The patient is a 53‐year‐old white woman with a history of systemic lupus erythematosus, WHO class 3A lupus nephritis on mycophenolate and pred‐nisone 10 mg/day. Two months prior to presentation she developed multiple erythematous nodules on her lower extremities, diagnosed as lupus panniculitis by skin biopsy. Prednisone was increased to 40 mg/day. She presented to us with worsening skin lesions on her lower abdomen and legs. Physical examination revealed extensive sloughing of the abdominal wall with areas of induration in the suprapubic area and multiple erythematous nodules in her lower extremities. Initial wound cultures grew group B Streptococcus. Blood cultures were negative for bacteria or fungi. Chest radiograph demonstrated small bilateral pleural effusions. Treatment was initiated with intravenous antibiotics against group B Streptococcus with no improvement. Serum histoplasma antibody was positive for H and M bands. Urine histoplasma antigen was moderately positive at 15.5 ng/mL (Miravista diagnostics assay). HIV serology was negative. Repeat biopsy obtained from the right thigh showed prominent inflammatory infiltrate involving the reticular dermis consisting of histiocytes, neutrophils, and numerous intracellular organisms that stained positive with GMS stain with morphological features of histoplasma. Culture grew Histoplasma capsulatum. She was treated with liposomal amphotericin B for 4 weeks followed by itraconazole, with significant clinical and laboratory improvement.
Cutaneous histoplasmosis is a disseminated disease primarily seen in immunocompromised patients such as transplant recipients, AIDS patients, or patients on chronic corticosteroid therapy. It is a rare manifestation of a disease that is endemic in specific geographic regions of the world, mainly North and Central America. In the United States it is endemic in the Ohio and Mississippi river valleys and seen more frequently in the Midwestern states. Histoplasmosis is commonly seen as a pulmonary infection but can disseminate to have gastrointestinal, cutaneous, and central nervous system involvement. Diagnosis is made by identification of mycelial growth phase on tissue or body fluid cultures grown on Sabouraud's dextrose agar. Staining exudates from the lesions with Giemsa and Wright stains and staining of biopsies from the lesions with hematoxylin and eosin and periodic‐acid–Schiff stains are diagnostic. Serum and urine Histoplasma antigen detection assays are more useful for diagnosis in disseminated cases. Disseminated histoplasmosis warrants therapy with antifun‐gal agents such as amphotericin B, liposomal amphotericin B, amphotericin B lipid complex, and itraconazole. Mortality is high at 95% in untreated cases.
A high degree of suspicion for Histoplasma capsulatum infection is needed in immunocompromised patients even in the absence of pulmonary signs and symptoms. This is especially important in the Midwestern region, where Histoplasma is highly endemic.
S. Hublikar ‐ none; P. Velagapudi ‐ none; M. Turagam ‐ none; S. Sundaram ‐none
To cite this abstract:Hublikar S, Velagapudi P, Turagam M, Sundaram S. Primary Cutaneous Histoplasmosis Masquerading As Lupus Panniculitis. Abstract published at Hospital Medicine 2011, May 10-13, Dallas, Texas. Abstract 297. Journal of Hospital Medicine. 2011; 6 (suppl 2). https://www.shmabstracts.com/abstract/primary-cutaneous-histoplasmosis-masquerading-as-lupus-panniculitis/. Accessed January 17, 2020.