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Michiaki Koga

Publications and source records attributed to Michiaki Koga.

At least 37 records · Page 2Linked to original sources
PubMed2004

Guillain-Barre syndrome with meningoencephalitis after Campylobacter jejuni infection.

A 14-year-old boy presented with progressive ascending muscle weakness, urinary retention and disturbed consciousness. Initially his cerebrospinal fluid showed pleocytosis, and protein-cellular dissociation developed later. Campylobacter jejuni was isolated from his stool and serum anti-ganglioside antibodies were positive. Our case suggests that coexistence of meningoencephalitis at an early stage of illness does not necessarily exclude the diagnosis of Guillain-Barre syndrome.

Adolescent↗
PubMed2004

[Clinical features of neuropathies in a group of patients associated with anti-GalNAc-GD1a antibody].

To clarify the clinical features of patients with anti-GalNAc-GD1a antibody, we retrospectively investigated which conditions were associated with anti-GalNAc-GD1a antibody in a large number of patients. Sixty-four out of 1,713 patients had anti-GalNAc-GD1a IgG antibody. Fifty-seven (89%) were diagnosed with Guillain-Barré syndrome (GBS) or atypical GBS with preserved deep tendon reflexes. These patients were characterized by young man, antecedent diarrhea, distal-dominant limb weakness, and absence of cranial nerve impairment and sensory disturbance. Some of sera from patients had anti-GM1, anti-GM1b, and anti-GD1a IgG antibodies associated with axonal GBS. Our study suggests that the anti-GalNAc-GD1a antibody testing is useful for supporting the diagnosis of GBS. In addition, fine specificity of the antibody also was clarified.

Autoantibodies↗
PubMed2003

The des-gamma-carboxy prothrombin index is a new prognostic indicator for hepatocellular carcinoma.

BACKGROUND: Des-gamma-carboxy prothrombin (DCP) has been reported to be an important prognostic factor in patients with hepatocellular carcinoma (HCC). Recently, a monoclonal antibody, 19B7, which recognizes the Gla domain of DCP, has been identified. The 19B7 antibody recognizes an epitope different from that recognized by MU-3, which is another antibody against DCP. In this study, the authors investigated the measurement of DCP using the antibodies MU-3 and 19B7, respectively, as a prognostic factor for patients with HCC who had solitary, small tumors and or Child Stage A HCC. METHODS: One hundred four patients with HCC who had solitary, small tumors or Child Stage A tumors were enrolled in the study between 1991 and 2001. All patients were treated and were followed for a mean of 3.2 years. The authors analyzed the correlation between the DCP Index (DCP measured by MU-3 and DCP measured by 19B7) and patient prognosis. The patients were classified into 3 groups based on their DCP Index: 1) DCP negative (DCP < 40 milli arbitrary unit (mAU)/mL)); 2) low DCP Index (DCP > or = 40 mAU/mL; MU-3:19B7 ratio, < 3.0; and 3) high DCP Index (DCP > or = 40 mAU/mL; MU-3:19B7 ratio, > or = 3.0). RESULTS: The survival rate for patients in the high DCP Index group was lower compared with the survival rate for patients in the DCP-negative group and was significantly lower compared with the survival rate for patients in the low DCP Index group. In a univariate Cox proportional hazards model, the positive factors were high DCP Index and low DCP Index. Among the positive predictive factors that were analyzed using a multivariate Cox proportional hazards model were age (hazard ratio, 3.27; P = 0.006), low DCP Index (hazard ratio, 2.87; P = 0.012), and high DCP Index (hazard ratio, 12.3; P < 0.0001). CONCLUSIONS: The prognosis of patients who had a high DCP Index score was poorer compared with patients who had a low DCP Index score and patients who were classified as DCP negative. The authors concluded that the DCP Index is a prognostic indicator for patients with HCC.

Aged↗
PubMed2003

Bickerstaff's brainstem encephalitis: clinical features of 62 cases and a subgroup associated with Guillain-Barré syndrome.

Bickerstaff reported eight patients who, in addition to acute ophthalmoplegia and ataxia, showed drowsiness, extensor plantar responses or hemisensory loss. This condition has been named Bickerstaff's brainstem encephalitis (BBE). One patient had gross flaccid weakness in the four limbs. Presumably because of the rarity of this disorder, there has been no reported study on a large number of patients with BBE. To clarify its clinical features, we reviewed detailed clinical profiles and laboratory findings for 62 cases of BBE diagnosed by the strict criteria of progressive, relatively symmetrical external ophthalmoplegia and ataxia by 4 weeks, and disturbance of consciousness or hyperreflexia. Ninety-two per cent of the patients involved had had an antecedent illness. Besides ophthalmoplegia and ataxia, disturbance of consciousness was frequent (74%), and facial diplegia (45%), Babinski's sign (40%) and pupillary abnormality and bulbar palsy (34%) were present. Almost all the patients had a monophasic remitting course and generally a good outcome. Serum anti-GQ1b IgG antibody was positive in 66%, and MRI showed brain abnormality in 30% of the patients. Another striking feature was the association with flaccid symmetrical tetraparesis, seen in 60% of the patients. An autopsy study of a BBE patient clearly showed the presence of definite inflammatory changes in the brainstem: there was perivascular lymphocytic infiltration with oedema and glial nodules. Electrodiagnostic study results suggested peripheral motor axonal degeneration. Limb weakness in the BBE cases studied was considered the result of overlap with the axonal subtype of Guillain-Barré syndrome. These findings confirm that BBE constitutes a clinical entity and provide additional clinical and laboratory features of BBE. A considerable number of BBE patients have associated axonal Guillain-Barré syndrome, indicative that the two disorders are closely related and form a continuous spectrum.

Adolescent↗
PubMed2003

Anti-GM1b IgG antibody is associated with acute motor axonal neuropathy and Campylobacter jejuni infection.

Anti-GM1 and anti-GM1b antibodies are frequently present in patients with Guillain-Barré syndrome (GBS) and accordingly, the two antibodies often coexist in the same patient. In order to study clinical and laboratory features of anti-GM1b-positive GBS, we analyzed the data of patients with anti-GM1b IgG antibody but no anti-GM1 IgG antibody. Of 86 consecutive patients, 10 had anti-GM1b antibody alone and frequently had acute motor axonal neuropathy (AMAN, 80%) and Campylobacter jejuni infection (60%). Of 10 patients with anti-GM1 antibody alone, four had AMAN, and two had C. jejuni infection. These results showed that GM1b could be a target molecule of autoantibody in the AMAN form of GBS subsequent to C. jejuni infection.

Adolescent↗
PubMed2003

Longitudinal changes of anti-ganglioside antibodies before and after Guillain-Barré syndrome onset subsequent to Campylobacter jejuni enteritis.

Anti-ganglioside antibodies frequently are present in sera from patients with Guillain-Barré syndrome (GBS) during the acute phase, but no patients in whom anti-ganglioside antibodies were tested before the onset of the syndrome have been reported. We describe the first case of GBS subsequent to Campylobacter jejuni infection, in which longitudinal changes in anti-ganglioside antibody titers were measured before and after the onset of limb weakness. Serum antibody titers against GM1 (IgM/IgG), GM1b (IgM/IgG), GalNAc-GD1a (IgM/IgG), and GD1b (IgG) were highest on the day of onset, but negative before onset. Anti-C. jejuni IgG and IgA antibody titers paralleled those of the anti-ganglioside antibodies, indicative that C. jejuni infection triggered anti-ganglioside antibody production. Press et al. [J. Neurol. Sci. 190 (2001) 41] reported that anti-ganglioside antibody titers peaked during the recovery phase, but our findings are counter to theirs. We speculate that anti-ganglioside antibodies are the primary effectors of nerve damage in GBS.

Antibodies↗
PubMed2003

Axonal pharyngeal-cervical-brachial variant of Guillain-Barré syndrome without Anti-GT1a IgG antibody.

We report two cases of pharyngeal-cervical-brachial (PCB) variant of Guillain-Barré syndrome (GBS). The patients developed dysphagia and weakness of the neck and arms subsequent to Campylobacter jejuni infection. Oropharyngeal palsy recovered poorly. Electrophysiological findings demonstrated axonal conduction failure. Anti-GD1a immunoglobulin G (IgG) antibody was detected in one case, and anti-GM1b IgG antibody in another. Anti-GT1a IgG and immunoglobulin M (IgM) antibodies were negative in both cases. The current cases suggest that the PCB and axonal variants of GBS form a continuous spectrum from the viewpoint of electrophysiological studies as well as antiganglioside serology.

Adult↗
PubMed2003

CDR3 spectratyping analysis of the T cell receptor repertoire in Guillain-Barré and Fisher syndromes.

Several autoimmune and infectious disorders show oligoclonal expansion of particular T cell phenotypes. The extent of T cell involvement in the pathogenesis of Guillain-Barré syndrome (GBS), a post-infectious autoimmune neuropathy, however, is not clear. To identify the pathogenic T cell phenotypes in GBS and Fisher syndrome (FS), variations in T cell receptor use of the V beta 1-24 and V delta 1-5 chain genes were analyzed at complementarity-determining region 3 level in 119 patients with GBS or FS. Overall, V beta and V delta spectratypes were expanded more frequently in patients with GBS (V beta in 77%, V delta in 53%) or FS (V beta in 75%, V delta in 65%) than in the healthy controls (V beta in 59%, V delta in 38%). No particular spectratype was significantly associated with GBS or FS. Subgrouping the patients by Campylobacter jejuni serology and anti-ganglioside IgG antibodies also failed to detect particular spectratype gene use. The frequency of V beta 5.2 expansion tended to be higher in patients with positive Haemophilus influenzae serology (50%) than in the controls (7%), but the difference was not significant. Our findings show that oligoclonal expansion of T cells bearing particular type T cell receptor V beta and V delta genes frequently occurs in GBS and FS, suggestive that T cells mediate the development of these neuropathies. The predominant phenotypes vary, even within subgroups of patients with a syndrome of single etiological origin or those with uniform serological features.

Acute Disease↗
PubMed2003

Hepatitis B virus of genotype C persistence after recovery from acute hepatitis B virus infection in Japan.

BACKGROUND/AIMS: this study aimed to determine the viremia status after clinical, biochemical and serological recovery from acute hepatitis B viral (HBV) infection. METHODS: we detected serum HBV-DNA in 19 patients with acute hepatitis B during followed-up 6-43 months after onset, and analyzed HBV genotypes. RESULTS: 13 (72%) of 19 patients had detectable HBV DNA at the point of 6 months after onset, and four (33%) of 12 patients had persisted viremia for more than 1 year although they were recovery with normalization of alanine transaminase (ALT), disappearance of hepatitis B surface antigen (HBsAg) and appearance of antibody against HBsAg (anti-HBs). Eighteen (95%) of 19 patients were infected with HBV genotype C, one (5%) with genotype B. CONCLUSIONS: these results suggest genotype C of HBV is the predominant genotype of acute hepatitis B in Nagasaki region in Japan. HBV can persist in the serum for more than one year after complete clinical and serological recovery from acute viral hepatitis.

Journal Article↗
PubMed2003

[High-dose intravenous immunoglobulin therapy in a child case of Bickerstaff's brainstem encephalitis].

We report an 11-year-old boy with Bickerstaff's brainstem encephalitis (BBE). He had gait disturbance, disturbed consciousness, and diplopia after upper respiratory tract infection. On admission, he showed multiple cranial nerve palsy, muscle weakness of arms, cerebeller ataxia and generalized areflexia. The cerebrospinal fluid on day 7 revealed albuminocytologic dissociation. IgG antibodies against GQ1b and GT1a were detected in the serum. Immunoglobulin was administered intravenously from day 11, and then his symptoms gradually diminished. When he was discharged on day 27, he had neither conscious disturbance nor limb weakness. There still were mild ophthalmoparesis and diminished deep tendon reflexes, but they disappeared by 10 months after the onset. Effective therapy for BBE has yet to be established. Our case had features of Guillain-Barré syndrome (GBS) and Miller Fisher syndrome, such as an acute monophasic course, limb weakness with areflexia, albuminocytologic dissociation in the cerebrospinal fluid, detection of serum anti-ganglioside antibodies and efficacy of intravenous immunoglobulin, indicating that BBE and GBS are closely related. Our case suggested that intravenous immunoglobulin therapy, an established treatment for GBS, should be considered in some patients with BBE.

Autoantibodies↗
PubMed2002

Acute isolated bulbar palsy with anti-GT1a IgG antibody subsequent to Campylobacter jejuni enteritis.

We describe a patient with acute isolated bulbar palsy following enteritis. A 29-year-old man developed dysphagia and nasal voice without limb weakness, ataxia, or areflexia. High titres of serum anti-GT1a and anti-Campylobacter jejuni IgG antibodies were detected. He was treated with plasmapheresis, resulting in rapid clinical improvement. This case suggests that an acute isolated bulbar palsy may be caused by a pathology relating to Guillain-Barré syndrome (GBS), in which anti-GT1a IgG antibody may have a role.

Adult↗
PubMed2002

Impact of aging on the development of hepatocellular carcinoma in patients with posttransfusion chronic hepatitis C.

BACKGROUND: Hepatitis C virus (HCV) infection is a heterogeneous disease, the natural history of which remains controversial. There is solid evidence that chronic HCV infection is responsible for the occurrence of hepatocellular carcinoma (HCC). The aim of the current cohort study was to determine the rate of the development of HCC from the time of primary HCV infection and to assess the risk factors for the development of HCC in chronic posttransfusion hepatitis C patients. METHODS: Four hundred sixty-nine patients with clinically compensated HCV, who had undergone a single blood transfusion comprised the current study cohort. Patients with other risk factors for chronic liver disease were excluded. All patients were referred to the liver center at the National Nagasaki Medical Center between December 1980 and December 1998 and were followed prospectively until the end of the analysis (June 2000). RESULTS: Follow-up data were obtained for 445 patients. The mean duration from HCV infection to the end of the observation was 28 years. Fifty-two patients (11.1%) progressed to HCC. The mean duration from the time of blood transfusion to the diagnosis of HCC was 31 years. Multivariate Cox regression analyses revealed age, fibrosis, duration from HCV infection to study entry, and alcohol consumption to be the independent factors affecting the development of HCC. The risk of developing HCC in patients age > or = 56 years was increased 7.8-fold compared with that in patients age < 56 years. The mean age of patients at the time of HCC diagnosis was 65 years (range, 58-79 years). CONCLUSIONS: At the time of diagnosis, 92% of the 52 HCC patients were age > 60 years and 38 of the HCC patients (73%) were in their 60s. There was a significantly negative correlation between the duration from HCV infection to the development of HCC and the age of the patient at the time of infection (correlation coefficient = 0.702; P < 0.0001; Y = 61.1-0.82X), indicating that the age of patients, rather than the duration of HCV infection, is more significant for HCC development in patients with posttransfusion HCV. Moreover, these data may contribute to the design of an optimal follow-up schedule for patients with posttransfusion HCV.

Adult↗
PubMed2002

Hyperreflexia in axonal Guillain-Barré syndrome subsequent to Campylobacter jejuni enteritis.

We describe a patient with the acute motor axonal neuropathy (AMAN) form of Guillain-Barré syndrome (GBS), who showed generalized hyperreflexia. A 24-year-old man developed acute paralysis following Campylobacter jejuni enteritis. He showed exaggerated tendon reflexes with abnormal reflex spread to other segments, and was initially diagnosed as having post-infectious myelitis. Nerve conduction studies showed motor axonal degeneration (the AMAN pattern), and increased soleus H-reflex amplitudes. His serum was positive for IgG antibodies to gangliosides GM1b and GalNAc-GD1a. He was treated with plasmapheresis, resulting in rapid recovery. Hyperreflexia was still present 12 months after onset when muscle strength was completely normal. This case provides further evidence that patients with AMAN can develop increased motor neuron excitability, and possible mechanisms for the hyperreflexia are discussed.

Adult↗
PubMed2002

Unilateral cranial and phrenic nerve involvement in axonal Guillain-Barré syndrome.

A 49-year-old woman developed acute left facial, hypoglossal, and phrenic nerve palsies, as well as dysphagia and weakness in the neck and arms. Electrophysiologic studies showed an acute motor axonal neuropathy. Serum anti-GM1 IgG antibody was positive. Intravenous immunoglobulin treatment resulted in good clinical recovery. The present report indicates that the cranial and phrenic nerves may be affected unilaterally in Guillain-Barré syndrome, and that there is clinical variability in the axonal subtype of this syndrome.

Axons↗