Objective Low-grade systemic inflammation is proposed as a component of metabolic syndrome (MS) and is reported as a predictor of diabetes. We studied the association between white blood cell count (WBC) and MS and diabetes in Japanese men and women.
Methods Cross-sectional associations between WBC and metabolic syndrome (MS) defined by revised NCEP criteria for Japanese, Japanese MS (JMS) defined by the Examination Committee for Criteria of Metabolic Syndrome, and diabetes were examined using medical check-up data from 1,880 men and 1,079 women.
Results The prevalence of MS, JMS, and diabetes was 6.4%, 5.5%, and 4.3%,13.2%, 11.5%, and 5.5%, 15.1%, 13.8%, and 5.1%, and 24.3%, 21.3%, and 8.5%, respectively through the quartiles of WBC in men (p<0.0001, <0.0001, and <0.01, respectively in comparison between the lowest quartile of WBC and the highest quartile of WBC) and 2.2%, 0.4%, and 0.4%, 4.5%, 0.7%, and 1.1%, 9.3%, 1.9%, and 1.5%, and 12.3%, 4.8%, and 3.3%, respectively through the quartiles of WBC in women (p<0.0001, <0.01, and <0.05, respectively in comparison between the lowest quartile of WBC and the highest quartile of WBC).
Conclusion The prevalence of MS, JMS, and diabetes increases through the quartiles of WBC in Japanese men and women. Thus, WBC may be useful as a marker of cardiovascular disease risk.

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Background Unilateral movement disorders and contralateral neuroimaging abnormalities of the striatum have been sporadically reported as a rare syndrome associated with diabetes mellitus. Despite characteristic imaging findings and clinical manifestations, the mechanism underlying this syndrome is still unclear.
Methods Six patients with this syndrome were studied clinically and subjected to MRI neuroimaging; one underwent biopsy of the striatum, and another underwent additional MR spectroscopy at 3.0T and FDG-PET.
Results Neuroimaging findings were characterized by a T1-hyperintense unilateral lesion restricted to the striatum, contralateral to the symptomatic limbs. The biopsied striatum contained patchy necrotic tissue, severe thickening of all layers of arterioles, and marked narrowing of vessel lumens. Hyaline degeneration of the arteriolar walls, extravasation of erythrocytes, and prominent capillary proliferation were also notable, together with lymphocytic infiltration and macrophage invasion. In one patient, PET examination revealed decreased accumulation of FDG in the lesion. The MR spectrum for the diseased striatum revealed a decrease in the NAA/Cr ratio (1.35), normal Cho/Cr ratio (1.22), and a peak for myoinositol, while the spectrum on the contralateral site revealed a decrease in the NAA/Cr ratio (1.48), increase in Cho/Cr (1.32), but no peak for myoinositol.
Conclusion The constellation of signs and symptoms and neuroimaging characteristics in previous reports and the six additional cases described here with neuropathological data and findings of MR spectroscopy appears unique enough to be termed "diabetic striatopathy." This syndrome appears in poorly controlled diabetics due to obliterative vasculopathy with prominent vascular proliferation, vulnerability to which is restricted to the striatum.

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A 66-year-old woman presented with jaundice, elevated liver enzymes, peripheral eosinophilia and increased levels of immunoglobulin (Ig) G4. The image findings of the biliary tree revealed multifocal strictures mimicking primary sclerosing cholangitis. A biopsy specimen of the liver demonstrated an infiltration of inflammatory cells consisting of several eosinophils and IgG4-positive plasma cells. The liver enzymes and eosinophil count were normalized immediately after the administration of an oral steroid. Finally, the patient was diagnosed with eosinophilic cholangitis based on the clinical manifestations, although she had features of both eosinophilic cholangitis and IgG4-related cholangitis. This case indicates that the two entities may show similar manifestations and thus they should be discriminated carefully.

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Cor triatriatum is a rare congenital cardiac malformation characterized by a fibromuscular membrane that divides the left atrium into two distinct chambers. In almost all cases, it is diagnosed in childhood, whereas adult cases are extremely rare. Herein, we describe an unusual case of cor triatriatum in a 55-year-old woman who presented with embolic cerebral infarction. The patient experienced sudden-onset, transient left-sided homonymous hemianopsia and echocardiography and multidetector computed tomography detected a membrane-like structure across the left atrium, confirming the diagnosis of a cor triatriatum. The laboratory examination for hypercoagulopathy was negative. She was conservatively treated with anticoagulation and her neurological manifestation gradually improved.

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A 39-year-old man received implantable cardioverter defibrillator (ICD) shocks during sinus rhythm, triggered by an increase in amplitude and oversensing of intracardiac T waves, caused by hyperkalemia. After treatment of hyperkalemia, the T wave morphology normalized, and oversensing and inappropriate ICD shocks were eliminated. Alteration of the intracardiac electrogram was well correlated to the surface electrocardiogram (ECG) changes. Intracardiac T waves can be altered by hyperkalemia and it seems that this alteration can be estimated by surface ECG analysis.

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Acute variant of human T lymphotropic virus type 1 (HTLV-1)-associated myelopathy (HAM) has been postulated as termed "acute HAM" or "rapidly progressive HAM". However, it remains controversial whether HAM itself could cause such rapid progression. We report a patient with HTLV-1 infection, in whom the diagnosis of neuromyelitis optica (NMO) could be made based on relapsing-remitting course of opticospinal disturbance and positive anti-aquaporin-4 (AQP4) antibody. Careful testing of anti-AQP4 antibody is necessary to establish whether or not acute HAM is a clinical variant of HAM.

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Lung parenchymal metastases are common manifestations; however, endobronchial metastasis is rare. We present herein a case of endobronchial metastasis from adrenocortical carcinoma. In the English language literature, this is the first case with such rare metastasis from adrenocortical carcinoma diagnosed antemortem. Although very rare, physicians should keep in mind the possibility of endobronchial metastasis in patients with a history of extrapulmonary malignancy including adrenocortical carcinoma.

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A 59-year-old woman was admitted to our hospital with a left lower lobe opacity and mediastinal shift on the chest X-ray. She had been complaining of intermittent nonproductive cough and exertional dyspnea. Chest computed tomography (CT) showed an endobronchial tumor of the left main to the lower bronchus, atelectasis of the left lower lobe, and mediastinal shift. Bronchoscopy revealed a polypoid tumor at the distal portion of the left main bronchus that occluded the bronchus. Biopsy specimens from the endobronchial tumor were shown to be serous papillary adenocarcinoma. Since the patient had been treated surgically for primary papillary serous carcinoma of the peritoneum (PSCP) 10 years earlier, immunohistochemical examinations were performed. The diagnosis of endobronchial metastasis of PSCP was confirmed by immunohistochemical staining with cancer antigen 125 (CA125), vimentin, and Wilms tumor-1 (WT-1). This is a rare case of endobronchial metastasis from PSCP.

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A 24-year-old man, who had suffered previous two episodes of non- Epstein-Barr virus (EBV)-associated hemophagocytic syndrome (HPS) at the ages of 16 and 18, developed EBV-induced infectious mononucleosis. His antibody pattern to EBV highlighted the initial infection. The disease took a self-limited course without developing into HPS. No reactivation of EBV infection was noted over the following 6 years. The patient may have attained immune competency in adulthood, which was somehow impaired during his adolescence.

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We report a 16-year-old woman patient with acute lymphoblastic leukemia (ALL) who developed severe critical illness polyneuropathy (CIP). She developed Bacillus cereus sepsis with multiple brain abscesses after chemotherapy. Although she was successfully treated and her general condition recovered, she could not stand. CIP was diagnosed based on the clinical course and electrophysiological studies. Since vincristine (VCR) was thought to have aggravated neurological symptoms, ALL treatment was continued without VCR. Five months from the onset of CIP, she could walk again with steppage gait. This case suggests that CIP can recover even while continuing ALL treatment, but omitting VCR.

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As a delayed neurologic complication following a high-voltage electrical injury, motor neuron disease-like spinal cord injury has often been reported. However, epileptic seizure as a delayed complication of electrical brain injury has not been reported. We report a 32-year-old man, who developed epilepsy 8 years after electrical brain injury. His electroencephalogram (EEG) recordings showed focus on the right side, in which the electrical current passed during the accident eight years earlier. He experienced cataract during these 8 years. On examination, the right side of his tongue was found to be atrophic, and he was unaware when it had started. Systemic EMG examination revealed neuropathic changes in both (interossei dorsalis) IODs, the right biceps, right tongue, and right masseter muscles.

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We describe a 17-year-old girl with Kleine-Levin syndrome (KLS), in which gabapentin was effective for the prevention of attacks. ⁹⁹mTc-ECD SPECT revealed hyperperfusion of the thalamus and nucleus accumbens presenting in the symptomatic period, suggesting epilepsy-like neuronal discharge from these structures. Treatment for KLS has not been established, although lithium has been used in limited cases with insignificant efficacy. Here, we report a case of recurrent hypersomnia in which gabapentin was effective for the prevention of attacks. We speculate that the recurrent hypersomnia and behaviour disturbance are related to epilepsy-like neuronal discharge from the thalamus due to dysfunction in GABAnergic receptors.

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Wernicke encephalopathy is caused by thiamine deficiency in the central nervous system, and is defined by the triad of confusional symptoms, ocular alterations and ataxia. Some other factors may also predispose alcoholic patients to this deficiency. We report two patients with hyperglicaemia and ketoacidosis due to diabetes mellitus decompensation and chronic alcoholism who developed Wernicke encephalopathy before their hospital admission. The outcome was successful after intravenous thiamine administration and insulinotherapy. The presence of Wernicke encephalopathy in alcoholics with diabetic ketoacidosis, suggests that metabolic decompensation is essential in the onset of the disease.

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