Internal Medicine
Online ISSN : 1349-7235
Print ISSN : 0918-2918
ISSN-L : 0918-2918
Volume 45, Issue 3
Displaying 1-14 of 14 articles from this issue
  • Noritoshi Nagaya, Masakazu Kojima, Kenji Kangawa
    2006 Volume 45 Issue 3 Pages 127-134
    Published: 2006
    Released on J-STAGE: March 01, 2006
    Ghrelin is a novel growth hormone (GH)releasing peptide, isolated from the stomach, which has been identified as an endogenous ligand for GH secretagogue receptor. The discovery of ghrelin indicates that the release of GH from the pituitary might be regulated not only by hypothalamic GHreleasing hormone, but also by ghrelin derived from the stomach. This peptide also stimulates food intake and induces adiposity through GHindependent mechanisms. In addition, ghrelin acts directly on the central nervous system to decrease sympathetic nerve activity. Thus, ghrelin plays important roles for maintaining GH release and energy homeostasis. Repeated administration of ghrelin improves body composition, muscle wasting, functional capacity, and sympathetic augumentation in cachectic patients with heart failure or chronic obstructive pulmonary disease. These results suggest that ghrelin has anticachectic effects through GHdependent and independent mechanisms. Thus, administration of ghrelin may be a new therapeutic strategy for the treatment of cardiopulmonaryassociated cachexia.
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  • Masafumi Ihara, Fumi Makino, Hideyuki Sawada, Takahiro Mezaki, Kotaro ...
    2006 Volume 45 Issue 3 Pages 135-140
    Published: 2006
    Released on J-STAGE: March 01, 2006
    Objective: Gluten sensitivity is associated with multiple neurological abnormalities including gluten ataxia, motor neuron diseaselike neuropathy, small fiber type neuropathy, cognitive impairment, and even parkinsonism. We investigated whether or not gluten sensitivity is involved in Japanese patients with idiopathic cerebellar ataxia with extracerebellar presentation.
    Patients or Materials: Fourteen patients with idiopathic cerebellar ataxia with extracerebellar presentation (autonomic instability, parkinsonism, or pyramidal dysfunction in varying combinations) were screened for antigliadin antibodies (AGA) to analyze for the presence or absence of gluten sensitivity. Patients with typical MR findings of multiple system atrophy of the cerebellar type were excluded. As disease controls without cerebellar ataxia, 9 patients with Parkinsons disease and 18 patients with amyotrophic lateral sclerosis were screened for AGA. Fortyseven normal controls were also screened for AGA.
    Results: We found a high prevalence of AGA in 5 (36%) of 14 cerebellar ataxia patients, but in only 1 (4%) of 27 disease controls without cerebellar ataxia (odds ratio, 14.4; 95% CI, 1.41147; p<0.05) and in only 1 (2%) of 47 normal controls (odds ratio, 25.6; 95% CI, 2.66246; p<0.001). Among the cerebellar ataxia patients, atypical features such as sensorimotor neuropathy and/or mild cognitive impairment were more prevalent in the AGApositive group (60%) than in the AGAnegative group (0%). In one of the ataxic patients with AGA, a glutenfree diet had positive effects on neurological symptoms and nutritional status.
    Conclusion: Gluten sensitivity is involved in at least some of the unexplained neurological symptoms of Japanese patients with adultonset, sporadic cerebellar ataxia.
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  • Tahamina Begum, Akio Ikeda, Jun Takahashi, Hidekazu Tomimoto, Shun Shi ...
    2006 Volume 45 Issue 3 Pages 141-144
    Published: 2006
    Released on J-STAGE: March 01, 2006
    Objective: To clarify the clinical significance of subclinical rhythmic EEG discharge of adults' (SREDA) by analyzing characteristics of SREDA and the outcome of patients based on retrospective analysis of EEG data base.
    Methods: EEGs were recorded soon after the onset of patient's initial symptoms and repeatedly recorded at various intervals of 23 months in all 4 patients. Neurological findings, MRI and SPECT were also investigated.
    Subjects: Out of 340 consecutive inpatient population who had EEGs, 4 patients (1.2%) showed SREDA. They had a diagnosis of syncope, transient global amnesia, generalized tonicclonic seizure and right temporal lobe epilepsy for each.
    Results: There was no consistent abnormality in the brain MRI, CT or SPECT among the 4 patients. The acute and transient symptoms disappeared and did not recur within the followup period of 28 months in any patient. In 2 patients SREDA disappeared in the followup EEG taken 714 days after the first EEG showing SREDA. In the other 2 patients, the followup EEGs taken 5 days after the first EEG with SREDA when clinical symptoms disappeared showed less frequent occurrence of SREDA.
    Conclusion: Being different from the previous reports suggesting the relation with cardiogenic insults or persistent ischemic abnormality, SREDA can occur in patients with various acute brain dysfunctions followed by a favorable clinical outcome.
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