammation.4,5 Our patient was started on tretinoin cream. Surgery is reserved for cases of lymphedema resistant to medical therapies, including debridement,6 lymphatic and lymphovenous anastomosis,7 lymphatic transplantation, and amputation for severe cases.

Malignancies can develop in areas of chronic lymphedema such as lymphangiosarcoma, squamous cell carcinoma, Kaposi sarcoma, B-cell lymphoma, and malignant fibrous histiocytoma. The morbidity and mortality usually are from the underlying medical problems rather than ENV itself. Our patient died 1 month after the diagnosis of ENV from his poorly controlled heart failure.

The Diagnosis: Elephantiasis Nostras Verrucosa

Elephantiasis nostras verrucosa (ENV) is a chronic deforming disorder characterized by hyperkeratosis and papillomatosis of the epidermis with underlying woody fibrosis of the dermis and the subcutaneous tissue in the setting of chronic nonfilarial lymphedema. Mossy papules, plaques, and cobblestonelike nodules are classic clinical features of ENV (Figure). The cobblestone lesion often is foul smelling and may be colonized with multiple bacteria and fungi.1

Verrucous cobblestonelike papules and nodules on the right lower limb.

The differential diagnosis includes filariasis, chromoblastomycosis, and venous stasis dermatitis. Filariasis is infection with the filarial worms Wuchereria bancrofti, Brugia malayi, or Brugia timori. These parasites are transmitted to humans through the bite of an infected mosquito and develop into adult worms in the lymphatic vessels, causing lymphedema. Elephantiasis, the classic sign of late-stage disease, also causes swelling of the legs and genital organs that can be disfiguring. Thus travel history to Southeast Asia and Africa regions is particularly important.

Chromoblastomycosis is a chronic fungal infection of the skin and subcutaneous tissue caused by traumatic inoculation of a specific group of dematiaceous fungi, usually Fonsecaea pedrosoi, Phialophora verrucosa, Cladosporium carrionii, or Fonsecaea compacta. Chromoblastomycosis-induced lymphedema may mimic elephantiasis. Thus it is important to perform fungal culture and fungal scraping, which will show typical thick-walled, cigar-colored, sclerotic cells (known as Medlar bodies).

The skin changes of venous stasis dermatitis include edema, varicosities, hyperpigmentation, atrophie blanche, diffuse red-brown discoloration representing deep dermal deposits of hemosiderin, and lipodermatosclerosis. Venous stasis dermatitis is caused by chronic venous insufficiency. It is one of the predispositions to ENV, as it can cause repeated infections and cellulitis leading to blockage of lymphatic drainage and secondary lymphedema. A study of 21 cases highlighted that chronic venous insufficiency may be an underappreciated risk factor in the pathogenesis of ENV.2

The development of verrucous cobblestonelike plaques in ENV occurs with chronic lymphedema. Chronic lymphedema can be caused by a variety of etiologies including infection, chronic venous stasis, congestive heart failure, obesity, trauma, tumor obstruction, and radiation. Our patient was obese with chronic venous stasis, congestive heart failure, and recurrent cellulitis that can lead to secondary lymphatic obstruction and edema, all contributing to the picture of ENV. Because of the unilateral presentation in our patient, we believe that recurrent infections and inflammation are the important risk factors that lead to fibrosis of the dermis and lymph channels, ultimately resulting in ENV.

The diagnosis of ENV is based on the patient’s history and characteristic skin changes. However, a biopsy should be performed if the diagnosis is not clinically apparent, if the lesion looks suspicious for malignancy, or if areas of chronic ulceration exist. Histologic findings include hyperkeratosis as well as a collarette of acanthotic epidermis extending around dilated lymph vessels in the upper dermis. Sometimes a few dilated lymph vessels present in the deeper or subcutaneous tissue. Bacterial and fungal culture should be done to exclude concomitant infection. Ultrasonography can be used to evaluate the lymphatic and venous systems.

Treatment of ENV aims at improving lymphedema and preventing infection. Physical therapy to improve lymphedema includes manual lymphatic drainage, massage, compression stockings, elastic bandages, and leg elevation. In cases associated with obesity, weight loss is recommended. In cases of recurrent cellulitis or lymphangitis, long-term antibiotic therapy with agents such as penicillins or cephalosporins is sometimes used.3 Success has been reported with the use of oral and topical retinoids, such as acitretin and tazarotene, which are thought to decrease epidermal proliferation, fibrogenesis, and inflammation.4,5 Our patient was started on tretinoin cream. Surgery is reserved for cases of lymphedema resistant to medical therapies, including debridement,6 lymphatic and lymphovenous anastomosis,7 lymphatic transplantation, and amputation for severe cases.

Malignancies can develop in areas of chronic lymphedema such as lymphangiosarcoma, squamous cell carcinoma, Kaposi sarcoma, B-cell lymphoma, and malignant fibrous histiocytoma. The morbidity and mortality usually are from the underlying medical problems rather than ENV itself. Our patient died 1 month after the diagnosis of ENV from his poorly controlled heart failure.

References
  1. Schissel DJ, Hivnor C, Elston DM. Elephantiasis nostras verrucosa. Cutis. 1998;62:77-80.
  2. Dean SM, Zirwas MJ, Horst AV. Elephantiasis nostras verrucosa: an institutional analysis of 21 cases. J Am Acad Dermatol. 2011;64:1104-1110.
  3. Olszewski WL, Jamal S, Manokaran G, et al. The effectiveness of long-acting penicillin (penidur) in preventing recurrences of dermatolymphangioadenitis (DLA) and controlling skin, deep tissues, and lymph bacterial flora in patients with “filarial” lymphedema. Lymphology. 2005;38:66-80.
  4. Feind-Koopmans A, van de Kerkhof PC. Successful treatment of papillomatosis cutis lymphostatica with acitretin. Acta Derm Venereol. 1995;75:411.
  5. Boyd J, Sloan S, Meffert J. Elephantiasis nostrum verrucosa of the abdomen: clinical results with tazarotene. J Drugs Dermatol. 2004;3:446-448.
  6. Iwao F, Sato-Matsumura KC, Sawamura D, et al. Elephantiasis nostras verrucosa successfully treated by surgical debridement. Dermatol Surg. 2004;30:939-41.
  7. Motegi S, Tamura A, Okada E, et al. Successful treatment with lymphaticovenular anastomosis for secondary skin lesions of chronic lymphedema. Dermatology. 2007;215:147-151.
References
  1. Schissel DJ, Hivnor C, Elston DM. Elephantiasis nostras verrucosa. Cutis. 1998;62:77-80.
  2. Dean SM, Zirwas MJ, Horst AV. Elephantiasis nostras verrucosa: an institutional analysis of 21 cases. J Am Acad Dermatol. 2011;64:1104-1110.
  3. Olszewski WL, Jamal S, Manokaran G, et al. The effectiveness of long-acting penicillin (penidur) in preventing recurrences of dermatolymphangioadenitis (DLA) and controlling skin, deep tissues, and lymph bacterial flora in patients with “filarial” lymphedema. Lymphology. 2005;38:66-80.
  4. Feind-Koopmans A, van de Kerkhof PC. Successful treatment of papillomatosis cutis lymphostatica with acitretin. Acta Derm Venereol. 1995;75:411.
  5. Boyd J, Sloan S, Meffert J. Elephantiasis nostrum verrucosa of the abdomen: clinical results with tazarotene. J Drugs Dermatol. 2004;3:446-448.
  6. Iwao F, Sato-Matsumura KC, Sawamura D, et al. Elephantiasis nostras verrucosa successfully treated by surgical debridement. Dermatol Surg. 2004;30:939-41.
  7. Motegi S, Tamura A, Okada E, et al. Successful treatment with lymphaticovenular anastomosis for secondary skin lesions of chronic lymphedema. Dermatology. 2007;215:147-151.
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Verrucous Cobblestonelike Papules and Nodules of the Right Lower Limb
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An obese 58-year-old man was admitted to the cardiology department for poorly controlled congestive heart failure. He was referred to the dermatology department with progressive painless swelling of the right lower limb of a year’s duration. He had chronic right lower limb insufficiency of 3 years’ duration with a history of a recurrent right medial malleolus ulcer and cellulitis. There was no notable travel or family history. Physical examination revealed woody edema of the right lower limb with verrucous cobblestonelike papules and nodules, foul-smelling odor, and thick crusts that were easily removed.

 

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Partially Blanchable Violaceous Lesions in an AIDS Patient

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The Diagnosis: Eruptive Disseminated Kaposi Sarcoma

There are 5 types of Kaposi sarcoma (KS): classic KS, African cutaneous KS, African lymphadenopathic KS, AIDS-related KS, and immunosuppression-associated KS. Immunosuppression-associated KS can occur in the setting of lymphoma or in conjunction with immunosuppressive therapy related to organ transplants and long-term corticosteroid treatment.1,2 Kaposi sarcoma associated with highly active antiretroviral therapy–induced immune reconstitution inflammatory syndrome also may occur.3

The possible causes of the manifestation of KS in our patient were 2-fold: (1) AIDS associated given the patient’s CD4 lymphocyte count of 7 cells/mm3, and (2) iatrogenic secondary to drug-induced immunosuppression that was temporally induced by 2 sustained periods of intravenous dexamethasone for cerebral edema in the setting of primary central nervous system lymphoma. It is unlikely that our patient experienced immune reconstitution inflammatory syndrome–induced KS, as the dysphagia interfered with the ability to take antiretroviral therapy during hospitalization. In patients who have experienced KS in the setting of steroid use or organ transplantation, KS lesions spontaneously improved or completely regressed several months after immunosuppression reduction or removal.1,2,4

Clinically and morphologically, our patient also clearly demonstrated the occasionally seen striking manifestation of perilesional, ecchymotic-appearing or bruiselike halos surrounding the KS lesions (Figure).

The initial differential diagnosis included hemorrhagic diathesis but later included KS in the setting of AIDS and immunosuppressive therapy with dexamethasone, bacillary angiomatosis, and cutaneous lymphoma. A biopsy of one of the cutaneous lesions confirmed the diagnosis of KS.

Three standard treatments of primary central nervous system lymphoma currently exist: radiation therapy, intrathecal and/or intraventricular chemotherapy, and steroid therapy.5 Given the patient’s risk for opportunistic infections and immunodeficient state, the medical team was constrained in its treatment options, as all of the therapies would further weaken the patient’s immune system.

Perilesional, ecchymotic-appearing or bruiselike halos surrounded some of the Kaposi sarcoma lesions on the trunk.

Treatment of KS can be local and/or systemic based on disease stage, progression, distribution, clinical type, and immune status.6,7 Our patient had generalized cutaneous KS covering more than 50% of the body, thus making local treatments such as radiation therapy, cryotherapy, intralesional chemotherapy with vincristine or vinblastine, excision, laser therapy, or alitretinoin gel impractical. Single- or multiple-agent systemic treatment options for disseminated cutaneous disease with or without internal organ involvement may include liposomal anthracyclines, paclitaxel, gemcitabine, vinblastine, vincristine, bleomycin, etoposide, and interferon-alfa.6,7 Potent combination antiretroviral therapy is the mainstay for treatment of AIDS-associated KS.8

References
  1. Nassar D, Schartz NEC, Bouche C, et al. Kaposi’s sarcoma after long-acting steroids: time until remission and drug washout. Dermatology. 2010;220:159-163.
  2. Trattner A, Hodak E, David M, et al. The appearance of Kaposi sarcoma during corticosteroid therapy. Cancer. 1993;72:1779-1783.
  3. Bower M, Nelson M, Young AM, et al. Immune reconstitution inflammatory syndrome associated with Kaposi’s Sarcoma. J Clin Oncol. 2005;23:5224-5228.
  4. Duman S, Töz H, Aşçi G, et al. Successful treatment of post-transplant Kaposi’s sarcoma by reduction of immunosuppression. Nephrol Dial Transplant. 2002;17:892-896.
  5. National Cancer Institute. Primary CNS lymphoma treatment. http://www.cancer.gov/cancertopics/pdq/treatment/primary-CNS-lymphoma/Patient/page4. Accessed June 10, 2014.
  6. Schwartz RA, Micali G, Nasca MR, et al. Kaposi sarcoma: a continuing conundrum. J Am Acad Dermatol. 2008;59:179-206.
  7. Lee F-C, Mitsuyasu RT. Chemotherapy of AIDS-related Kaposi’s sarcoma. Hematol Oncol Clin North Am. 1996;10:1051-1068.
  8. Dupont C, Vasseur E, Beauchet A, et al. Long-term efficacy on Kaposi’s sarcoma of highly active antiretroviral therapy in a cohort of HIV-positive patients. AIDS. 2000;14:987-993.
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Dr. Jones is from the General Internal Medicine Group, Arlington, Virginia. Mr. Willett is from the Uniformed Services University of the Health Sciences, Bethesda, Maryland. Dr. Decker is from the Division of Infectious Disease at Walter Reed National Military Medical Center, Bethesda. Dr. Turiansky is from the National Capital Consortium, Uniformed Services University of the Health Sciences, Bethesda.

The authors report no conflict of interest.

The views expressed in this article are those of the authors and do not reflect the official policy of the US Department of the Army, US Department of the Navy, US Department of Defense, or the US Government.

Correspondence: Kermit L. Jones, MD, JD, GIMG, 3022 Williams Dr, Ste 300, Fairfax, VA 22031 ([email protected]).

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The authors report no conflict of interest.

The views expressed in this article are those of the authors and do not reflect the official policy of the US Department of the Army, US Department of the Navy, US Department of Defense, or the US Government.

Correspondence: Kermit L. Jones, MD, JD, GIMG, 3022 Williams Dr, Ste 300, Fairfax, VA 22031 ([email protected]).

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Dr. Jones is from the General Internal Medicine Group, Arlington, Virginia. Mr. Willett is from the Uniformed Services University of the Health Sciences, Bethesda, Maryland. Dr. Decker is from the Division of Infectious Disease at Walter Reed National Military Medical Center, Bethesda. Dr. Turiansky is from the National Capital Consortium, Uniformed Services University of the Health Sciences, Bethesda.

The authors report no conflict of interest.

The views expressed in this article are those of the authors and do not reflect the official policy of the US Department of the Army, US Department of the Navy, US Department of Defense, or the US Government.

Correspondence: Kermit L. Jones, MD, JD, GIMG, 3022 Williams Dr, Ste 300, Fairfax, VA 22031 ([email protected]).

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The Diagnosis: Eruptive Disseminated Kaposi Sarcoma

There are 5 types of Kaposi sarcoma (KS): classic KS, African cutaneous KS, African lymphadenopathic KS, AIDS-related KS, and immunosuppression-associated KS. Immunosuppression-associated KS can occur in the setting of lymphoma or in conjunction with immunosuppressive therapy related to organ transplants and long-term corticosteroid treatment.1,2 Kaposi sarcoma associated with highly active antiretroviral therapy–induced immune reconstitution inflammatory syndrome also may occur.3

The possible causes of the manifestation of KS in our patient were 2-fold: (1) AIDS associated given the patient’s CD4 lymphocyte count of 7 cells/mm3, and (2) iatrogenic secondary to drug-induced immunosuppression that was temporally induced by 2 sustained periods of intravenous dexamethasone for cerebral edema in the setting of primary central nervous system lymphoma. It is unlikely that our patient experienced immune reconstitution inflammatory syndrome–induced KS, as the dysphagia interfered with the ability to take antiretroviral therapy during hospitalization. In patients who have experienced KS in the setting of steroid use or organ transplantation, KS lesions spontaneously improved or completely regressed several months after immunosuppression reduction or removal.1,2,4

Clinically and morphologically, our patient also clearly demonstrated the occasionally seen striking manifestation of perilesional, ecchymotic-appearing or bruiselike halos surrounding the KS lesions (Figure).

The initial differential diagnosis included hemorrhagic diathesis but later included KS in the setting of AIDS and immunosuppressive therapy with dexamethasone, bacillary angiomatosis, and cutaneous lymphoma. A biopsy of one of the cutaneous lesions confirmed the diagnosis of KS.

Three standard treatments of primary central nervous system lymphoma currently exist: radiation therapy, intrathecal and/or intraventricular chemotherapy, and steroid therapy.5 Given the patient’s risk for opportunistic infections and immunodeficient state, the medical team was constrained in its treatment options, as all of the therapies would further weaken the patient’s immune system.

Perilesional, ecchymotic-appearing or bruiselike halos surrounded some of the Kaposi sarcoma lesions on the trunk.

Treatment of KS can be local and/or systemic based on disease stage, progression, distribution, clinical type, and immune status.6,7 Our patient had generalized cutaneous KS covering more than 50% of the body, thus making local treatments such as radiation therapy, cryotherapy, intralesional chemotherapy with vincristine or vinblastine, excision, laser therapy, or alitretinoin gel impractical. Single- or multiple-agent systemic treatment options for disseminated cutaneous disease with or without internal organ involvement may include liposomal anthracyclines, paclitaxel, gemcitabine, vinblastine, vincristine, bleomycin, etoposide, and interferon-alfa.6,7 Potent combination antiretroviral therapy is the mainstay for treatment of AIDS-associated KS.8

The Diagnosis: Eruptive Disseminated Kaposi Sarcoma

There are 5 types of Kaposi sarcoma (KS): classic KS, African cutaneous KS, African lymphadenopathic KS, AIDS-related KS, and immunosuppression-associated KS. Immunosuppression-associated KS can occur in the setting of lymphoma or in conjunction with immunosuppressive therapy related to organ transplants and long-term corticosteroid treatment.1,2 Kaposi sarcoma associated with highly active antiretroviral therapy–induced immune reconstitution inflammatory syndrome also may occur.3

The possible causes of the manifestation of KS in our patient were 2-fold: (1) AIDS associated given the patient’s CD4 lymphocyte count of 7 cells/mm3, and (2) iatrogenic secondary to drug-induced immunosuppression that was temporally induced by 2 sustained periods of intravenous dexamethasone for cerebral edema in the setting of primary central nervous system lymphoma. It is unlikely that our patient experienced immune reconstitution inflammatory syndrome–induced KS, as the dysphagia interfered with the ability to take antiretroviral therapy during hospitalization. In patients who have experienced KS in the setting of steroid use or organ transplantation, KS lesions spontaneously improved or completely regressed several months after immunosuppression reduction or removal.1,2,4

Clinically and morphologically, our patient also clearly demonstrated the occasionally seen striking manifestation of perilesional, ecchymotic-appearing or bruiselike halos surrounding the KS lesions (Figure).

The initial differential diagnosis included hemorrhagic diathesis but later included KS in the setting of AIDS and immunosuppressive therapy with dexamethasone, bacillary angiomatosis, and cutaneous lymphoma. A biopsy of one of the cutaneous lesions confirmed the diagnosis of KS.

Three standard treatments of primary central nervous system lymphoma currently exist: radiation therapy, intrathecal and/or intraventricular chemotherapy, and steroid therapy.5 Given the patient’s risk for opportunistic infections and immunodeficient state, the medical team was constrained in its treatment options, as all of the therapies would further weaken the patient’s immune system.

Perilesional, ecchymotic-appearing or bruiselike halos surrounded some of the Kaposi sarcoma lesions on the trunk.

Treatment of KS can be local and/or systemic based on disease stage, progression, distribution, clinical type, and immune status.6,7 Our patient had generalized cutaneous KS covering more than 50% of the body, thus making local treatments such as radiation therapy, cryotherapy, intralesional chemotherapy with vincristine or vinblastine, excision, laser therapy, or alitretinoin gel impractical. Single- or multiple-agent systemic treatment options for disseminated cutaneous disease with or without internal organ involvement may include liposomal anthracyclines, paclitaxel, gemcitabine, vinblastine, vincristine, bleomycin, etoposide, and interferon-alfa.6,7 Potent combination antiretroviral therapy is the mainstay for treatment of AIDS-associated KS.8

References
  1. Nassar D, Schartz NEC, Bouche C, et al. Kaposi’s sarcoma after long-acting steroids: time until remission and drug washout. Dermatology. 2010;220:159-163.
  2. Trattner A, Hodak E, David M, et al. The appearance of Kaposi sarcoma during corticosteroid therapy. Cancer. 1993;72:1779-1783.
  3. Bower M, Nelson M, Young AM, et al. Immune reconstitution inflammatory syndrome associated with Kaposi’s Sarcoma. J Clin Oncol. 2005;23:5224-5228.
  4. Duman S, Töz H, Aşçi G, et al. Successful treatment of post-transplant Kaposi’s sarcoma by reduction of immunosuppression. Nephrol Dial Transplant. 2002;17:892-896.
  5. National Cancer Institute. Primary CNS lymphoma treatment. http://www.cancer.gov/cancertopics/pdq/treatment/primary-CNS-lymphoma/Patient/page4. Accessed June 10, 2014.
  6. Schwartz RA, Micali G, Nasca MR, et al. Kaposi sarcoma: a continuing conundrum. J Am Acad Dermatol. 2008;59:179-206.
  7. Lee F-C, Mitsuyasu RT. Chemotherapy of AIDS-related Kaposi’s sarcoma. Hematol Oncol Clin North Am. 1996;10:1051-1068.
  8. Dupont C, Vasseur E, Beauchet A, et al. Long-term efficacy on Kaposi’s sarcoma of highly active antiretroviral therapy in a cohort of HIV-positive patients. AIDS. 2000;14:987-993.
References
  1. Nassar D, Schartz NEC, Bouche C, et al. Kaposi’s sarcoma after long-acting steroids: time until remission and drug washout. Dermatology. 2010;220:159-163.
  2. Trattner A, Hodak E, David M, et al. The appearance of Kaposi sarcoma during corticosteroid therapy. Cancer. 1993;72:1779-1783.
  3. Bower M, Nelson M, Young AM, et al. Immune reconstitution inflammatory syndrome associated with Kaposi’s Sarcoma. J Clin Oncol. 2005;23:5224-5228.
  4. Duman S, Töz H, Aşçi G, et al. Successful treatment of post-transplant Kaposi’s sarcoma by reduction of immunosuppression. Nephrol Dial Transplant. 2002;17:892-896.
  5. National Cancer Institute. Primary CNS lymphoma treatment. http://www.cancer.gov/cancertopics/pdq/treatment/primary-CNS-lymphoma/Patient/page4. Accessed June 10, 2014.
  6. Schwartz RA, Micali G, Nasca MR, et al. Kaposi sarcoma: a continuing conundrum. J Am Acad Dermatol. 2008;59:179-206.
  7. Lee F-C, Mitsuyasu RT. Chemotherapy of AIDS-related Kaposi’s sarcoma. Hematol Oncol Clin North Am. 1996;10:1051-1068.
  8. Dupont C, Vasseur E, Beauchet A, et al. Long-term efficacy on Kaposi’s sarcoma of highly active antiretroviral therapy in a cohort of HIV-positive patients. AIDS. 2000;14:987-993.
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A 37-year-old AIDS patient (CD4 lymphocyte count, 7 cells/mm3 [reference range, 500–1000 cells/mm3]; viral load, >200,000 copies/mL) with a medical history of primary central nervous system lymphoma and recent Salmonella bacteremia was admitted with a 1-week history of dysphagia, generalized weakness, and a 15-lb weight loss over a 2-month period. Medications included prophylaxis with weekly azithromycin and daily atovoquone. The patient had a history of noncompliance with antiretroviral therapy, which included atazanavir sulfate, lamivudine, and zidovudine. One month prior to presentation the patient received a course of intravenous dexamethasone for cerebral edema secondary to mass effect from primary central nervous system lymphoma. On examination the patient was afebrile, cachectic, and in no acute distress. Initially, faint petechial lesions were noted on the torso and upper abdomen. Over the course of 10 days, after reintroduction of intravenous dexamethasone, the patient rapidly and diffusely developed partially blanchable, violaceous macules, patches, papules, and plaques that were most prominent on the trunk and lower extremities. Some of the lesions were surrounded by nonblanchable, yellowish brown, ecchymotic-appearing halos. Lesions spared the oral mucosa, face, and genitalia. There was no evidence of mucocutaneous involvement.

 

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Thrown From Motorcycle

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Several findings are evident from this radiograph. First, the quality is slightly diminished due to the patient’s size and artifact from the backboard. The patient’s mediastinum is somewhat widened, which is concerning for possible occult chest/vascular injury. There is some haziness within the left apical region suggestive of a hemothorax; no definite pneumothorax is seen. The left clavicle is fractured and displaced, and the left scapula is fractured as well.

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ANSWER
Several findings are evident from this radiograph. First, the quality is slightly diminished due to the patient’s size and artifact from the backboard. The patient’s mediastinum is somewhat widened, which is concerning for possible occult chest/vascular injury. There is some haziness within the left apical region suggestive of a hemothorax; no definite pneumothorax is seen. The left clavicle is fractured and displaced, and the left scapula is fractured as well.

ANSWER
Several findings are evident from this radiograph. First, the quality is slightly diminished due to the patient’s size and artifact from the backboard. The patient’s mediastinum is somewhat widened, which is concerning for possible occult chest/vascular injury. There is some haziness within the left apical region suggestive of a hemothorax; no definite pneumothorax is seen. The left clavicle is fractured and displaced, and the left scapula is fractured as well.

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Thrown From Motorcycle
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A 57-year-old man is brought to your facility as a trauma code. He was riding a motorcycle on the highway, traveling approximately 45 to 50 mph, when the car in front of him abruptly stopped. He hit the car and was thrown from his bike. He believes he briefly lost consciousness but recalls emergency personnel tending to him. On arrival, he is awake and alert, complaining of pain in his neck, left arm, and left lower leg. Medical history is significant for borderline hypertension and a previous accident that resulted in an emergency laparotomy. Primary survey reveals stable vital signs: blood pressure of 157/100 mm Hg; heart rate, 110 beats/min; respiratory rate, 20 breaths/min; and O2 saturation, 98% with supplemental oxygen. Pupils are equal and reactive; there are slightly decreased breath sounds on the left side. Abdominal exam appears benign. There is decreased mobility and pain in the patient’s left upper and left lower extremities, although no obvious deformity is noted. Preliminary chest radiograph is obtained before the patient is sent for CT. What is your impression?
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How Are Lesions and Seizures Related?

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How Are Lesions and Seizures Related?

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The correct answer is tuberous sclerosis (choice “d”), a genetic disorder affecting cellular differentiation and proliferation. As a result, hamartomas commonly form in organs such as the brain.

Von Recklinghausen disease (choice “a”; also known as neurofibromatosis type 1) presents with hyperpigmented macules and patches called café au lait macules. These and other findings differentiate it considerably from tuberous sclerosis.

“No unifying explanation” (choice “b”) is incorrect, because, as stated above, there is a unifying explanation for these findings!

Vitiligo (choice “c”) involves hypopigmented macules and patches. However, it does not present with some of the other findings seen in this case.

DISCUSSION
Tuberous sclerosis was first described in 1862 by von Recklinghausen, who noted the collection of findings we now term tuberous sclerosis complex (TSC) due to the wide variation in presentation.

In the United States, TSC occurs in an estimated one in 6,000 to one in 30,000 newborns. Usually, it manifests when the child is between ages 2 and 6, but genetic penetrance is highly variable—a major reason for the shift to the use of the term complex with this condition. (This case, with its late presentation, illustrates this variability.)

In about 60% of cases, TSC is transmitted in autosomal dominant mode, although at least 20% of cases may be due to spontaneous mutations. It has not shown any racial or gender predilections. Up to 90% of TSC patients will present with seizures, and 60% to 70% of those affected will demonstrate some developmental disability.

Skin is affected in at least 70% of TSC cases. This patient typifies the common dermatologic findings: dart-shaped hypopigmented macules (known as mountain ash leaf spots) and fleshy facial papules in the nasolabial region (originally called adenoma sebaceum and now called angiofibromas). Periungal fibromas are also common. Other major diagnostic criteria for TSC include cortical tubers seen on imaging and retinal hamartomas. Minor diagnostic criteria include pits in dental enamel and gingival fibromas.

Definitive diagnosis depends on identification of either two major manifestations or one major and two minor findings. There are no blood tests to confirm the diagnosis. In terms of treatment, the various elements that comprise TSC can be dealt with (eg, control of seizures and destruction or modification of skin lesions).

This patient received a diagnosis of TSC. She was returned to her primary care provider, who referred her for additional imaging of her lungs and heart and for ophthalmologic evaluation of her retinas. Genetic counseling was also arranged. With her seizures under control, she was able to continue matriculation through high school.

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ANSWER
The correct answer is tuberous sclerosis (choice “d”), a genetic disorder affecting cellular differentiation and proliferation. As a result, hamartomas commonly form in organs such as the brain.

Von Recklinghausen disease (choice “a”; also known as neurofibromatosis type 1) presents with hyperpigmented macules and patches called café au lait macules. These and other findings differentiate it considerably from tuberous sclerosis.

“No unifying explanation” (choice “b”) is incorrect, because, as stated above, there is a unifying explanation for these findings!

Vitiligo (choice “c”) involves hypopigmented macules and patches. However, it does not present with some of the other findings seen in this case.

DISCUSSION
Tuberous sclerosis was first described in 1862 by von Recklinghausen, who noted the collection of findings we now term tuberous sclerosis complex (TSC) due to the wide variation in presentation.

In the United States, TSC occurs in an estimated one in 6,000 to one in 30,000 newborns. Usually, it manifests when the child is between ages 2 and 6, but genetic penetrance is highly variable—a major reason for the shift to the use of the term complex with this condition. (This case, with its late presentation, illustrates this variability.)

In about 60% of cases, TSC is transmitted in autosomal dominant mode, although at least 20% of cases may be due to spontaneous mutations. It has not shown any racial or gender predilections. Up to 90% of TSC patients will present with seizures, and 60% to 70% of those affected will demonstrate some developmental disability.

Skin is affected in at least 70% of TSC cases. This patient typifies the common dermatologic findings: dart-shaped hypopigmented macules (known as mountain ash leaf spots) and fleshy facial papules in the nasolabial region (originally called adenoma sebaceum and now called angiofibromas). Periungal fibromas are also common. Other major diagnostic criteria for TSC include cortical tubers seen on imaging and retinal hamartomas. Minor diagnostic criteria include pits in dental enamel and gingival fibromas.

Definitive diagnosis depends on identification of either two major manifestations or one major and two minor findings. There are no blood tests to confirm the diagnosis. In terms of treatment, the various elements that comprise TSC can be dealt with (eg, control of seizures and destruction or modification of skin lesions).

This patient received a diagnosis of TSC. She was returned to her primary care provider, who referred her for additional imaging of her lungs and heart and for ophthalmologic evaluation of her retinas. Genetic counseling was also arranged. With her seizures under control, she was able to continue matriculation through high school.

ANSWER
The correct answer is tuberous sclerosis (choice “d”), a genetic disorder affecting cellular differentiation and proliferation. As a result, hamartomas commonly form in organs such as the brain.

Von Recklinghausen disease (choice “a”; also known as neurofibromatosis type 1) presents with hyperpigmented macules and patches called café au lait macules. These and other findings differentiate it considerably from tuberous sclerosis.

“No unifying explanation” (choice “b”) is incorrect, because, as stated above, there is a unifying explanation for these findings!

Vitiligo (choice “c”) involves hypopigmented macules and patches. However, it does not present with some of the other findings seen in this case.

DISCUSSION
Tuberous sclerosis was first described in 1862 by von Recklinghausen, who noted the collection of findings we now term tuberous sclerosis complex (TSC) due to the wide variation in presentation.

In the United States, TSC occurs in an estimated one in 6,000 to one in 30,000 newborns. Usually, it manifests when the child is between ages 2 and 6, but genetic penetrance is highly variable—a major reason for the shift to the use of the term complex with this condition. (This case, with its late presentation, illustrates this variability.)

In about 60% of cases, TSC is transmitted in autosomal dominant mode, although at least 20% of cases may be due to spontaneous mutations. It has not shown any racial or gender predilections. Up to 90% of TSC patients will present with seizures, and 60% to 70% of those affected will demonstrate some developmental disability.

Skin is affected in at least 70% of TSC cases. This patient typifies the common dermatologic findings: dart-shaped hypopigmented macules (known as mountain ash leaf spots) and fleshy facial papules in the nasolabial region (originally called adenoma sebaceum and now called angiofibromas). Periungal fibromas are also common. Other major diagnostic criteria for TSC include cortical tubers seen on imaging and retinal hamartomas. Minor diagnostic criteria include pits in dental enamel and gingival fibromas.

Definitive diagnosis depends on identification of either two major manifestations or one major and two minor findings. There are no blood tests to confirm the diagnosis. In terms of treatment, the various elements that comprise TSC can be dealt with (eg, control of seizures and destruction or modification of skin lesions).

This patient received a diagnosis of TSC. She was returned to her primary care provider, who referred her for additional imaging of her lungs and heart and for ophthalmologic evaluation of her retinas. Genetic counseling was also arranged. With her seizures under control, she was able to continue matriculation through high school.

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The parents of this 16-year-old girl first noticed the “spots” on their daughter’s thigh when she was 2. At that time, they expressed mild concern to the child’s pediatrician, who advised them to watch the lesions for change. In the absence of any, the spots were essentially ignored. But recently—and alarmingly—the patient experienced two grand mal seizures. Three months ago, she was hospitalized and underwent a thorough examination and workup, including imaging studies of the brain. These revealed presumed neural tumors, which are being followed with serial imaging. In the meantime, her primary care provider recommends a visit to dermatology for evaluation of the child’s skin—including the aforementioned spots on her thigh. Her parents deny any family history of similar problems with skin or seizures. The spots are located on the patient’s right lateral thigh. The largest is a dart-shaped 4 x 2.5–cm hypopigmented patch. It is surrounded by much smaller (< 1 cm in diameter) but similarly hypopigmented macules. The large lesion is symmetrical but has slightly serrated borders. Examination elsewhere reveals periungual fibromas on two of 10 fingers. Odd fleshy papules are noted in the bilateral nasolabial areas.

 

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Man’s Heart Rhythm Has Been “Strange”

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ANSWER
The ECG reveals sinus bradycardia with second-degree atrioventricular (AV) block (Mobitz I), also known as Wenckebach block.

Mobitz I heart block often occurs with reversible reasons of conduction block at the level of the AV node. While the P-P intervals remain constant, conduction fatigue within the AV node results in the P-R interval becoming progressively longer, until the AV node completely blocks conduction from the atria to the ventricles. The process then repeats itself in a pattern of P to QRS groups.

In this case, there are three P waves for every two QRS complexes, resulting in a 3:2 pattern. The PR interval is longest prior to the blocked QRS and shortest immediately after it. The diagnosis of sinus bradycardia results from a constant P-P interval of 58 beats/min.

Further questioning of the patient revealed that he had inadvertently doubled his dose of metoprolol. Correcting this resulted in the return of normal sinus rhythm. 

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Lyle W. Larson, PhD, PA-C, is clinical faculty in the Department of Medicine, Division of Cardiology, Cardiac Electrophysiology, at the University of Washington, Seattle.

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ANSWER
The ECG reveals sinus bradycardia with second-degree atrioventricular (AV) block (Mobitz I), also known as Wenckebach block.

Mobitz I heart block often occurs with reversible reasons of conduction block at the level of the AV node. While the P-P intervals remain constant, conduction fatigue within the AV node results in the P-R interval becoming progressively longer, until the AV node completely blocks conduction from the atria to the ventricles. The process then repeats itself in a pattern of P to QRS groups.

In this case, there are three P waves for every two QRS complexes, resulting in a 3:2 pattern. The PR interval is longest prior to the blocked QRS and shortest immediately after it. The diagnosis of sinus bradycardia results from a constant P-P interval of 58 beats/min.

Further questioning of the patient revealed that he had inadvertently doubled his dose of metoprolol. Correcting this resulted in the return of normal sinus rhythm. 

ANSWER
The ECG reveals sinus bradycardia with second-degree atrioventricular (AV) block (Mobitz I), also known as Wenckebach block.

Mobitz I heart block often occurs with reversible reasons of conduction block at the level of the AV node. While the P-P intervals remain constant, conduction fatigue within the AV node results in the P-R interval becoming progressively longer, until the AV node completely blocks conduction from the atria to the ventricles. The process then repeats itself in a pattern of P to QRS groups.

In this case, there are three P waves for every two QRS complexes, resulting in a 3:2 pattern. The PR interval is longest prior to the blocked QRS and shortest immediately after it. The diagnosis of sinus bradycardia results from a constant P-P interval of 58 beats/min.

Further questioning of the patient revealed that he had inadvertently doubled his dose of metoprolol. Correcting this resulted in the return of normal sinus rhythm. 

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A 74-year-old man presents to your outpatient clinic for a routine appointment. He’s been your patient for years, but you’ve had difficulty convincing him of the importance of taking his hypertension medications regularly. For the most part, he has been compliant; however, recently, with finances becoming tight toward the end of the month, he often takes his β-blocker and diuretic every other day in order to stretch his prescription before refilling it. His health has remained excellent since you last saw him a year ago. However, while performing a review of systems, you learn that his heart rhythm has been “funny” in the past two weeks. He states it hasn’t affected his ability to perform his daily activities, including farming, but it was just “strange.” He denies chest pain, shortness of breath, dizziness, syncope or near-syncope, and peripheral edema. He still manages his 450-acre farm, as he has for most of his adult life. Medical history includes hypertension but no angina, MI, or other cardiac disease. Surgical history is remarkable for a right inguinal hernia repair, an appendectomy, and a right hip replacement. His medications include furosemide, potassium chloride, and metoprolol. He has no known drug allergies and does not use recreational drugs or naturopathic herbs. The patient has been a widower for 12 years. His two sons live nearby and help him on his farm. Due to his religious affiliation, he has never used alcohol or tobacco. Review of systems is remarkable for palpitations and an occasional skipped beat. Vital signs include a blood pressure of 108/58 mm Hg; pulse, 50 beats/min and “irregular”; respiratory rate, 14 breaths/min-1; temperature, 98.4°F; and O2 saturation, 96% on room air. His weight is 176 lb and his height, 74 in. Physical exam reveals a pulse that is regularly irregular at a rate of 56 beats/min. There are no murmurs, rubs, or gallops. The neck veins are not distended, and there is no peripheral edema. His lungs are clear to auscultation, and the remainder of his physical exam is unchanged from his previous visit. Given the change in his heart rhythm since his previous visit, you order an ECG and note the following: a ventricular rate of 44 beats/min; PR interval, not measured; QRS duration, 106 ms; QT/QTc interval, 484/413 ms; P axis, 65°; R axis, 11°; and T axis, 6°. What is your interpretation of this ECG?

 

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Tender Thumbnail Papule

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The Diagnosis: Myxoid Cyst

Myxoid cysts, often called ganglion cysts or mucous cysts, are smooth translucent nodules that arise between the dorsal aspect of the distal interphalangeal joint and proximal nail fold.1 Lesions often have an associated distal depression or groove on the affected fingernail and typically appear on the middle and index fingers between the fourth and seventh decades of life.2,3 Acute lesions may present as tender nodules, whereas gradually developing lesions tend to be painless.3 Trauma to the distal interphalangeal joint, degenerative processes, and osteoarthritis may increase hyaluronic acid production and allow synovial fluid to escape the joint space, accumulating in the surrounding tissue. Subungual localization of a mucous cyst is rare and may be difficult to diagnose.4 The differential diagnosis includes benign and malignant tumors such as periungual fibroma, glomus tumor, basal cell carcinoma, squamous cell carcinoma, and amelanotic melanoma.5 Our patient declined treatment with cryotherapy or intralesional steroid injection and drainage. He was referred to the orthopedic surgery department for surgical removal of the cyst and imaging studies. Radiographs of the right thumb revealed severe osteoarthritis of the distal interphalangeal joint, demonstrating the association of digital mucous cysts.

References

1. Karrer S, Hohenleutner U, Szeimies RM, et al. Treatment of a digital mucous cyst with a carbon dioxide laser. Acta Derm Venereol. 1999;79:224-225.

2. Brown RE, Zook EG, Russell RC. Fingernail deformities secondary to ganglions of the distal interphalangeal joint (mucous cysts). Plast Reconstr Surg. 1991;87:718-725.

3. de Berker D, Goettman S, Baran R. Subungual myxoid cysts: clinical manifestations and response to therapy. J Am Acad Dermatol. 2002;46:394-398.

4. Lin YC, Wu TH, Scher RK. Nail changes and association of osteoarthritis in digital myxoid cyst. Dermatol Surg. 2008;34:364-369.

5. Kivanc-Altunay I, Kumbasar E, Gokdemir G. Unusual localization of multiple myxoid (mucous) cysts of toes. Dermatol Online J. 2004;10:23.

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Correspondence: Adam J. Tinklepaugh, MD ([email protected]).

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Correspondence: Adam J. Tinklepaugh, MD ([email protected]).

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Correspondence: Adam J. Tinklepaugh, MD ([email protected]).

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The Diagnosis: Myxoid Cyst

Myxoid cysts, often called ganglion cysts or mucous cysts, are smooth translucent nodules that arise between the dorsal aspect of the distal interphalangeal joint and proximal nail fold.1 Lesions often have an associated distal depression or groove on the affected fingernail and typically appear on the middle and index fingers between the fourth and seventh decades of life.2,3 Acute lesions may present as tender nodules, whereas gradually developing lesions tend to be painless.3 Trauma to the distal interphalangeal joint, degenerative processes, and osteoarthritis may increase hyaluronic acid production and allow synovial fluid to escape the joint space, accumulating in the surrounding tissue. Subungual localization of a mucous cyst is rare and may be difficult to diagnose.4 The differential diagnosis includes benign and malignant tumors such as periungual fibroma, glomus tumor, basal cell carcinoma, squamous cell carcinoma, and amelanotic melanoma.5 Our patient declined treatment with cryotherapy or intralesional steroid injection and drainage. He was referred to the orthopedic surgery department for surgical removal of the cyst and imaging studies. Radiographs of the right thumb revealed severe osteoarthritis of the distal interphalangeal joint, demonstrating the association of digital mucous cysts.

The Diagnosis: Myxoid Cyst

Myxoid cysts, often called ganglion cysts or mucous cysts, are smooth translucent nodules that arise between the dorsal aspect of the distal interphalangeal joint and proximal nail fold.1 Lesions often have an associated distal depression or groove on the affected fingernail and typically appear on the middle and index fingers between the fourth and seventh decades of life.2,3 Acute lesions may present as tender nodules, whereas gradually developing lesions tend to be painless.3 Trauma to the distal interphalangeal joint, degenerative processes, and osteoarthritis may increase hyaluronic acid production and allow synovial fluid to escape the joint space, accumulating in the surrounding tissue. Subungual localization of a mucous cyst is rare and may be difficult to diagnose.4 The differential diagnosis includes benign and malignant tumors such as periungual fibroma, glomus tumor, basal cell carcinoma, squamous cell carcinoma, and amelanotic melanoma.5 Our patient declined treatment with cryotherapy or intralesional steroid injection and drainage. He was referred to the orthopedic surgery department for surgical removal of the cyst and imaging studies. Radiographs of the right thumb revealed severe osteoarthritis of the distal interphalangeal joint, demonstrating the association of digital mucous cysts.

References

1. Karrer S, Hohenleutner U, Szeimies RM, et al. Treatment of a digital mucous cyst with a carbon dioxide laser. Acta Derm Venereol. 1999;79:224-225.

2. Brown RE, Zook EG, Russell RC. Fingernail deformities secondary to ganglions of the distal interphalangeal joint (mucous cysts). Plast Reconstr Surg. 1991;87:718-725.

3. de Berker D, Goettman S, Baran R. Subungual myxoid cysts: clinical manifestations and response to therapy. J Am Acad Dermatol. 2002;46:394-398.

4. Lin YC, Wu TH, Scher RK. Nail changes and association of osteoarthritis in digital myxoid cyst. Dermatol Surg. 2008;34:364-369.

5. Kivanc-Altunay I, Kumbasar E, Gokdemir G. Unusual localization of multiple myxoid (mucous) cysts of toes. Dermatol Online J. 2004;10:23.

References

1. Karrer S, Hohenleutner U, Szeimies RM, et al. Treatment of a digital mucous cyst with a carbon dioxide laser. Acta Derm Venereol. 1999;79:224-225.

2. Brown RE, Zook EG, Russell RC. Fingernail deformities secondary to ganglions of the distal interphalangeal joint (mucous cysts). Plast Reconstr Surg. 1991;87:718-725.

3. de Berker D, Goettman S, Baran R. Subungual myxoid cysts: clinical manifestations and response to therapy. J Am Acad Dermatol. 2002;46:394-398.

4. Lin YC, Wu TH, Scher RK. Nail changes and association of osteoarthritis in digital myxoid cyst. Dermatol Surg. 2008;34:364-369.

5. Kivanc-Altunay I, Kumbasar E, Gokdemir G. Unusual localization of multiple myxoid (mucous) cysts of toes. Dermatol Online J. 2004;10:23.

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A 71-year-old man presented to the dermatology clinic with mild tenderness and disfigurement of the right thumbnail of 6 months’ duration. The patient reported trauma to his thumb from closing a window on it during the time between onset of symptoms and presentation to the dermatology clinic. On physical examination the right thumbnail was atrophic with a flesh-colored papule involving the proximal nail bed. The nail plate overlying the papule was thinned by the underlying growth and there was a linear groove extending from the papule to the end of the nail. A biopsy was recommended for diagnosis and lidocaine was injected into the proximal aspect of the nail fold for local anesthesia. The lidocaine filled the papule, resulting in increased subungual pressure that caused the lesion to rupture through the nail plate, extruding a clear mucoid substance.
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Punctate Depigmented Macules

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The Diagnosis: Blaschkoid Punctate Vitiligo

Based on the patient’s clinical appearance as well as the histologic findings, the diagnosis of vitiligo was made. Although vitiligo is certainly not uncommon and punctate vitiligo is a known clinical presentation,1 punctate vitiliginous depigmentation conforming to lines of Blaschko is unique. Follicular repigmentation in a patch of vitiligo potentially could lead to this “spotty” appearance, but our patient maintained that the band was never confluently depigmented and that small macules arose within normally pigmented skin. The patient’s adult age at onset makes this case even more unusual.

Follicular repigmentation in vitiligo is fairly well understood, as the perifollicular pigment is formed by upward migration of activated melanoblasts in the outer root sheath.2 Follicular depigmentation as well as selective or initial loss of melanocytes around hair follicles in early vitiligo has not been described. It is unclear if the seemingly folliculocentric nature of the patient’s vitiliginous macules was a false observation, coincidental, or actually related to selective melanocyte loss around follicles.

Blaschkoid distribution has been described in numerous skin disorders and is known to be based on genetic mosaicism.3 Most of these disorders are X-linked and/or congenital. However, many acquired skin conditions have been described exhibiting blaschkoid distribution, such as vitiligo, psoriasis, lichen planus, atopic dermatitis, and mycosis fungoides.4,5

Confettilike depigmentation has been described as an unusual clinical variant of vitiligo.1 It also has been reported after psoralen plus UVA therapy in patients with more classic vitiligo,6 numerous domestic chemicals,7 and in association with mycosis fungoides.8 In these cases, punctate lesions were disseminated, symmetric on extremities, or limited to areas exposed to chemicals.

References

1. Ortonne J-P. Vitiligo and other disorders of hypopigmentation. In: Bolognia JL, Jorizzo JL, Rapini RP, eds. Dermatology. Vol 1. 2nd ed. St. Louis, MO: Mosby; 2003:913-938.

2. Cui J, Shen LY, Wang GC. Role of hair follicles in the repigmentation of vitiligo. J Invest Dermatol. 1991;97:410-416.

3. Happle R. X-chromosome inactivation: role in skin disease expression. Acta Paediatr Suppl. 2006;95:16-23.

4. Taieb A. Linear atopic dermatitis (“naevus atopicus”): a pathogenetic clue? Br J Dermatol. 1994;131:134-135.

5. Bolognia JL, Orlow SJ, Glick SA. Lines of Blaschko. J Am Acad Dermatol. 1994;31:157-190.

6. Falabella R, Escobar CE, Carrascal E, et al. Leukoderma punctata. J Am Acad Dermatol. 1988;18:485-494. 

7. Ghosh S, Mukhopadhyay S. Chemical leucoderma: a clinico-aetiological study of 864 cases in the perspective of a developing country. Br J Dermatol. 2009;160:40-47.

8. Loquai C, Metza D, Nashan D, et al. Confetti-like lesions with hyperkeratosis: a novel ultraviolet-induced hypomelanotic disorder? Br J Dermatol. 2005;153:190-193.

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The Diagnosis: Blaschkoid Punctate Vitiligo

Based on the patient’s clinical appearance as well as the histologic findings, the diagnosis of vitiligo was made. Although vitiligo is certainly not uncommon and punctate vitiligo is a known clinical presentation,1 punctate vitiliginous depigmentation conforming to lines of Blaschko is unique. Follicular repigmentation in a patch of vitiligo potentially could lead to this “spotty” appearance, but our patient maintained that the band was never confluently depigmented and that small macules arose within normally pigmented skin. The patient’s adult age at onset makes this case even more unusual.

Follicular repigmentation in vitiligo is fairly well understood, as the perifollicular pigment is formed by upward migration of activated melanoblasts in the outer root sheath.2 Follicular depigmentation as well as selective or initial loss of melanocytes around hair follicles in early vitiligo has not been described. It is unclear if the seemingly folliculocentric nature of the patient’s vitiliginous macules was a false observation, coincidental, or actually related to selective melanocyte loss around follicles.

Blaschkoid distribution has been described in numerous skin disorders and is known to be based on genetic mosaicism.3 Most of these disorders are X-linked and/or congenital. However, many acquired skin conditions have been described exhibiting blaschkoid distribution, such as vitiligo, psoriasis, lichen planus, atopic dermatitis, and mycosis fungoides.4,5

Confettilike depigmentation has been described as an unusual clinical variant of vitiligo.1 It also has been reported after psoralen plus UVA therapy in patients with more classic vitiligo,6 numerous domestic chemicals,7 and in association with mycosis fungoides.8 In these cases, punctate lesions were disseminated, symmetric on extremities, or limited to areas exposed to chemicals.

The Diagnosis: Blaschkoid Punctate Vitiligo

Based on the patient’s clinical appearance as well as the histologic findings, the diagnosis of vitiligo was made. Although vitiligo is certainly not uncommon and punctate vitiligo is a known clinical presentation,1 punctate vitiliginous depigmentation conforming to lines of Blaschko is unique. Follicular repigmentation in a patch of vitiligo potentially could lead to this “spotty” appearance, but our patient maintained that the band was never confluently depigmented and that small macules arose within normally pigmented skin. The patient’s adult age at onset makes this case even more unusual.

Follicular repigmentation in vitiligo is fairly well understood, as the perifollicular pigment is formed by upward migration of activated melanoblasts in the outer root sheath.2 Follicular depigmentation as well as selective or initial loss of melanocytes around hair follicles in early vitiligo has not been described. It is unclear if the seemingly folliculocentric nature of the patient’s vitiliginous macules was a false observation, coincidental, or actually related to selective melanocyte loss around follicles.

Blaschkoid distribution has been described in numerous skin disorders and is known to be based on genetic mosaicism.3 Most of these disorders are X-linked and/or congenital. However, many acquired skin conditions have been described exhibiting blaschkoid distribution, such as vitiligo, psoriasis, lichen planus, atopic dermatitis, and mycosis fungoides.4,5

Confettilike depigmentation has been described as an unusual clinical variant of vitiligo.1 It also has been reported after psoralen plus UVA therapy in patients with more classic vitiligo,6 numerous domestic chemicals,7 and in association with mycosis fungoides.8 In these cases, punctate lesions were disseminated, symmetric on extremities, or limited to areas exposed to chemicals.

References

1. Ortonne J-P. Vitiligo and other disorders of hypopigmentation. In: Bolognia JL, Jorizzo JL, Rapini RP, eds. Dermatology. Vol 1. 2nd ed. St. Louis, MO: Mosby; 2003:913-938.

2. Cui J, Shen LY, Wang GC. Role of hair follicles in the repigmentation of vitiligo. J Invest Dermatol. 1991;97:410-416.

3. Happle R. X-chromosome inactivation: role in skin disease expression. Acta Paediatr Suppl. 2006;95:16-23.

4. Taieb A. Linear atopic dermatitis (“naevus atopicus”): a pathogenetic clue? Br J Dermatol. 1994;131:134-135.

5. Bolognia JL, Orlow SJ, Glick SA. Lines of Blaschko. J Am Acad Dermatol. 1994;31:157-190.

6. Falabella R, Escobar CE, Carrascal E, et al. Leukoderma punctata. J Am Acad Dermatol. 1988;18:485-494. 

7. Ghosh S, Mukhopadhyay S. Chemical leucoderma: a clinico-aetiological study of 864 cases in the perspective of a developing country. Br J Dermatol. 2009;160:40-47.

8. Loquai C, Metza D, Nashan D, et al. Confetti-like lesions with hyperkeratosis: a novel ultraviolet-induced hypomelanotic disorder? Br J Dermatol. 2005;153:190-193.

References

1. Ortonne J-P. Vitiligo and other disorders of hypopigmentation. In: Bolognia JL, Jorizzo JL, Rapini RP, eds. Dermatology. Vol 1. 2nd ed. St. Louis, MO: Mosby; 2003:913-938.

2. Cui J, Shen LY, Wang GC. Role of hair follicles in the repigmentation of vitiligo. J Invest Dermatol. 1991;97:410-416.

3. Happle R. X-chromosome inactivation: role in skin disease expression. Acta Paediatr Suppl. 2006;95:16-23.

4. Taieb A. Linear atopic dermatitis (“naevus atopicus”): a pathogenetic clue? Br J Dermatol. 1994;131:134-135.

5. Bolognia JL, Orlow SJ, Glick SA. Lines of Blaschko. J Am Acad Dermatol. 1994;31:157-190.

6. Falabella R, Escobar CE, Carrascal E, et al. Leukoderma punctata. J Am Acad Dermatol. 1988;18:485-494. 

7. Ghosh S, Mukhopadhyay S. Chemical leucoderma: a clinico-aetiological study of 864 cases in the perspective of a developing country. Br J Dermatol. 2009;160:40-47.

8. Loquai C, Metza D, Nashan D, et al. Confetti-like lesions with hyperkeratosis: a novel ultraviolet-induced hypomelanotic disorder? Br J Dermatol. 2005;153:190-193.

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An otherwise healthy 54-year-old black man presented with a 10-year history of spotty pigmentary loss in a band on the left side of the abdomen, flank, and back. He denied a history of rash or inflammation in the area and had not experienced confluent depigmentation. He reported that initially he had only a few “white dots,” and over the next 5 to 7 years, he developed more of them confined within the same area. On presentation, he stated new areas of depigmentation had not developed in several years. The band was completely asymptomatic and had not been treated with any prescription or over-the-counter medications. On examination he had multiple 2- to 3-mm confettilike depigmented macules that seemed to be centered around follicles in a band with blaschkoid distribution extending across the left side of the abdomen, flank, and back. The band did not cross the midline and similar lesions were not present elsewhere. A punch biopsy of one of the depigmented macules revealed a markedly diminished number of melanocytes along the junction as well as a decrease in melanin, which was confirmed by Melan-A and Fontana stains, respectively.
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The image shows a comminuted and depressed fracture of the lateral tibial plateau. It is depressed approximately 6 to 7 mm. The patient was admitted, and orthopedic consultation was obtained. The patient subsequently underwent an open reduction and internal fixation of the fracture.

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The image shows a comminuted and depressed fracture of the lateral tibial plateau. It is depressed approximately 6 to 7 mm. The patient was admitted, and orthopedic consultation was obtained. The patient subsequently underwent an open reduction and internal fixation of the fracture.

ANSWER

The image shows a comminuted and depressed fracture of the lateral tibial plateau. It is depressed approximately 6 to 7 mm. The patient was admitted, and orthopedic consultation was obtained. The patient subsequently underwent an open reduction and internal fixation of the fracture.

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A 23-year-old man is brought in after being hit by a car. He was in the process of getting into his car when another vehicle coming from the opposite direction swerved into his lane. He tried to jump onto his hood to avoid the other car but was struck by the side mirror and landed on the ground. He is primarily complaining of left knee and lower leg pain. He denies any medical history. Primary survey appears to be stable except for scalp and facial lacerations. The patient is awake, alert, and oriented, and his vital signs are stable. His left lower extremity is in a splint immobilizer, placed by emergency medical personnel. There is a moderate amount of soft tissue swelling around the knee, which is exquisitely tender to palpation. The patient has limited flexion and extension of the knee due to pain. He is able to wiggle his toes, and distally in the leg and foot there appears to be no neurovascular compromise. Radiographs of the tibia are obtained. What is your impression?
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No Time for Chest Pain When There Are Chores to Do

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There are three significant findings on this ECG. First, the rhythm shows complete heart block. The ventricular rate is 56 beats/min, and the QRS complex is narrow, resulting in a junctional rhythm. The atrial rate is 98 beats/min (consistent with a sinus rhythm), and there is no relationship of the P waves to the QRS complexes.

The second finding is a rightward axis deviation. Note that the QRS complexes are negative in lead I and positive in lead aVF. To meet criteria for a right-axis deviation, the QRS complex must also be positive in lead aVR. In this case, the QRS complex appears to be isoelectric in aVR, so we call the axis rightward.

The presence of rightward axis deviation is a result of the third finding, an anterior MI. This is due to the LAD artery occlusion discovered at catheterization. It is evident on the ECG by the absence of significant R waves in leads V1 through V4.

Given the need for a β-blocker with titration of dose, the patient underwent implantation of a permanent pacemaker system.

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ANSWER

There are three significant findings on this ECG. First, the rhythm shows complete heart block. The ventricular rate is 56 beats/min, and the QRS complex is narrow, resulting in a junctional rhythm. The atrial rate is 98 beats/min (consistent with a sinus rhythm), and there is no relationship of the P waves to the QRS complexes.

The second finding is a rightward axis deviation. Note that the QRS complexes are negative in lead I and positive in lead aVF. To meet criteria for a right-axis deviation, the QRS complex must also be positive in lead aVR. In this case, the QRS complex appears to be isoelectric in aVR, so we call the axis rightward.

The presence of rightward axis deviation is a result of the third finding, an anterior MI. This is due to the LAD artery occlusion discovered at catheterization. It is evident on the ECG by the absence of significant R waves in leads V1 through V4.

Given the need for a β-blocker with titration of dose, the patient underwent implantation of a permanent pacemaker system.

ANSWER

There are three significant findings on this ECG. First, the rhythm shows complete heart block. The ventricular rate is 56 beats/min, and the QRS complex is narrow, resulting in a junctional rhythm. The atrial rate is 98 beats/min (consistent with a sinus rhythm), and there is no relationship of the P waves to the QRS complexes.

The second finding is a rightward axis deviation. Note that the QRS complexes are negative in lead I and positive in lead aVF. To meet criteria for a right-axis deviation, the QRS complex must also be positive in lead aVR. In this case, the QRS complex appears to be isoelectric in aVR, so we call the axis rightward.

The presence of rightward axis deviation is a result of the third finding, an anterior MI. This is due to the LAD artery occlusion discovered at catheterization. It is evident on the ECG by the absence of significant R waves in leads V1 through V4.

Given the need for a β-blocker with titration of dose, the patient underwent implantation of a permanent pacemaker system.

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Three days ago, a 62-year-old man was admitted with chest pain and an MI (confirmed by cardiac enzymes). The chest pain started while he was working on his farm, but he did not seek immediate help because he assumed it was heartburn and he had chores to finish. When the pain did not resolve overnight, he finally presented to the emergency department. Cardiac catheterization revealed an occluded left anterior descending (LAD) artery distal to the first diagonal branch and diffuse disease in the circumflex and right coronary arteries. An echocardiogram showed diffuse left ventricular hypokinesis and no evidence of valvular disease. His left ventricular ejection fraction was estimated to be 48%. Medical history is remarkable for hypertension and gout. Surgical history is remarkable for an appendectomy at age 7 and surgical repair of a fractured tibia from a high school football injury. Family history is positive for coronary artery disease; both parents died at young ages (father at 60, mother at 65) of MI, and his older brother had an MI at age 50 (but is currently doing well). The patient owns a 475-acre farm on which he grows corn and soybeans. He also tends to 23 cows and has a large chicken coop. There are five workers to help, but he states that he does most of the work himself. He is divorced and lives alone with five dogs, whom he refers to as his “kids.” He does not smoke, but he has one beer and one shot of bourbon with dinner each night. His only medication at the time of admission was ibuprofen. He had been prescribed lisinopril in the past but hadn’t taken it in six months because “it’s too far a drive to get it refilled.” He has no known drug allergies. Following admission, he was started on a β-blocker (metoprolol), aspirin, atorvastatin, and lisinopril. During rounds, you notice that his hypertension is well controlled. His blood pressure is 118/80 mm Hg, compared to 180/92 mm Hg on admission. He is comfortable and wants to know when he can go home. As you contemplate discharge, a technician hands you the patient’s daily ECG tracing. It shows a ventricular rate of 56 beats/min; QRS duration, 106 ms; QT/QTc interval, 400/386 ms; P axis, 36°; R axis, 120°; and T axis, 7°. What is your interpretation of this ECG?

 

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