- Email: [email protected]
Intralesional triamcinolone in the management of lipodermatosclerosis
166 Letters
J AM ACAD DERMATOL JULY 2006
Of note, the relationship between rosacea and dental disease has been reported in the literature. These rare reports indicate significant clinical improvement in rosacea after patients undergo treatment for their periodontal and dental disease.1 Unfortunately, because our patient refused dental evaluation, this potential association could not be verified.
Fig 1. Erythematous spongy plaque with multiple nodules and dilated pores covering the entire chin. Note poor dentition.
Erum N. Ilyas, MDa Matthew R. Hanson, BSb Naomi Lawrence, MDa Justin J. Green, MDa Division of Dermatology, Department of Medicine Cooper Health System, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson at Camdena Drexel University, College of Medicine Philadelphiab Funding sources: None. Conflicts of interest: None identified.
Fig 2. Two months after treatment with dermabrasion, CO2 laser, and wire loop electrocautery.
literature, images of this variant are not often seen. This distinct variant of rosacea may be overlooked because of its rare nature and unusual presentation. We report an unusual case of gnatophyma presenting in a young woman without other associated phymas. A 31-year-old woman was referred by her primary care physician for evaluation of a growth on her chin that had begun about 10 years earlier (Fig 1). Physical examination was also remarkable for overall poor dentition, including numerous dental caries and tooth decay for which the patient refused a dental referral. A biopsy was performed, which confirmed a diagnosis of rosacea. Initial treatment over the course of 3 months with doxycycline, subsequently switched to minocycline because of reported nausea, and topical metronidazole resulted in no response, prompting us to opt for surgical intervention. Dermabrasion performed initially resulted in slight improvement in contour, followed by carbon dioxide laser therapy with wire loop electrocautery 2 months later to debulk the lesion (Fig 2). She initially had a good response to this treatment with decreased tissue bulk and surface nodularity, as well as improved contour, but detailed observation could not be performed because the patient was lost to follow up.
Correspondence to: Erum N. Ilyas, MD Cooper Health System, Robert Wood Johnson University of Medicine and Dentistry of New Jersey at Camden Department of Medicine, Division of Dermatology 1811 Bethlehem Pike, Suite A104 Flourtown, PA 19031 E-mail: [email protected] REFERENCE 1. Lesclous P, Maman L. An unusual case of a relationship between rosacea and dental foci. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999;88:679-82. doi:10.1016/j.jaad.2005.09.037
Intralesional triamcinolone in the management of lipodermatosclerosis To the Editor: Lipodermatosclerosis is a common but confusing marker of venous insufficiency that presents with pain, erythema, edema, and increasing induration. Numerous therapies have been studied, including low-, medium- or high-pressure compression therapy,1 stanozolol,2,3 surgical correction of venous disease,4 Daflon 500 mg,5 pentoxifylline,6 oxandrolone,7 and total triterpenic fraction of Centella asiatica.8 Randomized controlled trials have shown improvement in symptoms of patients receiving compression therapy and stanozolol.2,3 One case utilizing intralesional triamcinolone with compression therapy for the treatment of pain associated with lipodermatosclerosis has been previously reported.9
Letters 167
J AM ACAD DERMATOL VOLUME 55, NUMBER 1
Table I. Characteristics and response of patients treated with intralesional triamcinolone* Pain
Initial clinical findings 26/28 Improvement after 25/26 therapy (1-3 visits)
Erythema Edema Induration
22/28 19/22
13/28 8/13
27/28 23/27
*Data expressed as number of patients.
We report a case series of 28 patients based on chart review who received intralesional triamcinolone for the management of lipodermatosclerosis. Twenty-three women and 5 men, 20 to 77 years of age, were included. All patients were initially diagnosed clinically. Twenty-six of 28 patients complained of pain on presentation. Additional clinical findings are listed in Table I. Intralesional triamcinolone was the sole treatment in 3 patients and was followed by Unna boot (10 patients), Profore compression wrap (1), compression stocking (13), or SurePress wrap (1) in the remaining patients. The strength of triamcinolone injected was not standardized and recorded in only 22 patients. Eleven of these received a concentration of 5 mg/mL, and 10 received a concentration of 10 mg/mL. The total volume injected varied with the size and number of lesions. Pain was alleviated in 25 of 26 patients after one or two treatments. Induration improved in 23 of 27, as did edema in 8 of 13 patients and erythema in 19 of 22 patients. Although most patients responded initially, ongoing therapy was required, with 21 receiving additional triamcinolone injections (frequency varied) and 26 patients utilizing some form of compression. The rationale for the use of intralesional steroids is based on the pathogenic role of inflammation in lipodermatosclerosis, particularly in the early stage of the disease (Fig 1, A). Triamcinolone, a glucocorticoid, decreases inflammation by increasing the production of inhibitory protein Ikba. This molecule serves to bind nuclear factor kb dimers, key proteins in signal transduction, preventing them from being released from cells. The decrease in activity of nuclear factor kb precludes the transcription of several primary inflammatory cytokines, including interleukin 1b and tumor necrosis factor-a.10 Early use of intralesional steroids reduced pain in our patients and prevented the progression of disease to induration and the potential bottleneck deformity associated with late-stage lipodermatosclerosis (Fig 1, B) (personal observation, O. F. M.) Our current approach consists of weekly, biweekly, or monthly therapy depending on the extent of cutaneous induration and associated pain. At each
Fig 1. A, Acute lipodermatosclerosis. lipodermatosclerosis.
B,
Chronic
visit, 1 to 2 mL of triamcinolone (10 mg/mL) is injected into indurated areas with a 30-gauge needle in 0.2- to 0.3-mL aliquots at approximately 1.5-cm intervals. An Unna boot or a 20 to 30 mm Hg compression stocking is then applied. This chart reviewebased case series is limited by its retrospective nature and lack of systematized data recording. Cesarone et al8 used a numerical scale to quantify pain, redness, skin alterations, and edema. This may be a useful gauge for future studies. Further study should also take place in a randomized control trial so that compression alone can be compared with steroid injection alone and injection with compression. Lisa B. Campbell, MD O. Fred Miller, III, MD Geisinger Medical Center Danville, Pennsylvania These data presented at the 2005 Pennsylvania Academy of Dermatology meeting. Reprint requests: O. Fred Miller, III, MD Department of Dermatology Geisinger Medical Center 100 N Academy Ave, Danville, PA 17822 E-mail: [email protected]
REFERENCES 1. Gniadecka M, Karlsmark T, Bertran A. Removal of dermal edema with class I and II compression stockings in patients with lipodermatosclerosis. J Am Acad Dermatol 1998;39:966-70. 2. Burnand K, Clemenson G, Morland M, Jarrett PE, Browse NL. Venous lipodermatosclerosis: treatment by fibrinolytic enhancement and elastic compression. Br Med J 1980;280:7-11. 3. Browse NL, Jarrett PE, Morland M, Burnand K. Treatment of liposclerosis of the leg by fibrinolytic enhancement: a preliminary report. Br Med J 1977;2:434-5.
168 Letters
J AM ACAD DERMATOL JULY 2006
4. Valencia IC, Falabella A, Kirsner RS, Eaglstein WH. Chronic venous insufficiency and venous leg ulceration. J Am Acad Dermatol 2001;44:401-21. 5. Bergan JJ, Schmid-Schonbein GW, Takase S. Therapeutic approach to chronic venous insufficiency and its complications: place of Daflon 500 mg. Angiology 2001;52(Suppl 1): S43-7. 6. Goldman MP. The use of pentoxifylline in the treatment of systemic sclerosis and lipodermatosclerosis: a unifying hypothesis? J Am Acad Dermatol 1994;31:135-6. 7. Segal S, Cooper J, Bolognia J. Treatment of lipodermatosclerosis with oxandrolone in a patient with stanozolol-induced hepatotoxicity. J Am Acad Dermatol 2000;43:558-9. 8. Cesarone MR, Belcaro G, De Sanctis MT, Incandela I, Cacchio M, Bavera P, et al. Effects of the total triterpenic fraction of Centella asiatica in venous hypertensive microangiopathy: a prospective, placebo-controlled, randomized trial. Angiology 2001;52(Suppl):S15-8. 9. Lewis JE. Treatment of postphlebitic lipodermatosclerosis. South Med J 1990;83:1489-90. 10. Williams IR, Rich BE, Kupper TS. Cytokines. In: Freedberg IM, Eisen AZ, Wolff K, Austen KF, Goldsmith LA, Katz SI, editors. Fitzpatrick’s Dermatology in general medicine. 6th ed. New York: McGraw-Hill; 2003. pp. 286-8. doi:10.1016/j.jaad.2005.09.043
Efficacy of anti-IgE therapy in patients with atopic dermatitis To the Editor: Atopic dermatitis (AD) or eczema is often the first manifestation of atopy, with approximately 80% of children eventually developing food allergies, asthma, or allergic rhinitis (AR). Since the discovery of the IgE molecule, its role as a crucial immune mediator of allergic inflammation has come to light. Although its exact role in the pathogenesis of asthma is unclear, previous studies have shown a strong correlation between the severity of AD, serum IgE levels, and concomitant allergic rhinitis and/or bronchial asthma.1 Even in the absence of known food allergies, eczema patients often have elevated
specific and total serum IgE levels.2 Factors that influence IgE production include cytokines (like interleukins-4 and -13) and inflammatory cells that are present in the milieu. When antigen cross-links the specific IgE bound to the FceRI on mast cells and basophils, these cells initiate and amplify the inflammatory response in both the airways and atopic skin. In the skin, these events are responsible for the hallmark features that include erythema, papulation, lichenification, exudation, and crusting. Omalizumab is a chimeric monoclonal antibody that binds IgE at the same binding site as FceRI and FceRII, thereby inhibiting mast cell or basophil activation. Recent studies have demonstrated a significant benefit from anti-IgE in the treatment of both atopic asthma and allergic rhinitis by decreasing serum IgE levels, nasal symptoms,3 and bronchoconstriction during both the early and late-phase responses to inhaled allergen.4 These translate to a reduction of asthma-related symptoms, corticosteroid dose, and improvement in quality of life. Because of similarities in the immune mechanisms underlying asthma and AD, we decided to look at the effect of anti-IgE therapy on cutaneous symptoms of AD. We report on 7 AD patients (aged 7-58 yrs) who received anti-IgE treatment for their persistent asthma. All patients had history of asthma, AR, and eczema since early childhood (\3 yrs old) and a strong family history of atopy. They had positive skin tests or RAST for common aeroallergens and high IgE titers (226-2020 kU/L or IU/mL). Physician assessments at 3 and 7 months were used to generate eczema scores (ranked 0-5 in increasing order of severity) using the Global Assessment (IGA) scoring system.5 All patients received omalizumab calculated according to patient’s mass and baseline IgE titers per manufacturer’s nomogram. Those whose IgE
Table I. Patients’ baseline characteristics Pt 1
Pt 2
Pt 3
Pt 4
Pt 5
Pt 6
Pt 7
Age (yrs)/sex 7/F 13/F 24/F 38/M 38/F 43/F 58/F Atopic conditions PAR, AD PAR, AD PAR, AD PAR, AD PAR, AD PAR, AD PAR, AD Cat, dog, Cat, dog, DM, Cat, dog Dog, trees Cat, dog, DM Aeroallergen Cat, dog, DM, Cat, DM, sensitivity trees, weeds, trees, weeds, ragweed, and trees, molds, and grasses molds and grasses molds, and grasses IgE titer (kU/L) 1375 2020 784 967 545 1484 265 Omalizumab 375 mg 375 mg 375 mg 375 mg 375 mg 375 mg 300 mg dose SQ q2wk SQ q2wk SQ q2wk SQ q2wk SQ q2wk SQ q2wk SQ q2wk Start mo. of November December November October October September December therapy Eczema severity Moderate Moderate Moderate Moderate Severe Severe Mild IGA score 3 3 3 3 4 4 2 AD, Atopic dermatitis; DM, dust mite; IGA, Investigator Global Assessment; PAR, perennial allergic rhinitis; SAR, seasonal allergic rhinitis.
J AM ACAD DERMATOL JULY 2006
Of note, the relationship between rosacea and dental disease has been reported in the literature. These rare reports indicate significant clinical improvement in rosacea after patients undergo treatment for their periodontal and dental disease.1 Unfortunately, because our patient refused dental evaluation, this potential association could not be verified.
Fig 1. Erythematous spongy plaque with multiple nodules and dilated pores covering the entire chin. Note poor dentition.
Erum N. Ilyas, MDa Matthew R. Hanson, BSb Naomi Lawrence, MDa Justin J. Green, MDa Division of Dermatology, Department of Medicine Cooper Health System, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson at Camdena Drexel University, College of Medicine Philadelphiab Funding sources: None. Conflicts of interest: None identified.
Fig 2. Two months after treatment with dermabrasion, CO2 laser, and wire loop electrocautery.
literature, images of this variant are not often seen. This distinct variant of rosacea may be overlooked because of its rare nature and unusual presentation. We report an unusual case of gnatophyma presenting in a young woman without other associated phymas. A 31-year-old woman was referred by her primary care physician for evaluation of a growth on her chin that had begun about 10 years earlier (Fig 1). Physical examination was also remarkable for overall poor dentition, including numerous dental caries and tooth decay for which the patient refused a dental referral. A biopsy was performed, which confirmed a diagnosis of rosacea. Initial treatment over the course of 3 months with doxycycline, subsequently switched to minocycline because of reported nausea, and topical metronidazole resulted in no response, prompting us to opt for surgical intervention. Dermabrasion performed initially resulted in slight improvement in contour, followed by carbon dioxide laser therapy with wire loop electrocautery 2 months later to debulk the lesion (Fig 2). She initially had a good response to this treatment with decreased tissue bulk and surface nodularity, as well as improved contour, but detailed observation could not be performed because the patient was lost to follow up.
Correspondence to: Erum N. Ilyas, MD Cooper Health System, Robert Wood Johnson University of Medicine and Dentistry of New Jersey at Camden Department of Medicine, Division of Dermatology 1811 Bethlehem Pike, Suite A104 Flourtown, PA 19031 E-mail: [email protected] REFERENCE 1. Lesclous P, Maman L. An unusual case of a relationship between rosacea and dental foci. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999;88:679-82. doi:10.1016/j.jaad.2005.09.037
Intralesional triamcinolone in the management of lipodermatosclerosis To the Editor: Lipodermatosclerosis is a common but confusing marker of venous insufficiency that presents with pain, erythema, edema, and increasing induration. Numerous therapies have been studied, including low-, medium- or high-pressure compression therapy,1 stanozolol,2,3 surgical correction of venous disease,4 Daflon 500 mg,5 pentoxifylline,6 oxandrolone,7 and total triterpenic fraction of Centella asiatica.8 Randomized controlled trials have shown improvement in symptoms of patients receiving compression therapy and stanozolol.2,3 One case utilizing intralesional triamcinolone with compression therapy for the treatment of pain associated with lipodermatosclerosis has been previously reported.9
Letters 167
J AM ACAD DERMATOL VOLUME 55, NUMBER 1
Table I. Characteristics and response of patients treated with intralesional triamcinolone* Pain
Initial clinical findings 26/28 Improvement after 25/26 therapy (1-3 visits)
Erythema Edema Induration
22/28 19/22
13/28 8/13
27/28 23/27
*Data expressed as number of patients.
We report a case series of 28 patients based on chart review who received intralesional triamcinolone for the management of lipodermatosclerosis. Twenty-three women and 5 men, 20 to 77 years of age, were included. All patients were initially diagnosed clinically. Twenty-six of 28 patients complained of pain on presentation. Additional clinical findings are listed in Table I. Intralesional triamcinolone was the sole treatment in 3 patients and was followed by Unna boot (10 patients), Profore compression wrap (1), compression stocking (13), or SurePress wrap (1) in the remaining patients. The strength of triamcinolone injected was not standardized and recorded in only 22 patients. Eleven of these received a concentration of 5 mg/mL, and 10 received a concentration of 10 mg/mL. The total volume injected varied with the size and number of lesions. Pain was alleviated in 25 of 26 patients after one or two treatments. Induration improved in 23 of 27, as did edema in 8 of 13 patients and erythema in 19 of 22 patients. Although most patients responded initially, ongoing therapy was required, with 21 receiving additional triamcinolone injections (frequency varied) and 26 patients utilizing some form of compression. The rationale for the use of intralesional steroids is based on the pathogenic role of inflammation in lipodermatosclerosis, particularly in the early stage of the disease (Fig 1, A). Triamcinolone, a glucocorticoid, decreases inflammation by increasing the production of inhibitory protein Ikba. This molecule serves to bind nuclear factor kb dimers, key proteins in signal transduction, preventing them from being released from cells. The decrease in activity of nuclear factor kb precludes the transcription of several primary inflammatory cytokines, including interleukin 1b and tumor necrosis factor-a.10 Early use of intralesional steroids reduced pain in our patients and prevented the progression of disease to induration and the potential bottleneck deformity associated with late-stage lipodermatosclerosis (Fig 1, B) (personal observation, O. F. M.) Our current approach consists of weekly, biweekly, or monthly therapy depending on the extent of cutaneous induration and associated pain. At each
Fig 1. A, Acute lipodermatosclerosis. lipodermatosclerosis.
B,
Chronic
visit, 1 to 2 mL of triamcinolone (10 mg/mL) is injected into indurated areas with a 30-gauge needle in 0.2- to 0.3-mL aliquots at approximately 1.5-cm intervals. An Unna boot or a 20 to 30 mm Hg compression stocking is then applied. This chart reviewebased case series is limited by its retrospective nature and lack of systematized data recording. Cesarone et al8 used a numerical scale to quantify pain, redness, skin alterations, and edema. This may be a useful gauge for future studies. Further study should also take place in a randomized control trial so that compression alone can be compared with steroid injection alone and injection with compression. Lisa B. Campbell, MD O. Fred Miller, III, MD Geisinger Medical Center Danville, Pennsylvania These data presented at the 2005 Pennsylvania Academy of Dermatology meeting. Reprint requests: O. Fred Miller, III, MD Department of Dermatology Geisinger Medical Center 100 N Academy Ave, Danville, PA 17822 E-mail: [email protected]
REFERENCES 1. Gniadecka M, Karlsmark T, Bertran A. Removal of dermal edema with class I and II compression stockings in patients with lipodermatosclerosis. J Am Acad Dermatol 1998;39:966-70. 2. Burnand K, Clemenson G, Morland M, Jarrett PE, Browse NL. Venous lipodermatosclerosis: treatment by fibrinolytic enhancement and elastic compression. Br Med J 1980;280:7-11. 3. Browse NL, Jarrett PE, Morland M, Burnand K. Treatment of liposclerosis of the leg by fibrinolytic enhancement: a preliminary report. Br Med J 1977;2:434-5.
168 Letters
J AM ACAD DERMATOL JULY 2006
4. Valencia IC, Falabella A, Kirsner RS, Eaglstein WH. Chronic venous insufficiency and venous leg ulceration. J Am Acad Dermatol 2001;44:401-21. 5. Bergan JJ, Schmid-Schonbein GW, Takase S. Therapeutic approach to chronic venous insufficiency and its complications: place of Daflon 500 mg. Angiology 2001;52(Suppl 1): S43-7. 6. Goldman MP. The use of pentoxifylline in the treatment of systemic sclerosis and lipodermatosclerosis: a unifying hypothesis? J Am Acad Dermatol 1994;31:135-6. 7. Segal S, Cooper J, Bolognia J. Treatment of lipodermatosclerosis with oxandrolone in a patient with stanozolol-induced hepatotoxicity. J Am Acad Dermatol 2000;43:558-9. 8. Cesarone MR, Belcaro G, De Sanctis MT, Incandela I, Cacchio M, Bavera P, et al. Effects of the total triterpenic fraction of Centella asiatica in venous hypertensive microangiopathy: a prospective, placebo-controlled, randomized trial. Angiology 2001;52(Suppl):S15-8. 9. Lewis JE. Treatment of postphlebitic lipodermatosclerosis. South Med J 1990;83:1489-90. 10. Williams IR, Rich BE, Kupper TS. Cytokines. In: Freedberg IM, Eisen AZ, Wolff K, Austen KF, Goldsmith LA, Katz SI, editors. Fitzpatrick’s Dermatology in general medicine. 6th ed. New York: McGraw-Hill; 2003. pp. 286-8. doi:10.1016/j.jaad.2005.09.043
Efficacy of anti-IgE therapy in patients with atopic dermatitis To the Editor: Atopic dermatitis (AD) or eczema is often the first manifestation of atopy, with approximately 80% of children eventually developing food allergies, asthma, or allergic rhinitis (AR). Since the discovery of the IgE molecule, its role as a crucial immune mediator of allergic inflammation has come to light. Although its exact role in the pathogenesis of asthma is unclear, previous studies have shown a strong correlation between the severity of AD, serum IgE levels, and concomitant allergic rhinitis and/or bronchial asthma.1 Even in the absence of known food allergies, eczema patients often have elevated
specific and total serum IgE levels.2 Factors that influence IgE production include cytokines (like interleukins-4 and -13) and inflammatory cells that are present in the milieu. When antigen cross-links the specific IgE bound to the FceRI on mast cells and basophils, these cells initiate and amplify the inflammatory response in both the airways and atopic skin. In the skin, these events are responsible for the hallmark features that include erythema, papulation, lichenification, exudation, and crusting. Omalizumab is a chimeric monoclonal antibody that binds IgE at the same binding site as FceRI and FceRII, thereby inhibiting mast cell or basophil activation. Recent studies have demonstrated a significant benefit from anti-IgE in the treatment of both atopic asthma and allergic rhinitis by decreasing serum IgE levels, nasal symptoms,3 and bronchoconstriction during both the early and late-phase responses to inhaled allergen.4 These translate to a reduction of asthma-related symptoms, corticosteroid dose, and improvement in quality of life. Because of similarities in the immune mechanisms underlying asthma and AD, we decided to look at the effect of anti-IgE therapy on cutaneous symptoms of AD. We report on 7 AD patients (aged 7-58 yrs) who received anti-IgE treatment for their persistent asthma. All patients had history of asthma, AR, and eczema since early childhood (\3 yrs old) and a strong family history of atopy. They had positive skin tests or RAST for common aeroallergens and high IgE titers (226-2020 kU/L or IU/mL). Physician assessments at 3 and 7 months were used to generate eczema scores (ranked 0-5 in increasing order of severity) using the Global Assessment (IGA) scoring system.5 All patients received omalizumab calculated according to patient’s mass and baseline IgE titers per manufacturer’s nomogram. Those whose IgE
Table I. Patients’ baseline characteristics Pt 1
Pt 2
Pt 3
Pt 4
Pt 5
Pt 6
Pt 7
Age (yrs)/sex 7/F 13/F 24/F 38/M 38/F 43/F 58/F Atopic conditions PAR, AD PAR, AD PAR, AD PAR, AD PAR, AD PAR, AD PAR, AD Cat, dog, Cat, dog, DM, Cat, dog Dog, trees Cat, dog, DM Aeroallergen Cat, dog, DM, Cat, DM, sensitivity trees, weeds, trees, weeds, ragweed, and trees, molds, and grasses molds and grasses molds, and grasses IgE titer (kU/L) 1375 2020 784 967 545 1484 265 Omalizumab 375 mg 375 mg 375 mg 375 mg 375 mg 375 mg 300 mg dose SQ q2wk SQ q2wk SQ q2wk SQ q2wk SQ q2wk SQ q2wk SQ q2wk Start mo. of November December November October October September December therapy Eczema severity Moderate Moderate Moderate Moderate Severe Severe Mild IGA score 3 3 3 3 4 4 2 AD, Atopic dermatitis; DM, dust mite; IGA, Investigator Global Assessment; PAR, perennial allergic rhinitis; SAR, seasonal allergic rhinitis.