genavence. was also elevated to 12.32 mg/dL. Computed tomography (CT) revealed consolidation in the inferior lobe of the left lung, hepatosplenomegaly, and multiple lymphadenopathies. Biopsies were performed in the cervical lymph nodes, liver, and lungs, but only nonspecific infiltration of inflammatory cells was observed. He was treated with 20 mg prednisolone (PSL) for suspected systemic autoimmune disease. Four months later, he noticed swelling around the dorsal skin of the left hand and was treated with antibiotics for the diagnosis of cellulitis at another hospital. He was also suspected of having hepatobiliary disease because of the elevated hepatobiliary enzyme level, leukocytosis [white blood cell (WBC) count 24,000 /L], and high serum CRP level (16.55 mg/dL), but there were no findings suggesting contamination or tumor in his gallbladder. Although high serum levels of soluble IL-2 receptor (13,400 U/mL) and multiple lymphadenopathies were observed, there were no findings of malignancy in the cervical lymph node biopsy. On admission to our department, physical examination revealed significant tabescence, skin pigmentation, and edema of the lower extremities. He also had swelling of the axillary lymph nodes and knee joint pain. He had no abdominal symptoms or numbness. His blood pressure was 112/66 mmHg, pulse was 98/min, heat was 36.4C, and O2 saturation was 96% on ambient air. Laboratory data revealed increased levels of serum CRP, erythrocyte sedimentation rate, WBCs (especially neutrophils), and elevated ALP and soluble IL-2 receptor levels (Table 1). He had anemia, but his mean corpuscular volume and haptoglobin levels were within the respective normal ranges. Total protein and albumin levels were low, his renal function was normal, and the brain natriuretic peptide level was slightly increased. Serum M protein (IgG- type Bence Jones protein) was also detected. We also examined the possibility of infectious diseases, including hepatitis B, hepatitis C, Epstein-Barr computer virus, HIV, human T-cell leukemia computer virus type 1, and tuberculosis, but all were negative. Table 1. Laboratory Mouse monoclonal to SYP Data on Admission. was identified from cultures of both gastric juice and subcutaneous abscesses using the EPZ004777 DNA-DNA hybridization method. Susceptibility testing using the broth microdilution method (BrothMIC NTM; Kyokuto, Tokyo, Japan) revealed that the minimum inhibitory concentrations for the drugs were as follows: rifampicin, 0.125 g/mL; levofroxacin, 0.25 g/mL; clarithromycin, 0.125 g/mL; and ethambutol, 1 g/mL. We diagnosed the patient with DNTM caused by complexFever, back pain, joint pain, myalgia, lung lesion, mediastinal lymphadenopathyRFP/EB/CAM/LVFX+drainageImproved(23)374/WNone complexFever, weight loss, lumbago, hepatosplenomegaly, edema, osteolytic lesionRFP/EB/CAM/STFX+RTXImproved(26)679/WNone was detected in the gastric juice and subcutaneous tissue. accounts for approximately EPZ004777 4% of nontuberculous mycobacterial disease cases in Japan (12). Many of the patients affected byM. kansasiiare middle-aged, and some background diseases, such as chronic obstructive lung disease and malignancy, are reported as risk factors (13). Aoki et al. reported that there were many cases of seropositivity for anti-IFN- neutralizing antibodies in DNTM in Japan, EPZ004777 the majority of which were caused by complex (70.3%), and only 1 1 of 31 cases was caused by (2.7%) (14). While skin lesions caused by are prone to manifest as raised lesions and ulcers in immune-responsive patients, there are reports of diffuse cellulitis and seroma in immunocompromised patients (15,16). In the current case, the skin lesions showed cellulitis and abscesses with a highly viscous milky white fluid, similar to those of immunocompromised patients with DNTM. The standard treatment regimen for DNTM is the same as that forM. kansasiipulmonary contamination, which includes isoniazid (300 mg/day), rifampicin (600 mg/day), and ethambutol (15 mg/kg/day), according to the official statement of.