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Myelodysplastic syndrome presenting as sarcoidosis

Dear Editor, A 64-year-old Caucasian woman presented to the clinic with intractable pruritus of her trunk and extremities for the previous 2 weeks. There was no associated rash. She experienced minimal improvement with antihistamines. She also reported an erythematous, indurated nodule on her right tibial region. She recently had a similar lesion on her left tibial area that spontaneously resolved. She was seen in consultation and sarcoidosis was highly suspected because of presumed erythema nodosum and persistent pruritis. An initial chest radiograph and angiotensin-converting enzyme (ACE) levels were normal, but computed tomography (CT) scan of the chest revealed multiple pulmonary nodules and both hilar and mediastinal lymphadenopathy. Subsequent mediastinoscopy and lymph node biopsy showed non-necrotizing granulomatous inflammation (Fig. 1a) consistent with sarcoidosis. Pulmonary function tests indicated a restrictive disease pattern. Three months after initial presentation, she developed acute unilateral iritis, further supportive of a diagnosis of sarcoidosis. She was started on a 6 week taper of oral steroids for pulmonary and ocular sarcoidosis, with plans for close clinical follow-up. The following month, she presented to the emergency department with 2 weeks of progressively worsening headaches. CT scan of the head did not reveal acute intracranial abnormalities, but magnetic resonance imaging (MRI) of the brain showed diffuse replacement of marrow fat, indicative of hematologic neoplasm or myelophthisic process. Complete blood count revealed new onset cytopenias, with a hemoglobin of 9.3 g/dL and platelets of 78 k/mcL. Bone marrow aspirate and biopsy revealed a hypercellular bone marrow (75% cellularity) with dyserythropoeisis and megakaryocytic atypia (Fig. 1b). An increase in immature blasts (8%) was noted (Fig. 1c). No granulomatous inflammation was seen. Cytogenetics revealed a complex karyotype with multiple chromosomal abnormalities, including del(5q), t(7;12), t(12,19), monosomy 3, monosomy 6 and monosomy 12. She was diagnosed with myelodysplastic syndrome refractory anemia with excess blasts (RAEB-1). Her international prognostic scoring system (IPSS) risk assessment score was 2, correlating with a median survival of 1.2 years. She completed 6 cycles of azacitidine, resulting in correction of peripheral blood counts. Repeat bone marrow biopsy no longer showed dysplastic features. She proceeded to matched unrelated donor allogeneic peripheral stem cell transplantation. Unfortunately, despite rapid engraftment, she relapsed on post-transplant day 70 and died due to progressive myelodysplasia on post-transplant day 105. Although non-caseating granulomata are a typical histopathologic finding of sarcoidosis, their development has also been observed in association with malignant disease. Granuloma formation has been seen with lymphoproliferative diseases and acute myeloid leukemia. Association with myelodysplastic syndrome is reported, but rare. Recognition of malignancy-related sarcoidosis often precedes diagnosis of the associated malignancy. However, the temporal relationship between the two conditions is difficult to ascertain, as both can remain asymptomatic for prolonged periods of time. The connection between sarcoidosis and malignancy remains uncertain. One hypothesis is that the impaired T-cell response associated with granuloma formation in