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Biomedical subjects

K Kanmatsuse

Publications and source records attributed to K Kanmatsuse.

At least 109 records · Page 6Linked to original sources

Appearance of nephrotic syndrome following interferon-alpha therapy in a patient with hepatitis B virus and hepatitis C virus coinfection.

A 59-year-old woman with hepatitis B surface antigen (HBsAg) and hepatitis C viral (HCV) antibody presented with proteinuria and hematuria. The patient was treated with interferon-alpha (INF-alpha) because plasma aminotransferase levels had been elevated and a liver biopsy had showed chronic active hepatitis. Her urinary protein excretion decreased as liver function normalized and her serum HCV-RNA was negative during treatment. Eleven weeks after completion of INF-alpha treatment, she suddenly presented with nephrotic-range proteinuria, although an improvement in the hepatic function was maintained. Renal pathologic findings were consistent with membranous glomerulonephritis (MGN), and HBsAg was detected in the glomeruli but not HCV. After treatment with prednisolone, her 24-hour protein excretion was below 0.7 g/day. To our knowledge this is the first report on hepatitis B virus MGN with nephrotic syndrome following IFN-alpha therapy for HCV. This suggests that treatment with INF-alpha might affect the immune processes and may be associated with the pathogenic mechanism in this patient.

Anti-Inflammatory Agents↗

Interleukin 12 upregulates the release of vascular permeability factor by peripheral blood mononuclear cells from patients with lipoid nephrosis.

The vascular permeability factor (VPF) is a lymphokine that has been shown to play a role in lipoid nephrosis (LN). Prior studies have shown that interleukin (IL) 12 promotes T helper type 1 differentiation and enhances production of T helper type 1 cytokines such as gamma interferon and IL-2. We, therefore, investigated the effects of recombinant human IL-12 on the release of VPF by peripheral blood mononuclear cells (PBMC) from LN patients. The VPF activity was measured according to the method of Ovary, with minor modifications. The goal of the present study was to examine the importance of IL-12 in concanavalin A induced VPF release in vitro. The levels of VPF were measured in a group of healthy subjects, LN patients with or without the nephrotic syndrome, and patients suffering from IgA nephropathy. There was a significantly increased concanavalin A induced release of VPF in LN and IgA nephropathy patients with nephrotic syndrome as compared with normal controls. Recombinant human IL-12 was found to enhance VPF release in a dose-dependent manner. Neutralization of endogenously produced IL-12 by anti-IL-12 antibody resulted in a decreased release of VPF by LN PBMC. These data indicate that endogenously produced IL-12 functions as a costimulatory molecule in vitro. Our data show that IL-12 can upregulate the release of VPF derived from LN PBMC. Thus IL-12 might be a potent adjuvant for inducing VPF. Therefore, IL-12 antagonists may interfere with newly initiated and ongoing VPF release associated with nephrotic syndrome.

Adolescent↗

Abnormal regulation of transforming growth factor-beta receptors on vascular smooth muscle cells from spontaneously hypertensive rats by angiotensin II.

The effects of angiotensin II (Ang II) on the expression and characteristics of transforming growth factor-beta (TGF-beta) receptors on vascular smooth muscle cells (VSMC) from Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) were investigated. TGF-beta-induced stimulation of DNA synthesis by VSMC from WKY rats was abolished with Ang II, whereas basal and TGF-beta-stimulated DNA synthesis by VSMC from SHR was increased with Ang II. Ang II stimulated DNA synthesis by VSMC from WKY rats in the presence but not in the absence of neutralizing antibody to TGF-beta1. Antibody to TGF-beta1 enhanced the stimulatory effect of Ang II on DNA synthesis by VSMC from SHR. Ang II increased the specific binding of TGF-beta to VSMC from WKY rats by increasing both the expression of the lower-affinity of TGF-beta receptors as well as the total number of TGF-beta binding sites. In contrast, VSMC from SHR showed a higher affinity and number of TGF-beta receptors in the absence of Ang II than did cells from WKY rats, and these parameters were not affected by Ang II. Ang II increased the expression of TGF-beta type I receptor mRNA in VSMC from WKY rats but had no effect of TGF-beta receptor type I or II mRNA in VSMC from SHR, which predominantly express the type II receptor. These results indicate that an increase in the expression of the TGF-beta type I receptor by Ang II may facilitate the ability of endogenous TGF-beta to counteract the stimulatory effect of Ang II on growth in VSMC from WKY rats, whereas endogenous TGF-beta induced by Ang II cannot counteract the growth-promoting action of Ang II in VSMC from SHR. The abnormal regulation of TGF-beta receptors by Ang II may be associated with the exaggerated growth of VSMC from SHR.

Angiotensin II↗

Angiographic study of mutant tissue-type plasminogen activator versus urokinase for acute myocardial infarction.

The effects and problems of intravenous thrombolytic therapy with a bolus injection of mutant tissue plasminogen activator (t-PA) were investigated in 34 patients with first acute myocardial infarction (AMI). In contrast, 114 patients were selected from 1,003 patients with AMI for treatment using intravenous infusion urokinase (UK). Angiography of these 148 patients revealed a complete occlusion of infarct-related artery with no clear contraindications to the study treatment. With the exception of thrombolysis in myocardial infarction (TIMI-3) recanalization 60 min after a bolus injection of mutant t-PA, the patients were given intracoronary UK in addition to mutant t-PA. The study comparisons were assessed using the following criteria: (1) 60-min assessment of recanalization rates, mutant t-PA vs UK; (2) time interval from initiation of thrombolysis to recanalization, mutant t-PA vs UK; (3) angiographic reocclusion rates within 1 month, mutant t-PA alone vs UK vs mutant t-PA plus UK; and (4) intracerebral hemorrhage rates, mutant t-PA alone vs UK vs mutant t-PA plus UK. There were no significant differences in the recanalization rates between mutant t-PA and UK, but there was a significant reduction in the time to recanalization with mutant t-PA (31.8 +/- 12.7 min) compared with UK (56.5 +/- 6.3 min). There was a significant difference in the reocclusion rates among the 3 treatment groups (20% mutant t-PA alone vs 4% UK vs 0% mutant t-PA plus UK). On the other hand, no significant differences in intracerebral hemorrhage rates among the 3 treatments were observed. In conclusion, thrombolytic therapy with a bolus injection of mutant t-PA achieved more rapid recanalization, but treatment with mutant t-PA led to a high rate of reocclusion.

Acute Disease↗

Calcium channel blockers shorten the periodicity of ultradian variation in blood pressure in patients with essential hypertension.

We studied ultradian and circadian variations in blood pressure (BP) in patients with essential hypertension who were receiving antihypertensive agents. No patient had previously received antihypertensive agents before this study began. After a 2-wk control period, we performed ambulatory blood pressure monitoring (ABPM) in 86 patients with essential hypertension (WHO stages I or II). The patients were then given a long-acting angiotensin converting enzyme inhibitor (ACEI) (captopril or imidapril), a beta-receptor blocker (arotinolol or bisoprolol), or a calcium channel blocker (nisoldipine or benidipine) twice daily to control BP. We evaluated the patients' BP once every 2 wk to ensure optimal control. After 12 wk, ultradian and circadian variations in BP were analyzed by the maximum entropy method (MEM). All antihypertensive agents decreased office systolic BP (SBP), office diastolic BP (DBP), 24-h SBP, and 24-h DBP. ACEI did not change office, 24-h, daytime, or nighttime pulse rate (PR). Arotinolol and bisoprolol decreased 24-h PR. All antihypertensive agents decreased 24-h, daytime, and nighttime pressure rate product. MEM showed that no antihypertensive agent affected the circadian variation in the 1st peak (24-h periodicity) of SBP, DBP, or PR. However, calcium channel blockers shortened the periodicity of circadian variations in the 2nd peak (12-h periodicity) of SBP and the 3rd peak (8 to 6 h periodicity) of SBP. Therefore, ultradian variations in BP should be carefully monitored in hypertensive patients treated with calcium channel blockers.

Activity Cycles↗

Intracoronary ST-segment alternans during coronary balloon angioplasty.

ST-segment alternans has been described in experimental coronary artery occlusion and in patients with variant angina. It is also seen during coronary angioplasty. This report describes a patient who on balloon inflation during coronary angioplasty demonstrated ST-segment alternans only on intracoronary electrocardiogram but did not on surface 12 lead electrocardiogram. Hemodynamic pulsus alternans of the aortic pressure tracing was not observed during electrical alternans.

Adult↗

[Effects of doxazosin and hydralazine on insulin sensitivity and sympathetic function in spontaneously hypertensive rat (SHR)].

Since insulin resistance and/or hyperinsulinemia may contribute to structural changes of the vascular wall, the influence of antihypertensive agents on insulin sensitivity could interfere with the long term outcome of blood pressure reduction. Although it is postulated that increased peripheral circulation due to vasodilating agents improves insulin sensitivity, reflex sympathetic activation elicited by blood pressure reduction may influence insulin sensitivity. Thus we investigated the different effects of an alpha blocker (doxazosin) as well as a direct vasodilation (hydralazine) on insulin sensitivity and on sympathetic function in spontaneously hypertensive rats (SHR). Doxazosin and hydralazine decreased mean arterial pressure to a similar extent. Doxazosin, but not hydralazine decreased steady state blood glucose. Plasma norepinephrine increased in doxazosin and hydralazine treated groups as compared to the control group. Thus, despite their similar effects on blood pressure and plasma norepinephrine, alpha-1 blocker improved insulin sensitivity while the direct vasodilator failed to do so, and this difference is probably related to blockade of the alpha-1 receptor rather than to peripheral vasodilation.

Adrenergic alpha-Antagonists↗

[The influence of correction of acidosis on plasma level of branched-chain amino acids in chronic hemodialysis patients].

Seven patients undergoing chronic hemodialysis three times a week and whose plasma bicarbonate concentration on predialysis was consistently under 18 mmol/l due to bicarbonate dialysis (BCD), were treated with BCD for 2 weeks, then switched to acetate-free biofiltration (AFB) for 8 weeks. In both periods, the same high flux dialyzer (AN69HF) was used. The treatment time, dialysate flow rate and blood flow rate were kept constant in each patient during both periods. Plasma bicarbonate concentration (HCO3-), serum urea nitrogen (SUN), serum creatinine (Cr) and plasma amino acids concentrations (AA) were measured before dialysis and KT/V was calculated on the 2nd days of the last week in both periods. HCO3- on AFB was significantly higher than that on BCD (16.4 +/- 0.9 vs 19.9 +/- 1.8 mmol/l; p < 0.05). SUN on AFB was significantly lower than that on BCD even though the dialysis schedule and dietary content were not changed (84.7 +/- 3.7 vs 76.6 +/- 3.8 mg/dl; p < 0.05). TP, Cr and KT/V were not significantly different. Plasma total amino acid concentration (TAA) and plasma essential amino acid concentration (EAA) were not significantly different in both periods. In contrast, plasma branched-chain amino acid concentrations (BCAA) on AFB were significantly higher than that on BCD (313.5 +/- 44.3 vs 390.3 +/- 50.7 mumol/l; p < 0.05). Plasma BCAA concentrations, valine (VAL), leucine (LEU) and isoleucine (ILE), were significantly higher on AFB than that on BCD, respectively (p < 0.05). These findings suggest that optimal correction of the metabolic acidosis in chronic hemodialysis patients by AFB leads to a significant increase in plasma BCAA concentration.

Acidosis, Lactic↗

[Pathogenesis of acute coronary syndromes].

Coronary artery diseases may categorized into asymptomatic disease, angina pectoris, myocardial infarction, chronic heart failure, and sudden coronary death. Unstable angina, acute myocardial infarction, and sudden cardiac death are known as the acute coronary syndromes. Coronary atheroma is unstable in the patients with acute coronary syndromes. Stable plaques will be unstable when dynamic alterations occur. The alterations are plaque rupture, plaque hemorrhage, coronary thrombosis and vasospasm. They act each other. We analysed the histopathology of coronary arteries who died of acute myocardial infarction in 85 cases. It showed that the risk factors of plaque rupture are clusters of form cells, eccentric plaque with soft lipid rich core, and thinning of fibrous cap in atheroma. Most of these cases ruptured at edge of the atheroma.

Acute Disease↗

[The issues of emergency medical system in patients with prehospital cardiac arrest complicating acute coronary syndrome in Japan].

Each year approximately 30,000 persons in Japan experience prehospital cardiac arrest complicating acute coronary syndrome, and about 96 percent of them die. The majority of these sudden cardiac deaths are the result of fatal arrhythmias that often can be stopped by rapid initial medical care. In Tokyo, however, the first responder to provide cardiopulmonary resuscitation are about 10 percent, the successful defibrillation rate by Japanese paramedics who are not authorized advanced cardiac life support (ACLS) with drugs are about 15 percent and there are very few cardiologists who have been engaged in ACLS and initial management of suspected acute coronary syndrome in the emergency department. Therefore, each community emergency medical system should develop a plan to provide rapid initial medical care to patients with cardiac arrest (those with and without acute coronary syndrome).

Acute Disease↗

[Beneficial effect of salazosulfapyridine (SASP) in a patient with secondary renal amyloidosis].

A 55-year old female with rheumatoid arthritis (RA) had presented with proteinuria since July 1996. She was referred to us for persistent edema on her face and legs in November 1996. On admission, her 24-hour urinary protein excretion was 4.4 g/day, total serum protein level was 5.3 g/dl, and serum level of amyloid A protein (SAA) was elevated to 45.8 mg/ml. A percutaneous renal biopsy was performed, and light microscopy revealed varying degrees of amyloid deposits in the mesangial areas and arteriolar walls. The diagnosis of secondary amyloidosis (AA amyloidosis) was based on immunohistochemical staining for amyloid A protein using monoclonal antibody against SAA. Four weeks after treatment with salazosulfapyridine (SASP) and dipyridamole, proteinuria began to decrease and the edema had disappeared. Finally she recovered from nephrotic syndrome. AA amyloidosis has been thought to have a poor prognosis, with progression to renal failure. Since there is no specific effective therapy for the disease, it is very important to reduce the activity of the underlying cause. In our patient with renal amyloidosis following RA, SASP was evidently effective for arthritis and improvement of renal function. SASP might have a beneficial effect on AA amyloidosis by suppressing inflammatory cytokines.

Amyloidosis↗

Level of red blood cells in the urinary sediment reflects the degree of renal activity in Wegener's granulomatosis.

Symptoms due to renal lesions often disappear and smolder by successful treatment during the first episode of Wegener's granulomatosis (WG). It is indispensable to recognize an increase in disease activity and provide adequate treatment to inhibit the progression of renal dysfunction as well as regulate disease activity in patients with WG. We gave attention to red blood cells in urinary sediment (U-RBC), a criterion in the diagnosis of WG, to more exactly determine the degree of renal activity. Comparison of level of U-RBC with other laboratory data and renal histology was performed in the clinical course of six cases. The level of U-RBC altered reversibly during the period studied and correlated with the C-reactive protein level and erythrocyte sedimentation rate which reflect disease activity in cases with microhematuria before treatment. When U-RBC disappeared within eight weeks after treatment, glomerular histological change remained small. The reported cases revealed that the alteration in U-RBC was more sensitive and more specific for renal involvement than the other disease markers. In conclusion, the level of U-RBC reflects the degree of renal activity in WG. We propose that the quantitation of U-RBC is extremely useful in following patients with WG.

Adult↗

Plaque rupture as a cause of apparent coronary aneurysm formation following directional coronary atherectomy.

Late coronary aneurysm formation was observed following treatment by directional coronary atherectomy. Intravascular ultrasound disclosed that the mechanism involved was plaque rupture. The cause of coronary aneurysm may be multifactorial after coronary interventions. Intravascular ultrasound imaging is useful for understanding the pathologic mechanism of coronary aneurysm production.

Aortic Dissection↗