Hyperpigmentation associated with intradermal tranexamic acid injections for treatment of melasma

Hyperpigmentation associated with intradermal tranexamic acid injections for treatment of melasma

P6784 P6797 Granulomatous variant of scleromyxedema mimicking a drug reaction Julia Shlyankevich, University of Washington School of Medicine, Seatt...

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P6784

P6797

Granulomatous variant of scleromyxedema mimicking a drug reaction Julia Shlyankevich, University of Washington School of Medicine, Seattle, WA, United States; Evan George, MD, University of Washington Medicine Department of Pathology, Seattle, WA, United States; Galina Stetsenko, MD, University of Washington Medicine Department of Medicine, Division of Dermatology, Seattle, WA, United States; Jay Vary, Jr., MD, PhD, University of Washington Medicine Department of Pathology, Seattle, WA, United States

Hyperpigmentation associated with intradermal tranexamic acid injections for treatment of melasma Richard Jamison, MD, Scott and White Healthcare; The Texas A&M Health Science Center College of Medicine, Temple, TX, United States; John Greene, Jr, MD, Scott and White Healthcare; The Texas A&M Health Science Center College of Medicine, Temple, TX, United States; Palak Parekh, MD, Scott and White Healthcare; The Texas A&M Health Science Center College of Medicine, Temple, TX, United States Melasma is a relatively common pigmentary disorder that remains a difficult condition to treat. A newer therapy that was initially reported in 2006 described intradermal injection of tranexamic acid as a promising approach for treatment of melasma. We report the first known case of melasma treated with intradermal tranexamic acid that resulted in disfiguring hyperpigmentation. Histologic evaluation of this case revealed a dual staining pattern of melanin and iron. We conclude this is a result of drug metabolite-protein-iron complexes similar to that seen in type II minocycline hyperpigmentation. Clinicians should be aware of the possible paradoxical hyperpigmentation that may occur with intradermal tranexamic acid injection for the treatment of melasma.

Scleromyxedema is a rare and progressive disease characterized by generalized waxy papules and skin induration. Cardinal histologic features include increased stellate fibroblasts, thickened collagen and mucin deposition. We present a case of a 54-year-old man with an erythematous, pruritic rash of 3 months duration, involving the face, upper extremities, and torso originally thought to be due to a drug eruption after the initiation of allopurinol. After discontinuation of this medication, his eruption persisted and worsened. On presentation to our clinic, the patient reported a 4-month history of skin redness and tightening as well as papules on the forehead, neck, back, torso, and arms. He endorsed a decreased ability to open his mouth because of stiffness of the skin, intermittent swelling of the abdomen, difficulty breathing, and hand and finger swelling. His medical history was significant for Crohn’s disease in remission, hypertension, and Graves disease status postablation on thyroid replacement. Physical examination revealed exaggerated wrinkling of the glabella, indurated skin on the sides of the nose, upper back and shoulders, and numerous 2- to 3-mm waxy papules diffusely scattered over the upper shoulders. Histologic examination of the lesional skin revealed increased deposition of collagen fibers, increased numbers of histiocytes with epithelioid and spindled cytology and dermal mucin deposits along with sparse perivascular lymphocytic inflammation. Laboratory evaluation was significant for monoclonal IgG and IgA lambda gammopathy on serum electrophoresis. Clinical findings of scleromyxedema with histologic findings of interstitial granulomatous changes with dermal mucinosis and monoclonal gammopathy fit best with a diagnosis of the granulomatous variant of scleromyxedema. The patient was initiated on lenalidomide and dexamethasone, as similar therapies directed at an underlying gammopathy have shown efficacy in patients with scleromyxedema. Although exceedingly rare, the findings in our patient lend further support to the existence of a granulomatous scleromyxedema variant and this diagnosis should be considered when faced with similar clinical and histologic findings.

Commercial support: None identified.

Commercial support: None identified.

P6989 Histiocytoid Sweet syndrome in a patient with myelofibrosis dominant myelodysplastic syndrome Sue May Ang, MBBS, Sheffield Teaching Hospital, Sheffield, United Kingdom; C. B. Chong, Chesterfield Royal Hospital, Calow, United Kingdom; Danesh Taraporewalla, Chesterfield Royal Hospital, Calow, United Kingdom; Robert Cutting, Chesterfield Royal Hospital, Derbyshire, United Kingdom; Vinod Elangasinghe, Chesterfield Royal Hospital, Derbyshire, United Kingdom We report a case of MDS-associated HSS in a 72-year-old man. He presented with an 8-year history of a progressive generalised rash that has only responded to intermittent oral steroids. This asymptomatic rash can be described as a mixture of multiple, urticated, erythematous purplish pink and oval shaped nodules (new lesions) and pinkish brown pigmented oval macules (old lesions). They were diffusely distributed all over his body and the macular lesions failed to demonstrate the Darier sign. He had no lymphadenopathy or hepatosplenomegaly. The diagnosis of myelofibrosis dominant MDS was made 10 years ago as an incidental finding when he was investigated for angina. His MDS had been managed with blood transfusions because of lethargy and weakness. Few years ago when he had presented with a less prominent rash it had been treated as Jessner lymphocytic infiltrate because of the inconclusive biopsy findings. The Sweetoid clinical appearance at presentation to us prompted a repeat biopsy. Histology showed a dermal infiltrate of ‘‘histiocyte looking’’ cells that stained CD68 and myeloperoxidase (MPO) but not S100. With the characteristic rash, histology and underlying MDS our patient met the criteria for the diagnosis of HSS. HSS is believed to be a variant of SS. Purplish pink juicy nodules and plaques are the characteristic feature of SS whereas urtication is the key differentiating feature in lesions of HSS. This is further supported by histology as the dermal infiltrate in SS is made up of mature neutrophils whereas CD68, MPO staining histiocytes form the bulk of the infiltrate in HSS. HSS has been reported in association with MDS and myeloproliferative disorders. Treatment of the underlying hematologic malignancy resolved the rash in most cases. Rare cases of HSS with MDS/MPD linking to Bortezomib, cryofibrinogenemia and pseudotumor/myxoma have been reported. Our patient has had few episodes of cutaneous vasculitis, had been on warfarin followed by scenocoumarol for AF for 6 to 7 years and had presented to the urologist for suspected Peyronie disease of his penis last year. The significance of these clinical elements in our case can be linked to the previous case reports but needs further understanding of this haematological phenomenon which may be linked to a possible B cell dyscrasia. This case highlights key clinical features of rare HSS and provides new insights into its aetiopathogenesis. Commercial support: None identified.

AB86

J AM ACAD DERMATOL

P6355 Immunohistochemical staining in cutaneous marginal zone B-cell lymphoma Stephanie Frisch, MD, Saint Louis University, Saint Louis, MO, United States; Claudia Vidal, MD, PhD, Saint Louis University Department of Dermatology, Saint Louis, MO, United States; Eric Armbrecht, PhD, Saint Louis University, Saint Louis, MO, United States; Yadira Hurley, MD, CAE, Saint Louis University Department of Dermatology, Saint Louis, MO, United States Background: Cutaneous marginal zone B-cell lymphomas share histopathologic and immunophenotypic characteristics with splenic and nodal marginal zone B cell lymphomas. CD43 in particular has been studied in cutaneous, splenic, and nodal marginal zone B cell lymphomas and its positivity in skin has been suggestive of malignancy. Staining of CD43 in all types is variable, some reporting about 50%. CD23 and CD30 have rarely been studied in cutaneous marginal zone B-cell lymphomas. Objective: We sought to compare immunohistochemical markers seen in splenic and nodal types of marginal zone B-cell lymphoma with cutaneous marginal zone Bcell lymphoma as well as evaluate CD30 positivity. Methods: We performed a retrospective chart review of our computerized dermatopathology lab data base searching for all reports with ‘‘marginal zone lymphoma.’’ Cutaneous marginal zone B cell lymphoma cases that were available for additional staining were collected and if not already done CD23, CD30, and CD43 were performed. Results: Of the cases queried, 8 cases were identified as marginal zone B-cell lymphoma available for additional staining. Two dermatopathologists reviewed the cases for consistency. Of the 8 cases, 7 were partial (10-50%) or completely positive ([50%) for CD43. All 8 cases were negative for CD30. CD23 was negative in 3 cases, partially positive in 2 cases, and completely positive in 3 cases. Limitations: We evaluated only 8 cases of this entity. The result of immunohistochemical stains may be affected by deeper tissue sectioning. It is difficult to evaluate the significance of partial positive staining. Conclusion: Variable CD43 staining in the skin is consistent with spleen and lymph node types as well as other reports of cutaneous marginal zone B-cell lymphomas. CD30 is negative in all cases. There is no clear trend or pattern with CD23 staining. Commercial support: None identified.

APRIL 2013