論文

We report a case of recurrent disseminated Mycobacterium avium complex (DMAC) disease with anti-gamma interferon autoantibodies. To our knowledge, this is the first reported case caused by reinfection with a separate isolate of M. avium. DMAC disease activity was monitored using serum IgG antibody titers against lipid antigens extracted from a MAC strain.

BACKGROUND: Pulmonary nocardiosis frequently occurs in immunocompromised hosts and in some immunocompetent hosts with chronic lung disease; however, few reports have described pulmonary nocardiosis with nontuberculous mycobacterial lung infection. Here we report for the first time two cases of pulmonary nocardiosis caused by Nocardia cyriacigeorgica associated with Mycobacterium avium complex (MAC) lung disease caused by M. avium.CASE PRESENTATION: Case 1 is that of a 72-year-old Japanese man with untreated MAC lung disease, who was diagnosed with rheumatoid arthritis and initiated on methotrexate. After 3 years of methotrexate therapy, the patient remained smear-negative and culture-positive for MAC, but also became smear-positive for Nocardia species. He received trimethoprim/sulfamethoxazole, and his symptoms and lung infiltrates improved. Case 2 is that of an immunocompetent 53-year-old Japanese woman with MAC lung disease, who was treated with a combined therapy of clarithromycin, rifampicin, ethambutol, and levofloxacin. MAC sputum culture was negative after 1 year of combined treatment, which was maintained for 2 years. After four treatment-free years, Nocardia species were occasionally isolated from her sputum, although MAC was rarely isolated from sputum cultures over the same period. In both cases, the Nocardia species were identified as the recently defined N. cyriacigeorgica by 16S ribosomal RNA gene sequencing.CONCLUSION: We report two cases of pulmonary nocardiosis caused by N. cyriacigeorgica associated with MAC lung disease caused by M. avium and suggest that N. cyriacigeorgica may be a major infective agent associated with MAC lung disease.

Prostaglandin E2 (PGE2) is an important biological mediator involved in the defense against Mycobacterium tuberculosis (Mtb) infection. Previously, we reported that in macrophages (Mφs), infection with avirulent Mtb H37Ra resulted in inhibition of necrosis by an inhibitory effect on mitochondrial permeability transition via the PGE2 receptor EP2. However, human Mφs also express EP4, a PGE2 receptor functionally closely related to EP2 that also couples to stimulatory guanine nucleotide binding protein, but the functional differences between EP2 and EP4 in Mtb-infected Mφs have been unclear. EP4 antagonist addition to H37Rainfected Mφs inhibited the expression of cyclooxygenase 2 (COX2) and microsomal prostaglandin E synthase- 1 (mPGES-1), which are involved in PGE2 production. Moreover, H37Ra infection induced PGE2 production through the Toll-like receptor (TLR) 2/p38 mitogen-activated protein kinase (MAPK) signaling pathway. Induction of COX2 and mPGES-1 expression by TLR2 stimulation or Mtb infection was increased after additional stimulation with EP4 agonist. Hence, in Mtb-infected Mφs, PGE2 production induced by pathogen recognition receptors/p38 MAPK signaling is upregulated by EP4-triggered signaling to maintain an effective PGE2 concentration.-Nishimura, T., Zhao, X., Gan, H., Koyasu, S., and Remold, H. G. The prostaglandin E 2 receptor EP4 is integral to a positive feedback loop for prostaglandin E2 production in human macrophages infected with Mycobacterium tuberculosis.

In vivo control of Mycobacterium tuberculosis reflects the balance between host immunity and bacterial evasion strategies. Effector Th1 cells that mediate protective immunity by depriving the bacterium of its intracellular niche are regulated to prevent overexuberant inflammation. One key immunoregulatory molecule is Tim3. Although Tim3 is generally recognized to down-regulate Th1 responses, we recently described that its interaction with Galectin-9 expressed by M. tuberculosis-infected macrophages stimulates IL-1β secretion, which is essential for survival in the mouse model. Why IL-1β is required for host resistance to M. tuberculosis infection is unknown. In this article, we show that IL-1β directly kills M. tuberculosis in murine and human macrophages and does so through the recruitment of other antimicrobial effector molecules. IL-1β directly augments TNF signaling in macrophages through the upregulation of TNF secretion and TNFR1 cell surface expression, and results in activation of caspase-3. Thus, IL-1β and downstream TNF production lead to caspase-dependent restriction of intracellular M. tuberculosis growth.

Two different forms of death are commonly observed when Mycobacterium tuberculosis (Mtb)-infected macrophages die: (i) necrosis, a death modality defined by cell lysis and (ii) apoptosis, a form of death that maintains an intact plasma membrane. Necrosis is a mechanism used by bacteria to exit the macrophage, evade host defenses, and spread. In contrast, apoptosis of infected macrophages is associated with diminished pathogen viability. Apoptosis occurs when tumor necrosis factor activates the extrinsic death domain pathway, leading to caspase-8 activation. In addition, mitochondrial outer membrane permeabilization leading to activation of the intrinsic apoptotic pathway is required. Both pathways lead to caspase-3 activation, which results in apoptosis. We have recently demonstrated that during mycobacterial infection, cell death is regulated by the eicosanoids, prostaglandin E 2 (proapoptotic) and lipoxin (LX)A 4 (pronecrotic). Although PGE 2 protects against necrosis, virulent Mtb induces LXA 4 and inhibits PGE 2 production. Under such conditions, mitochondrial inner membrane damage leads to macrophage necrosis. Thus, virulent Mtb subverts eicosanoid regulation of cell death to foil innate defense mechanisms of the macrophage.

Background: Patients with Mycobacterium avium-intracellulare complex (MAC) pulmonary disease often suffer from weight loss. Adipokines are factors secreted by adipocytes, including leptin and adiponectin, as well as some inflammatory cytokines, tumor necrosis factor-α (TNF-α) and interleukin 6 (IL-6). Body mass index (BMI) is known to be inversely correlated with adiponectin and positively with leptin, TNF-α, and IL-6. Objective: We aimed to evaluate the levels of serum adipokines, including adiponectin, leptin, TNF-α, and IL-6 in patients with MAC pulmonary disease. Methods: Forty consecutive patients with MAC pulmonary disease (8 males; median age 62 years; median BMI 18.1) were examined. Serum levels of adiponectin, leptin, TNF-α, and IL-6 were measured with ELISA. Age-, sex- and BMI-matched healthy subjects served as controls. Results: Serum adiponectin was significantly elevated in patients with MAC pulmonary disease compared with the controls (p < 0.01). In both the patients and controls, serum adiponectin levels were inversely correlated with BMI (p < 0.05). No significant correlation was observed between serum adiponectin levels and C-reactive protein or lung function. Serum leptin levels, which were positively correlated with BMI, did not differ between patients and controls. Serum levels of TNF-α and IL-6 were significantly greater in patients with MAC pulmonary disease than in controls. The levels of TNF-α and IL-6 were not correlated with BMI and other adipokines examined. Conclusion: The results of the present study indicate that, in patients with MAC pulmonary disease, adiponectin is inappropriately secreted and may play a role in the pathophysiology of the disease.

Background: The objective of this study was to find an optimal initial combination chemotherapy that includes clarithromycin (CAM) for treatment-naive patients with Mycobacterium avium complex (MAC) pulmonary disease, as assessed by microbiological conversion using a Mycobacterium growth indicator tube (MGIT). Methods: Thirty-four patients with treatment-naive MAC pulmonary disease (determined using 1997 American Thoracic Society criteria) were evaluated retrospectively. They demonstrated a nodular and bronchiectatic pattern without cavity on high-resolution CT (HRCT) scans. The following three regimens were administered: regimen A (n = 9) consisted of CAM (400 mg/d), ethambutol (EB) [750 mg/d], and rifampicin (RFP) [450 mg/d]; regimen B (n = 12) consisted of CAM (800 mg/d), EB (750 mg/d), and RFP (450 mg/d); and regimen C (n = 13) consisted of CAM (800 mg/d), EB (1,000 mg/d), and RFP (600 mg/d) during the first 2 months followed by a reduction of the dosage of EB from 1,000 to 750 mg/d. Gender, age, BMI, and HRCT scan finding scores were not significantly different among the three groups. Chemotherapy was continued for 18 months. Sputum culture was periodically assessed by MGIT. Results: Culture conversion at 18 months in regimen A (55.6%), which included a daily dosage of 400 mg of CAM (9.5 mg/kg), was significantly inferior to that in regimen B (91.7%), which included daily 800 mg of CAM (17.6 mg/kg; p < 0.05), but regimen B and C (92.3%) showed no between-group difference after > 18 months of chemotherapy. Conclusions: The higher dose of CAM allowed for better culture conversion. Daily combination chemotherapy that includes CAM (800 mg) seems appropriate as an initial treatment against treatment-naive patients with nodular and bronchiectatic MAC pulmonary disease.

We studied the effects of TNF-converting enzyme inhibition with Y-41654, which down-regulates the production of soluble TNF-α (sTNF-α), on acute lung injury induced by intratracheal administration of LPS. We first verified in vitro that pretreatment of isolated alveolar macrophages from Sprague-Dawley male rats with 20 μL of 0.1-mM Y-41654, decreased significantly (P < 0.05) the concentration of sTNF-α in cell supernatants induced by 10 μg/mL of LPS. We then studied four groups of rats (each n = 10) including 1) a control group, 2) an LPS group (300 μg /kg, instilled intratracheally), 3) a Y-41654 group, and 4) a treatment group treated with Y-41654 after LPS instillation. Y-41654, 10 mg/kg in 0.7 mL of phosphate-buffered saline, was administered (i.v.), 15 min before and 0.5, 1.5, 2.5, and 3.5 h after saline or LPS instillation. The animals were observed for 4 h. In the animals treated with Y-41654, the concentrations of sTNF-α and protein in bronchoalveolar lavage fluid, and the number of neutrophils in lung tissue and bronchoalveolar lavage fluid were significantly lower at 4 h than in the LPS group (P < 0.05). In conclusion, sTNF-α plays an important role in the development of acute lung injury induced by intratracheal administration of LPS, in part modulating neutrophil kinetics.

Background. Although the incidence of pulmonary tuberculosis is decreasing, the number of immunocompetent patients with Mycobacterium avium complex (MAC) pulmonary disease is steadily increasing. Therefore, albeit not contagious, MAC pulmonary disease needs to be diagnosed rapidly and accurately. We examined the serodiagnostic contributions of serum immunoglobulin G antibody titers against the species-specific and -common mycobacterial lipid antigens in the diagnosis of MAC pulmonary disease. Methods. Serum samples were obtained from 65 patients with MAC pulmonary disease, 15 patients with suspected MAC disease, 25 patients with pulmonary tuberculosis, 10 patients with Mycobacterium kansasii disease, and 100 healthy volunteers (control subjects). We measured the serum immunoglobulin G antibody titers against trehalose monomycolate (TMM-M) and apolar-glycopeptidolipid (GPL), lipid antigens extracted from MAC. Results. In patients with MAC pulmonary disease, the antibody titers against TMM-M and apolar-GPL were significantly higher than those in the other patient groups or in the control subjects. By receiver operator characteristic curve analysis, an optical density of 0.27, corresponding to the optimal cutoff antibody titer against TMM-M, was associated with a sensitivity of 89.2% and a specificity of 97.0%, and an optical density of 0.33, corresponding to the optimal cutoff antibody titer against apolar-GPL, was associated with a sensitivity of 89.2% and a specificity of 94.0%. Conclusions. Measurements of antibody titers against TMM-M and apolar-GPL would be useful in the diagnosis of MAC pulmonary disease and in the differential diagnosis of mycobacterial pulmonary disease.

Objectives: Clarithromycin (CAM) is widely accepted for the treatment of Mycobacterium avium complex (MAC) pulmonary diseases. This study measured (a) the concentrations of CAM and its active metabolite (14OH-CAM) in bronchial epithelial lining fluid (ELF) obtained by bronchoscopic microsampling (BMS), and (b) the minimal inhibitory concentrations (MIC) of CAM for each MAC isolate. Methods: We studied eight patients with MAC pulmonary disease treated with oral CAM, 400 (n = 4) or 800 (n = 4) mg/day. BMS was performed 3 h after the last CAM dose, and the concentrations of CAM and 14OH-CAM were measured in ELF collected from the diseased and normal contralateral pulmonary segments, and in serum. Results: The mean ± SEM ELF concentrations of CAM (23.85 ± 7.64 μg/ml) and CAM + 14OH-CAM (28.71 ± 8.37 μg/ml) in the 800 mg/day treatment group were significantly higher than in the 400 mg/day group (7.48 ± 2.58 μg/ml and 9.63 ± 2.99 μg/ml, respectively; both p < 0.05), while the serum concentrations were similar in both groups. In both treatment groups, the mean ELF concentrations sampled from diseased and normal segments were higher than the MIC against MAC isolates. The mean ELF concentration of CAM in the 400 mg/day treatment group was <8 μg/ml (the breakpoint concentration of CAM against M. avium recommended by the Clinical Laboratories Standards Institute), while the mean concentration in the 800 mg/day treatment group was >8 μg/ml. Conclusion: These observations suggest that CAM, 800 mg/day, is an appropriate dose to treat MAC pulmonary disease, and prevent its spread from diseased to non-diseased lung segments.

Background: A new bronchoscopic microsampling (BMS) probe has recently been developed, which allows the minimally invasivecollection of epithelial lining fluid (ELF) simultaneously from multiple sites. While the number of immunocompetent patients with pulmonary Mycobacterium avium complex(MAC) disease is growing, the precise pathogenesis of the disease remains to be clarified. Objectives: This study aimed to measure biochemical markers in the ELF of patients with pulmonary MAC disease using BMS. Methods: We studied 8 healthy volunteers (controls) and 8 patients with pulmonary MAC disease. In the patients, ELF was collected from visibly abnormal (involved) and normal (uninvolved) sites using high-resolution computed tomography (HRCT). Results: The concentration of IFN-γ (means ± SEM) was significantly higher in patient ELF sampled from involved (26.62 ± 9.66 pg/ml) than from uninvolved sites (5.33 ± 1.44 pg/ml; p < 0.05) or from normal controls (<1.56 pg/ml; p < 0.05). In most patients, there was no difference in IFN-γ concentrations between the involved and uninvolved sites. The concentration of KL-6 in ELF was significantly higher in the involved (793 ± 108 U/ml) than in the uninvolved sites (192 ± 43 U/ml;p < 0.05) or in normal controls (186 ± 38 U/ml;p < 0.05). Conclusions: The specific inflammatory reaction caused by MAC infection might not be limited to sites that were visibly abnormal on HRCT. Although further improvement has to be considered, BMS may help to increase the understanding of the pathogenesis of various respiratory disorders.

OBJECTIVE: To examine the performance of an interferon-gamma (IFN-γ) release assay (QuantiFERON-TB 2G assay [QFT-G]) to detect Mycobacterium tuberculosis infection in a Japanese general hospital, for the diagnosis of active pulmonary tuberculosis (PTB) and extrapulmonary tuberculosis (EPTB). DESIGN: We prospectively examined the performance of QFT-G in 194 patients suspected of active TB. Diagnosis was confirmed by 1) positive M. tuberculosis cultures, or 2) clinical manifestations or laboratory or pathological findings consistent with active TB and response to specific therapy. RESULTS: Three patients with indeterminate QFT-G results were excluded. Among the remaining 191 patients, 77 had active TB. When the cut-off concentration of IFN-γ was set at 0.35 IU/ml, as recommended by the manufacturer, the assay was positive in 69 patients and negative in 122. The sensitivity of the assay was 76.6% in all patients, 74.5% in the 47 patients with PTB and 80.0% in the 30 patients with EPTB. The overall specificity of the assay was 91.2%. CONCLUSION: Although the specificity of the QFT-G to detect active TB was high and its sensitivity low, it was as accurate for the detection of active EPTB as for PTB when the 0.35 IU/ml INF-γ cut-off concentration was used.

[Objective]: This study was conducted in patients of secondary infection with chronic respiratory disease in order to compare 5 day short-course therapies employing gatifloxacin(GFLX) and levofloxacin(LVFX). In addition to the shortening of treatment periods, we also investigated the economic efficiency of this medical treatment. [Materials and methods]: A total of 74 patients with secondary infection in chronic respiratory disease were enrolled and treated with the study drugs. The study was conducted between September, 2006 and April, 2007 at Keio University Hospital and its affiliated hospitals and clinics. This was a randomized study in which patients were randomly assigned to one of the following two treatment groups: GFLX group (200 mg twice daily for patients aged ≧ 65 years and 400 mg twice daily in patients aged < 65 years), LVFX group (400 mg twice daily). The duration of antibiotic therapy was 5 days. [Results]: 61 patients (GFLX group: 32, LVFX group: 29) were evaluated for the efficacy of the medications, 74 patients (GFLX group: 37, LVFX group: 37) were evaluated for side effects, and 63 patients (GFLX group: 30, LVFX group: 33) were evaluated for abnormal laboratory results from a total of 74 patients. Clinical efficacy was 90.6% (29/32) in the GFLX group and 89.7% (26/29) in the LVFX group. Side effects were observed in 2 cases in the GFLX group, and 2 abnormal laboratory results were observed (1 in the GFLX group and 1 in the LVFX group). These cases were all mild in nature. [Conclusion]: Conventional management recommends 7-14 days of antibiotic therapy for secondary infection in patients with chronic respiratory disease. However, the optimum duration of treatment is less clear. This study suggests that for secondary infection in chronic respiratory disease, 5 day short-course therapy employing antibiotics therapy can be clinically successful. In terms of the economic efficiency of this medical treatment, GFLX is superior to LVFX due to the lower cost of this drug. These results show that therapy involving a 5 day short-course using GFLX is of greater benefit than therapy involving the use of LVFX.

Background: The diagnosis of pneumocystis pneumonia (PCP) is difficult because it requires microscopic examination to identify pneumocystis from induced sputum or BAL fluid. Study objective: To evaluate the usefulness of four serum markers - lactate dehydrogenase (LDH), (1→3) β-D-glucan (β-D-glucan), KL-6, and C-reactive protein (CRP) - in the diagnosis of PCP. Design: Case-control retrospective study. Patients and measurements: We reviewed the medical records of 295 consecutive patients who underwent BAL for the diagnosis of PCP. Differential cell counts in BAL fluid and serum levels of LDH, β-D-glucan, KL-6, and CRP were examined. Oxygenation index was determined using arterial oxygen tension and inspiratory oxygen concentration. Results: Based on the microscopic examination of BAL fluid, 57 patients were PCP positive and 238 patients were PCP negative. There were no significant differences in cell count or differentials in BAL fluid between the positive and negative cases. Serum levels of LDH, β-D-glucan, and KL-6 were significantly higher in PCP-positive patients (p < 0.01). Receiver operating characteristic curves suggest that β-D-glucan was the most reliable indicator. The cut-off level of β-D-glucan was estimated to be 31.1 pg/mL, with which the positive and negative predictive values were 0.610 and 0.980, respectively. In PCP-positive patients, the oxygenation index was decreased and correlated with LDH. Both LDH and β-D-glucan levels were correlated with the proportion of neutrophils in BAL fluid. Conclusions: Serum β-D-glucan is a reliable marker for the diagnosis of PCP. Since BAL procedure is invasive, measuring β-D-glucan should be considered as a primary modality for a diagnosis of PCP, especially for patients with severe respiratory failure.

Recently, we had developed a polymerase chain reaction (PCR)-immunochromatographic assay (ICA) method for Mycobacterium tuberculosis and examined its clinical utility among 138 sputa of patients under suspicion of pulmonary tuberculosis. According to the results of fluorochrome staining of acid-fast bacillus, which were confirmed by Ziehl-Neelsen staining, these were 83 specimens (-), 7 specimens (±), 30 specimens (1+), 8 specimens (2+), and 10 specimens (3+). These specimens included 4 groups: group 1, 41 specimens of smear (±)∼(3+) with culture-positive M. tuberculosis; group 2, 11 specimens of smear (-) with culture-positive M. tuberculosis; group 3, 12 specimens of smear (±)∼(1+) with culture-positive nontuberculosis mycobacterium (NTM); and group 4, 9 specimens of smear (-) with culture-positive NTM. The positive results of PCR-ICA test and Amplicor M. tuberculosis (Amplicor MTB) test for M. tuberculosis are as follows: group 1, 40 positive by PCR-ICA and 39 positive by Amplicor MTB from 41 specimens; group 2, 1 positive by PCR-ICA and 5 positive by Amplicor MTB from 11 specimens; group 3, 0 positive by both tests from 12 specimens; and group 4, 0 positive by both tests from 9 specimens. None of NTM-positive specimens from groups 3 and 4 reacted on the PCR-ICA test for M. tuberculosis.

A 72-year-old man was admitted to our hospital with complaints of dry mouth, muscle weakness of the lower limbs and gait disturbance. The patient had dry mouth, dry eyes, positive anti-SS-B antibody and salivary gland inflammation. Sjögren's syndrome was diagnosed. Since muscle weakness of the lower limbs and gait disturbance were not compatible with Sjögren's syndrome, we considered the possibility of paraneoplastic syndrome. Serum levels of CEA, NSE and ProGRP were elevated. Chest roentgenogram and CT showed a nodular lesion in the right upper lobe of the lung and swollen lymph nodes in the hilum and mediastinum. Small cell lung cancer was diagnosed by bronchoscopy. Anti-P/Q-type Ca2+ channel antibody was positive. Electromyogram showed a reduction in the amplitude of the evoked muscle action potential response after slow repetitive stimulation and did not show a reduction after rapid repetitive stimulation. Based on these findings, we made a diagnosis of Lambert-Eaton myasthenic syndrome (LEMS). Concurrent chemoradiotherapy induced an improvement of muscle weakness of the lower limbs. LEMS is frequently associated with a malignant tumor and an autoimmune disorder. We thought that in this patient, the presentation of LEMS was apparent because he had both Sjögren's syndrome and small cell lung cancer.

Systemic lupus erythematosus (SLE) is often associated with various opportunistic infections, particularly during treatment with corticosteroids or immunosuppressants. We studied the clinical characteristics of 15 patients with SLE who underwent diagnostic bronchoalveolar lavage (BAL) and compared 6 patients with confirmed Pneumocystis pneumonia (PcP+), with 9 patients without Pneumocystis pneumonia (PcP-). The serum concentrations of beta-D-glucan and KL-6 were significantly higher in PcP+ than in PcP- patients, whereas serum LDH was similar in both groups. The serum concentrations of complement, a marker of SLE activity, and of IgG did not predict the presence of PcP. In all patients, the overall cell and lymphocyte counts were increased in the BAL fluid, without any significant difference between the PcP+ and PcP- groups. Ground-glass opacities on chest computed tomography, and oxygenation impairment (PaO2/FiO2<200Torr) were more common in PcP+ than PcP- patients. We concluded that, in patients with SLE, serum beta-D-glucan and KL-6 might be useful in the diagnosis of PcP, particularly when severe hypoxemia precludes BAL.

We hypothesized that the extent of acute lung injury (ALI) caused by lipopolysaccharide (LPS) is modified with its initial passage through the liver. We tested this hypothesis by administering LPS, 5 mg/kg, or saline to 120 male Wistar rats via the portal vein (PV) or the inferior vena cava (IVC) over 1 h. Four experimental groups of rats were administered saline into the PV, saline into the IVC, LPS into the PV (LPS-PV group), and LPS into the IVC (LPS-IVC group), respectively. At 15 and 30 min after onset of Chromium-LPS infusion, the γ counts in the liver were higher in the LPS-PV group than that in the LPS-IVC group. The ratio of Iodine-albumin counts in lung tissue to that in plasma per unit of weight (as an assessment of pulmonary microvascular permeability) at 240 min after onset of LPS stimulation, the accumulation of polymorphonuclear cell (assessed by myeloperoxidase activity) and the concentration of tumor necrosis factor α in the lung at 60 and 240 min after onset of LPS infusion, were higher in the LPS-IVC group than in the LPS-PV group. Significant differences in several factors indicative of inflammation and in the extent of LPS-induced ALI were observed after the onset of LPS infusion, depending on whether it was delivered via the PV or the IVC. These observations suggest that the entrapping of LPS during its initial passage through the hepatic circulation may attenuate LPS-induced ALI within 4 h of initiation of LPS stimulation.

[Purpose]: This study examined the usefulness of QuantiFERON®TB-2G (QFT) i.e., a novel technique for detecting tuberculosis infection based on the whole blood interferon-gamma response to specific antigens, in the investigation of a tuberculosis outbreak among university students. [Subjects and Method]: One university student was diagnosed as smear-positive pulmonary tuberculosis. In order to determine the extent of tuberculosis infection among contact students, tuberculin skin tests and QFT were performed on the close-contact group (220 people), as well as on the non-close-contact group (242 people). [Results]: Nine students were found to be TB either clinically or on the X-ray screening in the contact investigation. In the close-contact group, the QFT-positive rate was 32.7%. The proportion of those exhibiting tuberculin reactions with erythema diameters of 30 mm or larger was 57.7%. In the non-close-contact group, the QFT-positive rate was only 0.8 %, as expected from the current healthy Japanese youths of this age. In contrast, strong tuberculin reactions with erythema of 30 mm or larger were seen in 18.2% in the latter group, most likely due to the previous history of BCG vaccination. [Conclusion]: QFT was clearly demonstrated to be a useful method for diagnosing tuberculosis infection, especially among subjects who show tuberculin reactivity due to past BCG vaccination. At the same time, the current criteria for the indication of chemoprophylaxis based on the strong tuberculin reaction were considered to be unreliable, causing many subjects with strong reactions to be given unnecessary preventive medications.

A 47-year-old woman was admitted to our hospital with complaints of fever, upper abdominal pain, and back pain. The serum amylase, C-reactive protein (CRP), and IgG (especially IgG4) were elevated, and abdominal computed tomography (CT) revealed diffuse enlargement of the pancreas and pseudocysts. Endoscopic retrograde pancreatography (ERP) revealed diffuse irregular narrowing of the main pancreatic duct. Histopathological examination of the pancreatic tissue showed fibrotic change with lymphocytic infiltration. Based on these findings, we diagnosed this case as a case of autoimmune pancreatitis. This case also fully satisfied the diagnostic criteria for autoimmune pancreatitis established by the Japan Pancreas Society in 2002. Few reports have been published on cases of autoimmune pancreatitis complicated by the formation of pseudocysts in the pancreas. We, therefore, report this case here to emphasize that cases of autoimmune pancreatitis can be complicated by the development of pseudocysts.