An iliopsoas abscess caused by Parvimonas micra: a case report.

BACKGROUND: Parvimonas micra, a Gram-positive anaerobic coccus, is a rare pathogen for psoas abscess. We describe a case of a patient with iliopsoas abscess caused by P. micra. CASE PRESENTATION: An 81-year-old Asian man presented to our department with complaints of fever since the preceding day. Abdominal computed tomography revealed the presence of a low-density mass in the right iliopsoas muscle indicative of a psoas abscess. Computed tomography-guided percutaneous drainage of the psoas abscess was performed. Results of organism cultures of the abscess and blood were positive for P. micra. However, our patient had no known primary focus of infection. On the basis of these findings, a primary psoas abscess caused by P. micra was diagnosed, and treatment with ampicillin/sulbactam 1.5 g, administered intravenously every 8 h, was initiated. By day 7, the patient's white blood cell count normalized. By day 20, his C-reactive protein level was decreased to 0.35 mg/dl. CONCLUSION: Iliopsoas abscesses caused by anaerobic bacteria are relatively rare, and iliopsoas abscesses caused by P. micra are especially rare. Our patient's case revealed that P. micra can cause iliopsoas abscess. Therefore, clinicians should be aware of the possibility that P. micra may cause iliopsoas abscess.

Miliary tuberculosis with co-existing pulmonary cryptococcosis in non-HIV patient without underlying diseases: a case report.

BACKGROUND: Tuberculosis and cryptococcosis co-infection usually occurs in immunosuppressed patients with impaired cell-mediated immunity. However, there are few reports about such co-infection in non-HIV patients without underlying diseases. Here, we report a case of miliary tuberculosis with co-existing pulmonary cryptococcosis in non-HIV patient without underlying diseases. CASE PRESENTATION: An 84-year-old Asian female presented to our hospital with complaints of a 1-week history of abdominal pain and appetite loss. Chest computed tomography (CT) showed diffuse micronodules in random patterns in both lung fields. Liver, skin and bone marrow biopsies showed epithelioid cell granuloma. Polymerase chain reaction of gastric aspirate was positive for Mycobacterium tuberculosis. According to these findings, miliary tuberculosis was suspected and antimycobacterial therapy was initiated. After a 6-month treatment course, chest radiograph showed new multiple nodules in the right middle lung field. Chest CT showed that a right S6 small nodule was increased and new multiple nodules appeared in the right lower lobe. Flexible fiberoptic bronchoscopy was subsequently perfomed. Cytology of the bronchial lavage showed a small number of Periodic acid-Schiff-positive bodies, suggesting Cryptococcus species. Moreover, serum cryptococcal antigen testing was positive. According to these findings, pulmonary cryptococcosis was diagnosed, although the culture was negative. Oral fluconazole therapy was subsequently initiated. After a 6-month treatment course, chest radiograph showed gradual improvement. CONCLUSION: Although tuberculosis and cryptococcosis co-infection is relatively rare in immunocompromised hosts, such as those with acquired immunodeficiency syndrome, clinicians should be aware that these infections can co-exist even in non-HIV patients without underlying diseases.

Relationship between UGT1A1*27 and UGT1A1*7 polymorphisms and irinotecan-related toxicities in patients with lung cancer.

BACKGROUND: The objective of this study was to evaluate the effects of gene polymorphisms, including UGT1A1*7, *27, and *29, on the safety of irinotecan therapy. METHODS: The eligibility criteria were: lung cancer patients scheduled to undergo irinotecan therapy, aged ≥ 20 years, with a performance status of 0-2. Thirty-one patients were enrolled and their blood was collected and used to examine the frequency of UGT1A1*6, *7, *27, *28, and *29 polymorphisms and the concentrations of irinotecan, SN-38, and SN-38G after irinotecan therapy. RESULTS: The patients' characteristics were as follows: male/female 25/6, median age 71 years (range 55-84), stage IIB/IIIA/IIIB/IV 2/6/11/12, and adenocarcinoma/squamous cell carcinoma/small cell carcinoma/other 14/10/3/4, respectively. The -/-, *6/-, *7/-, *27/-, *28/-, and *29/- UGT1A1 gene polymorphisms were observed in 10 (32%), 10 (32%), 2 (6%), 2 (6%), 7 (23%), and 0 (0%) cases, respectively. The UGT1A1*27 polymorphism occurred separately from the UGT1A1*28 polymorphism. The lowest leukocyte counts of the patients with the UGT1A1*27 and UGT1A1*6 gene polymorphisms were lower than those observed in the wild-type patients. SN-38 tended to remain in the blood for a prolonged period after the infusion of irinotecan in patients with UGT1A1*27 or UGT1A1*28 polymorphisms. No severe myelotoxicity was seen in the patients with UGT1A1*7. CONCLUSION: UGT1A1*27 can occur separately from UGT1A1*28 and is related to leukopenia during irinotecan treatment. UGT1A1*7 is less relevant to irinotecan-induced toxicities, and UGT1A1*29 seems to have little clinical impact.

Intraabdominal abscess caused by Stenotrophomonas maltophilia: A case report.

INTRODUCTION: Stenotrophomonas maltophilia usually causes nosocomial infections, but intraabdominal abscesses or organ/space surgical site infection (SSI) secondary to this organism has been rarely reported. Here, we reported a rare case of SSI that presented as intraabdominal abscess caused by S. maltophilia. PRESENTATION OF CASE: A 68-year-old woman presented to our hospital with transverse colon cancer. Further work up with abdominal computed tomography (CT) revealed left renal cell carcinoma. Transverse colon resection and left kidney partial resection were performed. On post-operative day 10, she started to have fever at 38°C and repeat abdominal CT showed intraabdominal abscess. Empiric treatment with piperacillin/tazobactam (TAZ/PIPC) was initiated. However, fever persisted and the abscess size did not change despite 10 days of antibiotic. On post-operative day 20, drainage of intraabdominal abscess was performed. TAZ/PIPC was then shifted to meropenem (MEPM). After two days, S. maltophilia was identified in the culture of the abscess, and MEPM was shifted to minocycline (MINO). Fever disappeared after 7days of treatment and abdominal CT after 14 days showed almost complete resolution of the abscess. DISCUSSION: S. maltophilia is a multi-drug resistant, aerobic, non-glucose fermenting, non-sporulating, Gram-negative bacillus. S. maltophilia may cause a variety of infections, but intraabdominal abscesses as a manifestation of SSI due to this organism is relative rare. CONCLUSION: Although usually a non-pathogenic organism or colonizer, S. maltophilia can cause organ/space SSI in an immunocompromised host. Therefore, clinicians should be aware of the possibility that S. maltophilia may cause organ/space SSI.

Detection of high serum levels of ß-D-Glucan in disseminated nocardial infection: a case report.

BACKGROUND: ß-D-glucan (BDG) is a helpful diagnostic marker for many invasive fungal infections, but not for nocardiosis. Here, we reported the first case of nocardial infection with high serum level of BDG. CASE PRESENTATION: A 73-year-old man was hospitalized because of fever, headache, and appetite loss after 10 months of steroid and immunosuppressive therapy for cryptogenic organizing pneumonia. With a diagnosis of bacterial pneumonia, treatment with ampicillin/sulbactam was initiated. There was improvement on chest radiograph, but fever persisted. Further work-up revealed multiple brain abscesses on cranial magnetic resonance imaging (MRI). Serum galactomannan and BDG were elevated at 0.6 index and 94.7 pg/ml, respectively. Voriconazole was initiated for presumed aspergillus brain abscess. However, fever persisted and consciousness level deteriorated. Drainage of brain abscess was performed; based on the Gram stain and Kinyoun acid-fast stain, disseminated nocardiosis was diagnosed. Voriconazole was then shifter to trimethoprim/sulfamethoxazole. The presence of Nocardia farcinica was confirmed by the 16S rRNA gene sequence. Treatment course was continued; BDG level normalized after 1 month and cranial MRI showed almost complete improvement after 2 months. CONCLUSION: BDG assay is widely used to diagnose invasive fungal infection; therefore, clinicians should be aware that Nocardia species may show cross-reactivity with BDG assay on serum.

Sisters who developed piloerection after administration of milnacipran.

OBJECTIVE: We previously reported the first case of piloerection in a patient receiving milnacipran hydrochloride (MLP). Here, we now present a second case of MLP-induced piloerection. We discuss this effect in terms of α1-adrenoceptor occupancy. CASE SUMMARY: After the first case of MLP-induced piloerection, we monitored occurrence of piloerection in our patients taking MLP. In response to our interview, a 43-year-old woman who had been prescribed MLP by a psychiatrist for depression mentioned that piloerection occurred frequently all over her body, starting soon after initiation of MLP administration (50 mg/day). Although she was concerned at the time, she assumed it might be related to her depression or to coldness in winter. She also mentioned that the incidence of piloerection increased with MLP dose escalation. The piloerection disappeared after several months. Interestingly, the previous patient and the current patient are biological sisters. DISCUSSION: Changes in α1-adrenoceptor occupancy by endogenous norepinephrine (as an index of the risk of piloerection) in the presence of MLP were estimated. The occupancy values increased with MLP dose escalation, in accordance with the patient's report of the phenomenon. other concomitant drugs, such as nortriptyline, had little effect. Since the two patients were sisters, genetic factors might influence the risk of piloerection. CONCLUSION: The incidence of piloerection appeared to increase with MLP dose escalation in this patient, who was the biological sister of the previously reported patient. Clinicians should recognize the possibility of MLP-induced piloerection in view of its potential impact on patients' quality of life and on drug compliance.

Autoimmune pulmonary alveolar proteinosis co-existing with breast cancer: a case report.

INTRODUCTION: Pulmonary alveolar proteinosis is a rare pulmonary disease characterized by excessive alveolar accumulation of surfactant due to defective alveolar clearance by macrophages. There are only a few published case reports of pulmonary alveolar proteinosis occurring in association with solid cancers. To the best of our knowledge, there are no previously reported cases of pulmonary alveolar proteinosis associated with breast cancer. CASE PRESENTATION: A 48-year-old Asian woman, a nonsmoker, presented to our institution with a right breast mass. Biopsy examination of the lesion revealed scirrhous carcinoma. A chest computed tomography scan for metastases showed abnormal shadows in both upper lung fields. As a result of flexible fiberscopic bronchoscopy, this patient was diagnosed as having pulmonary alveolar proteinosis. This case was categorized as autoimmune pulmonary alveolar proteinosis due to the positive anti-granulocyte-macrophage colony-stimulating factor antibody. Pulmonary alveolar proteinosis decreased gradually after mastectomy. CONCLUSIONS: The present case involved the coincident occurrence of autoimmune pulmonary alveolar proteinosis with breast cancer; breast cancer may be a factor during pulmonary alveolar proteinosis development.

A retrospective comparative study of recombinant human thrombomodulin and gabexate mesilate in sepsis-induced disseminated intravascular coagulation patients.

The novel biological agent recombinant human thrombomodulin (rhTM) has been used clinically in Japan to treat disseminated intravascular coagulation (DIC) since 2008. Previous studies have shown the efficacy of rhTM versus heparin therapy or non-rhTM therapy. We retrospectively evaluated and compared the efficacies of rhTM and gabexate mesilate (GM) in patients diagnosed with sepsis-induced DIC. From September 2010 to October 2012, patients with sepsis-induced DIC who were treated with rhTM (n = 13) or GM (n = 10) at Nagasaki Municipal Hospital were extracted. Patients receiving other anticoagulants in combination were excluded. Clinical information, laboratory data, Sequential Organ Failure Assessment (SOFA) scores, and DIC scores were obtained from the medical records. Mortality at days 7 and 30 after DIC diagnosis and changes in laboratory data and SOFA scores from days 1-7 were evaluated. The groups' clinical characteristics did not differ, except for the relatively higher C-reactive protein (CRP) levels in the rhTM group (P = 0.0508). The survival rates of the rhTM and GM groups on days 7 and 30 were 92.3%, 69.2% and 80%, 70%, respectively, both group indicated similar mortality. However, on day 7, the platelet counts, SOFA scores, and CRP levels significantly improved in the rhTM group; the platelet counts and SOFA scores did not improve significantly in the GM group. The platelet counts of the rhTM group significantly improved compared to the GM group (P = 0.004). Recombinant human thrombomodulin might be more effective for sepsis-induced DIC than GM.

A case of community-acquired pneumonia due to influenza A virus and Nocardia farcinica co-infection.

Nocardia spp. has not been reported previously as a cause of post-influenza pneumonia. Here we present a first case of post-influenza bacterial pneumonia due to Nocardia farcinica. Initial reason for hospitalization of the 90 year old female patient was a pneumonia with the symptoms of fever and productive cough. A rapid test for influenza antigen was positive for influenza A virus. Treatment with Zanamivir and piperacillin was initiated. However, after 1 week of treatment, the infiltration shadows on chest X-ray had worsened. Because the expectorated sputum collected on admission for culture was found to be positive for Nocardia spp., piperacillin was replaced with trimethoprim/sulfamethoxazole, and a chest X-ray showed some improvement. Although pulmonary nocardiosis with co-infection with influenza A is extremely rare, clinicians should be alert to the possibility.

Differential airway inflammatory responses in asthma exacerbations induced by respiratory syncytial virus and influenza virus a.

BACKGROUND: Although respiratory viral infections cause acute exacerbations of asthma, the inflammatory responses vary depending on the causative virus. The purpose of this study was to compare the inflammatory responses in the airways of acute exacerbations of asthma induced by respiratory syncytial virus (RSV) and influenza A virus. METHODS: Sputum induction was performed in asthmatic patients with acute exacerbations induced by RSV (n = 6), influenza A (n = 7), and non-upper respiratory infection (URI)-related factors (n = 8). Sputum concentrations of cysteinyl leukotrienes (cysLTs), TNF-α and IFN-γ were measured. RESULTS: Sputum cysLTs were significantly higher in RSV-induced exacerbations than in influenza A- and non-URI-induced exacerbations. Sputum TNF-α was significantly higher in influenza A-induced exacerbations than in RSV- and non-URI-induced exacerbations. Sputum IFN-γ was significantly lower in RSV-induced exacerbations than in the others. CONCLUSIONS: RSV and influenza A cause acute exacerbations and have different effects on airway inflammation in asthmatic patients. RSV significantly increased cysLTs, while influenza A significantly increased TNF-α in the airway. The underlying mechanism in virus-induced asthma might depend on the viral species.

Retrospective cohort study of leukotriene receptor antagonist therapy for preventing upper respiratory infection-induced acute asthma exacerbations.

Upper respiratory tract infections (URIs) represent the most frequent cause of acute asthma exacerbations. It has yet to be determined whether leukotriene receptor antagonist (LTRA) treatment prevents URI-induced acute asthma exacerbations in adults. The objective of the present study was to evaluate the preventive effects of LTRA treatment on URI-induced acute asthma exacerbations. The incidences of URI alone, acute asthma exacerbation without URI, and URI-induced acute asthma exacerbation were determined retrospectively by analyzing diary and medical records of 321 adult asthmatic patients (mean age, 56.3 ± 17.2 years; male/female ratio, 117:204) over 1 year. Results were compared between patients who had been taking an LTRA (n = 137) and those who had never taken any LTRA (n = 184) during the study periods. Significantly fewer URIs alone and acute asthma exacerbations without URI occurred in patients with than in those without prophylactic daily use of LTRA. LTRA treatment significantly reduced the durations of URIs alone and of total acute asthma exacerbations, as well as the incidence of mild exacerbations of asthma. In contrast, in patients with URI-induced acute asthma exacerbations, LTRA treatment failed to significantly reduce the interval between URI onset and acute asthma exacerbation, as well as the duration and severity of both URIs and acute asthma exacerbations. Use of an LTRA for adult asthmatic patients appears to reduce the incidences of URIs alone and acute asthma exacerbations without URI, but it failed to prevent URI-induced acute asthma exacerbations once a URI occurred.

Effects of a short course of pranlukast combined with systemic corticosteroid on acute asthma exacerbation induced by upper respiratory tract infection.

BACKGROUND: Upper respiratory tract infections (URIs) represent the most frequent cause of acute asthma exacerbation. Systemic corticosteroid (CS) is presently recommended for URI-induced asthma exacerbation, although it might inhibit cellular immunity against respiratory virus infection. OBJECTIVES: To determine the effects of adding a short course (2 weeks) of a leukotriene receptor antagonist (LTRA) to systemic CS on URI-induced acute asthma exacerbation. METHODS: Twenty-three adult asthmatics (mean age, 42.8 ± 9.8 y; Male:Female, 10:13) with URI-induced acute asthma exacerbation confirmed by a questionnaire and physical findings were randomly assigned to receive either oral prednisolone (PSL) alone or oral PSL plus the LTRA pranlukast (PRL) for 2 weeks (PSL + PRL). The cumulative doses of PSL and the amount of time required to clear asthma-related symptoms were determined. Levels of respiratory syncytial virus (RSV) RNA and influenza viral (IV) antigen in nasopharyngeal swabs were also determined. RESULTS: Adding PRL significantly reduced the cumulative dose of PSL and tended to reduce the time required to clear asthma-related symptoms. Either RSV or IV was detected in about one-third of the patients. CONCLUSION: The combination of an LTRA and CS might be more useful than CS alone for treating URI-induced acute exacerbation of asthma and reducing the cumulative CS dose.

The first surgical treatment case of pulmonary Mycobacterium malmoense infection in Japan.

Mycobacterium malmoense is a very rare pathogen of pulmonary infectious disease in Japan. We encountered a case of M. malmoense infectious lung disease which could be cured by surgical operation without chemotherapy. M. malmoense strains were isolated in both the bronchial washing lavage and the removed lung specimen, and it were identified using 16S rRNA gene and rpoB gene sequencing. This case might indicate that pulmonary infectious disease caused by a rare non-tuberculous mycobacteria pathogen should be positively considered to be treated surgically as an initial therapy when the patient's condition is admissive, and also indicated the importance of identification of the causative pathogen from surgical specimens. In addition, this was the second report of M. malmoense infectious disease, and the first case of surgical treatment case of M. malmoense lung disease in Japan, as far as we could determine.

Observational study of the additive effects of pranlukast on inflammatory markers of clinically stable asthma with inhaled corticosteroids and long-acting beta 2 agonists.

BACKGROUND: Little is understood about the additive effects of leukotriene receptor antagonists (LTRA) on asthmatics currently medicated with inhaled corticosteroids (ICS) and long-acting beta(2)-agonists (LABA). OBJECTIVES: The present study examines the anti-inflammatory effects of the LTRA pranlukast in addition to ICS and LABA, among asthmatic patients with normal pulmonary function and unremarkable clinical symptoms. METHODS: Fifteen adult asthmatics participated in a 2-month, open-label, uncontrolled, prospective, multicenter, observational trial. Patients stabilized (predicted forced expiratory volume in 1 s >80%) by medication with ICS and LABA were also given pranlukast (450 mg daily). Asthma-related symptoms, pulmonary function, blood eosinophil counts and several inflammatory markers in sputum were monitored at week 0, as well as at 4 and 8 weeks after starting therapy with pranlukast. RESULTS: Adding pranlukast did not further improve blood eosinophil counts, pulmonary function and symptoms, but significantly attenuated sputum cysteinyl leukotrienes, tumor necrosis factor-alpha and interleukin-5 concentrations. CONCLUSIONS: Although the clinical relevance remains obscure, adding an LTRA attenuates allergic airway inflammation in some asthmatics undergoing treatment with ICS and LABA.

[Case of idiopathic bronchiolitis obliterans successfully treated by medication].

A 53-year-old woman visited a clinic for stridor and dyspnea, and was treated with steroid and heparin for bronchial asthma and pulmonary embolism. She was later admitted to our hospital for progressive dyspnea. Blood gas analysis showed severe hypoxemia with hypercapnia. Pulmonary funtion tests revealed severe obstractive pulmonary dysfunction. Chest computed tomography showed a mosaic perfusion pattern. Ventilation-perfusion scanning showed bilateral multiple matched defects, especially in the basal region. Since specimens of Video-assisted thoracoscopic surgical (VATS) lung biopsy showed lymphocytic infiltration in membranous bronchiole and occlusion of the membranous bronchiole lumen, bronchiolitis obliterans was diagnosed. We initiated treatment with steroids, macrolides and bronchodilators and her condition stabilized. Although these therapies did not cure the BO, they did retard its progression.

[Case of idiopathic chylothorax successfully treated with surgical ligation of thoracic ducts].

A 72-year-old woman visited a clinic for anorexia and general fatigue but no particular abnormality was detected by routine examination at that time. Thereafter, she experienced gradually increasing dyspnea and chest X ray showed right pleural effusion. Idiopathic chylothorax was diagnosed due to the milky effusion with a high concentration of triglyceride (2618 mg/dl) and no apparent causative disease. Irrespective of treatments including dietary restriction, drainage of the pleural space, and somatostatin injections, her effusion did not reduce. The leakage of lymph fluid from the right posterior mediastinum was identified by lymphatic scintigraphy and she was successfully treated with surgical ligation of the thoracic ducts.

Piloerection induced by replacing fluvoxamine with milnacipran.

AIMS: To present a case of piloerection after replacing fluvoxamine maleate with milnacipran hydrochloride, and to analyse this effect based on receptor occupancy theory. METHODS: A 40-year-old female with a 3-year history of panic disorder was prescribed fluvoxamine 50 mg day(-1) in addition to clorazepate dipotassium and sulpiride. Depression was not improved and she complained of fatigue, lack of energy and drowsiness. These symptoms worsened within a few days of an increase in the dose of fluvoxamine to 50 mg twice daily. Since an interaction between fluvoxamine and tizanidine, prescribed by another clinic, was suspected, fluvoxamine was replaced with milnacipran 50 mg day(-1). Although her drowsiness improved, she complained of piloerection throughout her body. This symptom gradually abated within a week and when the dosage of milnacipran was increased to 100 mg day(-1) at 2 months, no further piloerection occurred. We calculated the changes in alpha(1)-adrenoceptor occupancy by endogenous norepinephrine during treatment with the usual doses of milnacipran, fluvoxamine and imipramine by using pharmacokinetic and pharmacodynamic parameters obtained from the literature. RESULTS: The ratios of alpha(1)-adrenoceptor occupancy by endogenous norepinephrine during the treatment with milnacipran, fluvoxamine and imipramine to that without drug were estimated to be 7.13, 1.00 and 4.12, respectively. The alpha(1)-adrenoceptor occupancy by endogenous norepinephrine was increased in a dose-dependent manner by milnacipran, whereas fluvoxamine had essentially no effect. CONCLUSIONS: The piloerection observed after the replacement of fluvoxamine with milnacipran in this patient appears to have been due to an increase in the alpha(1)-adrenoceptor occupancy by endogenous norepinephrine induced by milnacipran.

A clinical evaluation of definitive and clinical allergic bronchopulmonary mycosis.

OBJECTIVE: The present study aims to overcome problems associated with the early diagnosis of allergic bronchopulmonary mycosis (ABPM) using the current criteria. PATIENTS AND METHODS: Clinical features including radiographic findings from 10 patients with definitive ABPM based on the diagnostic criteria of Rosenberg-Patterson were compared with those from 9 patients with ABPM clinically diagnosed by respiratory allergy specialists. RESULTS: ABPM should be considered in patients with peripheral blood eosinophilia and pulmonary infiltration and/or central bronchiectasis when serum total IgE is elevated. Complication by bronchial asthma suggested ABPM, but was not essential. The expectoration of sputum containing solid components was a critical factor in patients with a history in ABPM. Evaluation of sputum cultures, serum specific IgE antibodies, skin tests and precipitating antibodies were required to establish a diagnosis, but the positive rate of these tests remained low. CONCLUSIONS: Even when a definitive diagnosis cannot be established, systemic corticosteroid therapy should be initiated for clinically diagnosed ABPM to prevent irreversible pulmonary dysfunction.