Kazuma Ishikawa

Spontaneous cholesterol crystal embolism to lymph node

A 65-year-old male diagnosed with hypertension and hypertrophic cardiomyopathy in April 2010 at a different hospital was administered angiotensin II receptor blocker and low-dose aspirin. Although laboratory data at that time showed eosinophilia (2,860/lL), further examination was not performed. He had a history of smoking 1.5 packs of cigarettes a day for 45 years, but no history of diabetes mellitus. He developed cerebral infarction in January 2012, but recovered uneventfully with conservative treatment, including statins for dyslipidemia. He was subsequently referred to our hospital to investigate the eosinophilia. On physical examination, he had several swollen lymph nodes in bilateral inguinal regions, but no cutaneous lesion was observed. Laboratory data were as follows: WBC 10,600/ lL, eosinophil 840/lL, Hb 11.2 g/dL, Plt 8.8 9 10/lL, FDP 12.0 lg/mL, LDH 352 U/L, BUN 17.5 mg/dL, Cr 1.00 mg/dL, IgE 8,600 IU/mL, ACTH 15.3 pg/mL and cortisol 9.4 lg/dL, as well as negative test results for ANA and MPO-ANCA. The urinalysis showed proteinuria and microhematuria. Parasite eggs were not detected in the feces. Bone marrow examination showed 9.1 % eosinophils among all nucleated cells without dysplasia, and FIP1L1-PDGFRa and BCR-ABL chromosomal aberrations were not detected by FISH analysis. Chest and abdominal CT showed several enlarged inguinal lymph nodes up to 18 mm in the minor axis. Although he stated that he had recognized these inguinal masses about 10 years previously and that they had not changed markedly in size, we performed biopsy from the right inguinal lymph node. Histopathological findings revealed needle-shaped clefts in the lumen of arterioles with multinucleated giant cell infiltration surrounded by normal lymphoid follicles (Fig. 1a–c). Perivascular inflammatory cell infiltration, mainly of eosinophils, was also observed. Flow cytometric analysis of lymph node showed no abnormality. The diagnosis of cholesterol crystal embolism (CCE) to lymph node was made. As he presented no other clinical manifestations of CCE, no further therapeutic intervention was performed. CCE is a rare systemic disease caused by occlusion of small arteries by cholesterol crystals released from atheromatous plaques of the aorta or major branches. Chest CT in this patient also showed calcification and wall thickness of the thoracic aorta, which can be a source of cholesterol crystals (Fig. 2). The common manifestations of CCE are characteristic skin lesions, such as livedo reticularis, cyanosis or ulceration, renal impairment, and gastrointestinal disorder. CCE involvement of lymph node is extremely rare. Only a few preand postmortem cases of CCE to lymph node have been reported to date [1, 2]. CCE usually occurs following an invasive vascular procedure, or anticoagulant or thrombolytic therapy, but it can also occur spontaneously. We surmised that the CCE in this patient was spontaneous, as he had not undergone any such intervention during this clinical course. The exact time at which the CCE developed was unclear, but pathological findings of lymph nodes showing CCE with giant cell infiltration and no signs of fibrosis suggested that it had been a relatively recent event. Hence, we suspect that the A. Fujimi (&) A. Hashimoto Y. Kanisawa Department of Hematology and Oncology, Oji General Hospital, 3-4-8 Wakakusa-cho, Tomakomai 053-8506, Japan e-mail: Akihito.fujimi@ojihosp.or.jp

Hepatitis C virus reactivation due to antiemetic steroid therapy during treatment of hepatocellular carcinoma

Hepatitis C virus (HCV) reactivation is relatively rare compared with hepatitis B reactivation in patients treated with immunosuppressive or anticancer drugs. Here, we present the first case of genotype 2 HCV reactivation due to antiemetic steroid therapy during chemotherapy for hepatocellular carcinoma (HCC), which was verified by not only increased viral load but also pathological exacerbation of liver injury during HCV reactivation. Further chemotherapy for HCC could be continued without steroid therapy. This present case highlights the awareness of HCV reactivation and the management of complex situation.

Cases of primary malignant melanoma and melanocytosis of the esophagus observed by magnifying endoscopy: Application to differential diagnosis

Rationale: Primary malignant melanoma of the esophagus (PMME) is a rare disease with an extremely poor prognosis. In contrast, melanocytosis is a benign condition defined as melanocytic proliferation with melanin deposition. PMME is often accompanied by melanocytosis, but differentiating between them is difficult because of their similar appearance. Patient concerns: Here, we reported 3 PMME cases, 2 with melanocytosis. Diagnoses: Magnifying endoscopy revealed characteristic non-uniform pigmented spots along deformed intrapapillary capillary loops (IPCLs) in PMME, while melanocytosis showed fine granule-like or linearly arranged spots and intact IPCLs. Interventions: The patients underwent endoscopic or surgical resection of each lesion. Outcomes: Histologically, magnified images reflected melanocyte growth. For cases 1 and 2, the patients remained disease-free for 61 and 15 months after endoscopic resection, respectively. In case 3, liver metastases developed two months after surgery, and the patient died from liver failure after six months. Lessons: This is the first report describing differences in magnified views of the 2 diseases, which aids a differential diagnosis.