Objective The purpose of this study was to test the hypothesis that lack of microvascular reperfusion following revascularization might be associated with a poor clinical outcome in diabetic patients with acute myocardial infarction (AMI).
Methods We studied 134 patients with a first anterior AMI who underwent successful revascularization within 6 hours. We assessed microvascular reperfusion by using electrocardiogram recordings just before revascularization and on return to the coronary care unit. Lack of microvascular reperfusion was defined as the absence of decrease of ≥20% in the sum of ST segment elevation (ΣST).
Results Twenty-four patients had diabetes and 110 patients did not. ΣST before revascularization was similar between diabetic and nondiabetic patients. After revascularization, reduction of ΣST was significantly smaller (1.3±8.4 mm vs 6.5±10.8 mm, p=0.03), and lack of microvascular reperfusion was significantly more frequent (62.5% vs 33.6%, p=0.01) in diabetic patients. A multivariate analysis showed that diabetes was associated with insufficient microvascular reperfusion (odds ratio 3.18, p=0.03). Major adverse cardiac events occurred more frequently in patients with a lack of microvascular reperfusion (30.8% vs 15.9%, p=0.04).
Conclusion These findings suggest that lack of microvascular reperfusion following revascularization may be one of the mechanisms of a poor clinical outcome in diabetic patients with AMI.
(Internal Medicine 42: 554-559, 2003)

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Objective Orthostatic hypotension is caused by autonomic nerve dysfunction, mainly by severe sympathetic nerve dysfunction in diabetic patients. Diabetes affects the peripheral nerves in a length-dependent manner. Quantitative sudomotor axon reflex test (QSART) is one of the sensitive tests for detecting sympathetic nerve function. We examined the relation between Orthostatic hypotension and QSART at the foot and hand in type 2 diabetic patients.
Methods Thirty-eight type 2 diabetic patients (age, 48.9±11.9 years; duration of diabetes, 13.4±8.6 years) and 13 age-matched non-diabetic controls were evaluated. All subjects aged under 65 years old were recruited. All subjects underwent Schellong tests and quantitative sudomotor axon reflex tests (QSART) at the back of the hand and dorsum of the foot.
Results The sweating volume at the foot dorsum, but not the back of the hand, during the first 10 minutes of QSART was significantly related to the orthostatic hypotension on the Schellong test. In patients with normal, borderline and abnormal blood pressure response to standing, 6 out of 17 (35.3%), 9 out of 12 (75.0%) and 9 out of 9 (100%) had decreased sweating volume of the foot dorsum, respectively.
Conclusions Our results suggest that orthostatic hypotension may be detected early by QSART at the dorsum of the foot in type 2 diabetic patients.
(Internal Medicine 42: 560-564, 2003)

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Objective Idiopathic pulmonary fibrosis (IFF) is a slowly progressive disease with a poor prognosis. Acute exacerbation is the worst stage in the clinical course of IFF, as the condition is unresponsive to most conventional therapies. Corticosteroids and other immunosuppressive drugs have been attempted for the treatment of acute exacerbation, but only with very limited effectiveness. This study was performed to examine the effect of cyclosporin A (CsA) on acute exacerbation of IPF.
Patients and Methods Thirteen patients with acute exacerbation of IFF were retrospectively studied. All 13 patients received pulse-therapy with methylprednisolone (1, 000 mg per day for 3 days), followed by oral prednisolone (40-60 mg per day). Seven patients were received CsA (1.0-2.0 mg/kg per day) after the treatment with corticosteroids. We attempted to keep the blood trough level of CsA between 100 and 150 ng/ml.
Results Among the 7 patients treated with CsA, 4 patients have survived for 60, 120, 276 and 208 weeks, respectively; 2 did not respond to pulse-therapy with methylprednisolone and died within 8 weeks after the start of CsA treatment. The other patient experienced re-exacerbation and died 87 weeks after the discontinuation of CsA due to the development of viral encephalitis. In contrast, all 6 patients treated without CsA died within 66 weeks after the onset of acute exacerbation. Four of these patients responded to pulse-therapy with methylprednisolone, but their condition deteriorated again while the subsequent prednisolone was being tapered.
Conclusion CsA seems to prevent re-exacerbation of IPF and improve the patients' chances for long-term survival.
(Internal Medicine 42: 565-570, 2003)

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Objective Chlamydia pneumoniae (Cp) is an important pathogen for infections of the respiratory tract; recently, also a number of reports suggesting its relation to atherosclerosis. This study was performed to clarify the relation between Cp infection and ischemic stroke.
Patients Forty elderly patients with ischemic stroke (age 75±6.6; male 57.5%) and 85 elderly control subjects without a history of ischemic stroke (age 74±8.1; male 43.5%) were investigated.
Methods Patients were divided into four groups according to clinical diagnosis: 1) atherothrombotic infarction, 2) lacunar infarction, 3) those with cardiac embolism, and 4) non-classifiable. Cp infection was determined by measuring the anti-Cp IgG specific antibody level (Cp IgG index) using enzyme-linked immunosorbent assay (ELIZA) method. Those below the 1.10 Cp IgG index were determined as seronegative and those above 1.10 as seropositive.
Results We found that 20 cases (87.0%) of atherothrombotic infarction, 6 (66.7%) of lacunar infarction, 3 (50.0%) others and 52 (61.2%) control were Cp seropositive. Cp seropositiveness, as adjusted by multiple regression analysis using various known risk factors, was a significant independent contributing factor for ischemic stroke (p=0.017) and was associated with an increased risk for atherothrombotic infarction (odds ratio, 12.6; 95% CI, 2.0-79.3).
Conclusion This suggests that Cp infection is also an important risk factor for ischemic stroke, particularly atherothrombotic infarction in elderly Japanese.
(Internal Medicine 42: 571-575, 2003)

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Objectives The underlying cause of lobar intracerebral hemorrhage (ICH) is often difficult to determine, since these vascular abnormalities are not necessarily visualized in radiographic studies. We sought to determine the clinical features of hypertensive and non-hypertensive lobar ICH, and further predict the presence or absence of vascular abnormalities in terms of clinical features and radiographic abnormalities.
Patients and Methods Eighty-one patients with lobar ICH were retrospectively assigned to either hypertensive or non-hypertensive groups based on their blood pressure levels during the chronic phase or a history of antihypertensive medication. The clinical and radiographic features of these two groups were compared.
Results Forty-nine patients (60%) were hypertensive, and the other thirty-two (40%) were non-hypertensive. In the non-hypertensive group, amyloid angiopathy (n= 6), aneurysms (n=5), arteriovenous malformation (n=4), use of anticoagulants (n=2), liver cirrhosis (n=2) and thrombasthenia (n=l) were found as underlying causes. There were no significant differences between these two groups in the frequencies of stroke risk factors except for hypertension, clinical features and initial neurological findings. On the contrary, subarachnoid extension of the hematoma on CT was significantly more frequent in the non-hypertensive lobar ICH group than in the hypertensive group (p<0.001). The patients with subarachnoid extension were more likely to have vascular abnormality than those without subarachnoid extension (p<0.01).
Conclusion Subarachnoid extension of the hematoma on CT strongly indicates a non-hypertensive cause, and more specifically, it suggests lobar ICH caused by vascular abnormalities.
(Internal Medicine 42: 576-580, 2003)

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In 1997, a 27-year-old homosexual man contracted acute hepatitis B that developed into chronic hepatitis. Because of repeated flares, administration of lamivudine was started in March 2002. Hepatitis B virus (HBV) DNA immediately decreased, but the serum level of alanine aminotransferase gradually increased. Drug-induced hepatitis due to lamivudine was excluded. It was suspected that the progression of liver damage was caused by hepatitis delta virus (HDV), because the patient was positive for both anti-HDV antibody and HDV RNA. Coinfection of HDV should be considered a possibility if liver injury is not improved by lamivudine therapy.
(Internal Medicine 42: 581-586, 2003)

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Multisystemic lipid storage disease is a rare disorder of lipid metabolism. We report one case of a Japanese man with systemic lipid storage in skeletal muscle and heart as well as in leukocytes (Jordans' anomaly). Positron emission tomography (PET) using ¹⁸F-fluoro-2-deoxyglucose (FDG) clearly revealed an abnormal increase of uptake during fasting in the left ventricle, suggesting changes in the energy metabolism in the heart.
(Internal Medicine 42: 587-590, 2003)

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This is a case report of a 19-year-old man who presented with acute myocardial infarction with obstruction of one coronary artery and rapid progression to three vessels in 8 months. He was proved to have sitosterolemia, a rare hereditary disease with plant sterol storing, resulting in juvenile coronary artery disease. Atherosclerotic complications can be preventable by administration of bile acid-binding resin, after the correct diagnosis is made. We introduce this disease with a review of the literature.
(Internal Medicine 42: 591-594, 2003)
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We encountered two patients with abnormally low glycohemoglobin levels in spite of normal plasma glucose levels. Since the presence of an abnormal hemoglobin was suggested by high-performance liquid chromatography (HPLC), gene analysis of these two patients was conducted by single-strand conformation polymorphism (SSCP) analysis followed by direct sequencing, and Hb Kamakura with one base substitution (β3 Leu→Val) in the β globin gene was detected in both patients. There has been only one report of Hb Kamakura in Kanagawa Prefecture, and our patients represent the second and third cases, respectively.
(Internal Medicine 42: 595-598, 2003)

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We herein report a case of aceruloplasminemia in a 27-year-old man who had a 10-year history of diabetes mellitus. The patient developed a convulsion, most likely as a result of hypoglycemia. Unexpectedly, this episode left him in a prolonged state of unconsciousness, which necessitated neurological testing and imaging. Brain MRI showed bilateral hypo-intensities in the basal ganglia and thalamus. Molecular analysis revealed a novel splicing mutation in the ceruloplasmin (CP) gene that would result in the skipping of exon 3 during transcription. This case suggests that diabetes associated with aceruloplasminemia can become manifest in the teens.
(Internal Medicine 42: 599-604, 2003)

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A 64-year-old Japanese man suffering from IgD λ myeloma and renal failure requiring chronic hemodialysis was treated with thalidomide. Serum IgD concentration was 4, 050 mg/dl and myeloma cells constituted 95.6% of nucleated cells in bone marrow at the start of treatment. These parameters improved markedly to 1, 590 mg/dl and 22.0%, respectively, in the 4 months immediately prior to his death due to pneumonia. Thalidomide caused peripheral neuropathy and constipation at a dose of 100 mg daily in the first week of treatment, but adverse effects resolved upon dose reduction. Thalidomide represents a valid therapeutic option for some myeloma patients receiving hemodialysis.
(Internal Medicine 42: 605-608, 2003)

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We report a rare case of bilateral primary adrenal non-Hodgkin's lymphoma with adrenal failure. A 66-year-old woman developed symptoms of adrenal failure. The cause of adrenal failure was suspected to be malignant lymphoma based on the high levels of serum soluble interleukin-2 receptor and LDH. Bilateral adrenalectomy was performed and pathological examination showed intravascular large B-cell lymphoma (IVL). Although complete remission was achieved, recurrence occurred three months later with brain metastases. IVL should be suspected in patients with bilateral adrenal tumors who present with rapidly progressive adrenal failure.
(Internal Medicine 42: 609-614, 2003)

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We report a 35-year-old man with gliomatosis cerebri, of which fluid-attenuated inversion-recovery (FLAIR) and T2-weighted magnetic resonance (MR) images revealed diffuse and high signal intensity areas in the bilateral cerebral hemispheres, bilateral middle cerebellar peduncles, cerebellum and lumbosacral spinal cord. Malignant features were not detected by ¹²³I-IMP SPECT, ²⁰¹TI SPECT, ¹⁸F-fluorodeoxyglucose PET or MR spectroscopy. Histopathological examination of biopsy specimens from the right frontal lobe demonstrated diffuse infiltration of neoplastic cells with relative preservation of the underlying cytoarchitecture. Gliomatosis cerebri demonstrating a lumbosacral spinal cord lesion on MR images is rare and thus this case is important from the aspect of the differential diagnosis of spinal cord lesions.
(Internal Medicine 42: 615-618, 2003)

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We describe a rare case of systemic vasculitis associated with α1-antitrypsin (α1-AT) deficiency. Mutational analysis of the α1-AT gene in this patient revealed a homozygous α1-AT Mnichinan variant. α1-AT possesses broad-spectrum inhibitory activity against many serine proteases, including human neutrophil elastase, to help maintaining the crucial balance between proteases and protease inhibitors. The increase in free protease activity in the context of α1-AT deficiency may induce exacerbation of the vasculitis. This serious genetic defect severely affects the balance between a protease and a protease inhibitor at the pathological site.
(Internal Medicine 42: 619-623, 2003)

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