Obihiro Kousei Hospital

Obihiro, Japan

Obihiro Kousei Hospital

Obihiro, Japan
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Harada T.,Hokkaido Social Insurance Hospital | Oizumi S.,Hokkaido University | Ito K.,Obihiro Kousei Hospital | Takamura K.,Obihiro Kousei Hospital | And 13 more authors.
Oncologist | Year: 2013

Amrubicin, a third-generation synthetic anthracycline agent, has favorable clinical activity and acceptable toxicity for the treatment of patients with non-small cell lung cancer (NSCLC) and small cell lung cancer. We conducted this study to evaluate the efficacy and safety of amrubicin for advanced NSCLC patients as a third- or fourth-line therapy. Eligible patients had recurrent or refractory advanced NSCLC after second- or third-line therapy. Patients received amrubicin, 35 mg/m2 i.v. on days 1-3 every 3 weeks. The primary endpoint was the disease control rate (DCR). Secondary endpointswerethe overall survival (OS) time, progression-free survival (PFS) time, response rate, and toxicity profile. Of the 41 patients enrolled, 26 received amrubicin as a third-line and 15 received it as a fourth-line therapy. The median number of treatment cycles was two (range, 1-9). Objective responses were complete response (n = 0), partial response (n = 4), stable disease (n = 21), progressive disease (n=15), and not evaluable (n1), resulting in a DCR of 61.0% (95% confidence interval, 46.0%-75.9%). The overall response rate was 9.8% (95% confidence interval, 0.6%-18.8%). The median PFS interval was 3.0 months, median OS time was 12.6 months, and 1-year survival rate was 53.7%. Grade 3 or 4 hematological toxicities were neutropenia (68%), anemia (12%), thrombocytopenia (12%), and febrile neutropenia (17%). Nonhematological toxicities were mild and reversible. No treatment-related deaths were observed. Amrubicin showed significant clinical activity with manageable toxicities as a third- or fourth-line therapy for patients with advanced NSCLC. This study provides relevant data for routine practice and future prospective trials evaluating third- or fourth-line treatment strategies for patients with advanced NSCLC. © AlphaMed Press 2013.


Ogasawara N.,Sapporo Medical University | Ogasawara N.,Obihiro Kousei Hospital | Takano K.-I.,Sapporo Medical University | Kobayashi H.,Obihiro Kousei Hospital | And 4 more authors.
Auris Nasus Larynx | Year: 2016

We present two cases of an HIV-associated parotid gland cyst. One case was a 36-year-old HIV infected woman. She was diagnosed with HIV infection and presented with slowly enlarged parotid gland cysts together with elevation of HIV viral RNA copies/mL in her serum. She was performed parotid gland biopsy under the general anesthesia. The histopathologic analysis revealed negative HIV p24-antigen in her parotid gland tissue. The other case was a 43-year-old man found his parotid gland swelling shortly after highly active antiretroviral therapy (HAART). He was diagnosed with HIV infection 2 years previously. He had started HAART several days before. He showed exceeding elevation of IgE in his serum. We treated him with medication using anti-histamic drugs for his cyst. A computed tomography scan revealed a complete response of his parotid gland cyst 4 weeks after the medication. His serum IgE level was decreased to half of the level before the medication. These findings suggested that the parotid gland swelling associated with HIV was due to various factors including immune reconstitution inflammatory syndrome (IRIS). In case such a parotid gland swelling, we could avoid invasive treatments. © 2016 Elsevier Ireland Ltd.


Kikuchi H.,Obihiro Kousei Hospital | Kikuchi K.,Obihiro Kousei Hospital
Journal of Japanese Society of Gastroenterology | Year: 2012

A 57-year-old man presented with jaundice. Abdominal computed tomography showed a 10-cm left hepatic lobe heterogeneous solid mass with low attenuated areas in the mass, multiple liver metastases and lung metastasis. Serology for hepatitis B and C were negative. Serum alpha-fetoprotein, CEA and CA19-9 were normal. The patient died a few weeks later of progressive liver failure and an autopsy was performed. Histologically, the tumor consisted of sarcomatoid mononuclear cells and osteoclast-like giant cells. The liver tissue surrounding the tumor showed no cirrhotic pattern. The osteoclast-like giant cells were uniformly and strongly immunoreactive with CD68. The mononuclear cells demonstrated expression of vimentin but were negative for CAM5.2. The MIB-1 index was 20% for the mononuclear cells. In conclusion, the histopathological diagnosis revealed an osteoclast-like giant cell tumor of the liver.


Uzuki Y.,Obihiro Kousei Hospital | Uctakc K.,Obihiro Kousei Hospital | Toshihiro T.,Hokkaido University
Acta Endocrinologica | Year: 2012

Introduction: Prader-Willi syndrome (PWS) is one of the most common known genetic causes of morbidly obese, resulting in diabetes mellitus (DM) and the management of DM in PWS is difficult. Recently, glucagon-like peptide I (GLP-I) receptor agonists have been introduced for the treatment of type 2 DM. Here, we report the use of liraglutidc, a GLP-I receptor agonist, in a patient with DM in PWS. Case report: A Japanese male patient was diagnosed as having PWS at the age of 1 year. He was mentally rctarted and developed morbid obesity. When he was 18 years old, his weight was 79 kg and height was 152 cm (BMI 34.1 kg/m 2). His HbAlc level was 6.2 % and thus DM was diagnosed. Despite several medications, the control of DM worsened and thus at the age of 22 years his body weight and HbAlc further increased (83 kg and 10.8%, respectively). At this time, liraglutide was initiated. His weight and BMI did not change, however his HbAlc level decreased to 7.4 % after one year treatment. He did not have any side effects of liraglutidc. This case indicates that GLP-1 receptor agonists may be useful for the treatment of DM with PWS.


Matsuo S.,Obihiro Kousei Hospital | Nakamura Y.,Obihiro Kousei Hospital | Matsuo K.,Obihiro Kousei Hospital | Oguro H.,Sapporo University
Japanese Journal of Clinical Ophthalmology | Year: 2013

Purpose: To report spontaneous closure of macular hole in a case of diabetic retinopathy. Case: A 77-year-old female was referred to us for diabetic retinopathy. She had been diagnosed with diabetes mellitus 26 years before and had been under medical treatment. Corrected visual acuity was 1.0 right and 0.2 left. The fundus showed diabetic retinopathy of B2 grade after Fukuda. Both eyes received panretinal photocoagulation. The left eye became blind due to endophthalmitis. The right eye developed cataract and macular edema with visual acuity down to 0.2 Nine years after her initial visit, the right eye developed macular hole by funduscopy and optical coherence tomograph (OCT). No proliferative membrane was present in the posterior fundus. A bridge formed across the macular hole 4 months later. The macular hole closed spontaneously another 2 months later with visual acuity stabilized at 0.2 Conclusion: Bridge formation appeared to have induced spontaneous closure of macular hole in the present case.


Kawano O.,Obihiro Kyokai Hospital | Nakamura A.,Hokkaido University | Morikawa S.,Hokkaido University | Uetake K.,Obihiro Kousei Hospital | And 2 more authors.
American Journal of Medical Genetics, Part A | Year: 2015

Spondyloepiphyseal dysplasia congenita (SEDC) is a group of rare inherited chondrodysplasias characterized by short stature, abnormal epiphyses, and flattened vertebral bodies. SEDC is usually caused by substitution of glycine residue with another amino acid in the triple helical domains of alpha 1 chains, which consist of type II collagen (COL2A1). Herein, we describe a unique case of SEDC with mild coxa vara (SEDC-M) caused by double de novo COL2A1 mutations located on the same allele. One mutation, p.G504S, was previously described in patients with SEDC, whereas the other, p.G612A, was a novel mutation; both were located in the triple helical domain. Neither mutation was identified in the parents and appeared to be de novo. To the best of our knowledge, this is the first study involving a patient with a type II collagenopathy with two COL2A1 mutations on the same allele. The case was characterized by a more severe phenotype compared with previously reported cases involving a single p.G504S mutation, which may have been the result of the double mutation. © 2015 Wiley Periodicals, Inc.


PubMed | Obihiro Kousei Hospital and Sapporo Medical University
Type: | Journal: Auris, nasus, larynx | Year: 2016

We present two cases of an HIV-associated parotid gland cyst. One case was a 36-year-old HIV infected woman. She was diagnosed with HIV infection and presented with slowly enlarged parotid gland cysts together with elevation of HIV viral RNA copies/mL in her serum. She was performed parotid gland biopsy under the general anesthesia. The histopathologic analysis revealed negative HIV p24-antigen in her parotid gland tissue. The other case was a 43-year-old man found his parotid gland swelling shortly after highly active antiretroviral therapy (HAART). He was diagnosed with HIV infection 2 years previously. He had started HAART several days before. He showed exceeding elevation of IgE in his serum. We treated him with medication using anti-histamic drugs for his cyst. A computed tomography scan revealed a complete response of his parotid gland cyst 4 weeks after the medication. His serum IgE level was decreased to half of the level before the medication. These findings suggested that the parotid gland swelling associated with HIV was due to various factors including immune reconstitution inflammatory syndrome (IRIS). In case such a parotid gland swelling, we could avoid invasive treatments.


PubMed | Obihiro Kousei Hospital
Type: Case Reports | Journal: Rinsho shinkeigaku = Clinical neurology | Year: 2012

A 53-year-old woman was admitted to our hospital with headache and convulsion. Advanced anemia with a Hb level of 3.5 g/dl had been detected about a month earlier, and it had been treated by iron administration to achieve a Hb level of 8.9 g/dl. The patient developed status epilepticus on admission. The blood pressure was elevated, and brain diffusion weighted imaging and fluid attenuated inversion recovery imaging revealed high intensity areas in the bilateral posterior and parietal lobes, right frontal lobe, and right basal ganglia. The cerebrospinal fluid protein was elevated. The convulsions settled after continuous infusion of thiamylal under mechanical ventilation. Subsequently, the patient became conscious, and the brain MRI abnormalities gradually disappeared. While a number of factors such as hypertension, medication and others have been reported as causes of posterior reversible encephalopathy syndrome (PRES), comparatively rapid anemia correction could also possibly precipitate PRES as like as this case. Thus anemia correction needs to be undertaken carefully.


PubMed | Obihiro Kousei Hospital
Type: Case Reports | Journal: Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology | Year: 2012

A 57-year-old man presented with jaundice. Abdominal computed tomography showed a 10-cm left hepatic lobe heterogeneous solid mass with low attenuated areas in the mass, multiple liver metastases and lung metastasis. Serology for hepatitis B and C were negative. Serum alpha-fetoprotein, CEA and CA19-9 were normal. The patient died a few weeks later of progressive liver failure and an autopsy was performed. Histologically, the tumor consisted of sarcomatoid mononuclear cells and osteoclast-like giant cells. The liver tissue surrounding the tumor showed no cirrhotic pattern. The osteoclast-like giant cells were uniformly and strongly immunoreactive with CD68. The mononuclear cells demonstrated expression of vimentin but were negative for CAM5.2. The MIB-1 index was 20% for the mononuclear cells. In conclusion, the histopathological diagnosis revealed an osteoclast-like giant cell tumor of the liver.


PubMed | Obihiro Kousei Hospital, Obihiro Kyokai Hospital and Hokkaido University
Type: Case Reports | Journal: American journal of medical genetics. Part A | Year: 2015

Spondyloepiphyseal dysplasia congenita (SEDC) is a group of rare inherited chondrodysplasias characterized by short stature, abnormal epiphyses, and flattened vertebral bodies. SEDC is usually caused by substitution of glycine residue with another amino acid in the triple helical domains of alpha 1 chains, which consist of type II collagen (COL2A1). Herein, we describe a unique case of SEDC with mild coxa vara (SEDC-M) caused by double de novo COL2A1 mutations located on the same allele. One mutation, p.G504S, was previously described in patients with SEDC, whereas the other, p.G612A, was a novel mutation; both were located in the triple helical domain. Neither mutation was identified in the parents and appeared to be de novo. To the best of our knowledge, this is the first study involving a patient with a type II collagenopathy with two COL2A1 mutations on the same allele. The case was characterized by a more severe phenotype compared with previously reported cases involving a single p.G504S mutation, which may have been the result of the double mutation.

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