Hepatitis C virus (HCV) infection is one of the major causes of chronic liver disease worldwide. The critical role of innate as well as adaptive immunity has been reported in HCV persistence and liver injury. In the early phase of acute infection, HCV continues to replicate in the liver, suggesting the HCV capability of inhibiting innate immunity. The sustained, vigorous and multiepitopespecific CD4+ and CD8+ T cell responses are essential for spontaneous HCV clearance. HCVspecific CD8+ T cells are primary elements for HCV clearance by inducing hepatocyte apoptosis, in which Fas/CD95 is fundamentally involved. However, once HCV persistency develops, HCV utilizes multifaceted arms to subvert various immune effectors. During IFNαbased therapy, the enhancement of HCVspecific CD4+ T cell response followed by HCV eradication has been reported, however, it remains obscure whether the therapeutic HCV clearance is able to restore the durable immune competency to HCV. Further investigation is still warranted to establish the means to direct HCVspecific immune responses in the desired way.
Objective: Evidence suggests that the effectiveness of angiotensinconverting enzyme (ACE) inhibition diminishes with time, resulting in increasing angiotensin II levels, the action of which can be inhibited by the addition of an angiotensin receptor blocker (ARB). In the present study, the renal protective effects of ACE inhibitors and ARBs were compared over a fiveyear period in a prospective, randomized, openblind study in 68 nondiabetic Japanese patients with elevated serum creatinine levels. Patients and Methods: Japanese patients with renal insufficiency were randomly assigned to receive either an ACE inhibitor (benazepril 1.25 to 5 mg daily or trandolapril 0.5 to 4 mg daily) or ARB (candesartan 2 to 8 mg daily or losartan 25 to 100 mg daily) at the Kidney Disease Center at Saitama Medical School Hospital. The primary study endpoint was a change in glomerular filtration rate (GFR) between the baseline value and the last available value obtained during the fiveyear treatment period, as estimated by the CockcraftGault equation. Secondary endpoints included the annual changes in GFR, serum creatinine level, urinary protein excretion, and blood pressure, as well as the rate of development of endstage renal disease. Results: There were no significant differences in the primary endpoint between the two groups. However, after 4 years, the decline in GFR in patients treated with ARBs was significantly greater than that seen in patients treated with an ACE inhibitor (p<0.05). Furthermore, the rate of introduction of dialysis therapy was also significantly greater in the ARBtreated patients (52.7% in ACE inhibitor and 81.2% in ARB group at year 5. p<0.01). Conclusion: While our data suggested that ARB, like ACE, treatment might slow the progression of renal dysfunction, it also pointed to the necessity to be alerted to the progression to endstage renal disease with longterm medication.
Objective: Our objectives were to investigate the therapeutic effects of low protein diet (LPD) for chronic renal failure (CRF) in compliant patients with the diet, and to clarify the relationships to the sociopsychological factors. Patients and Methods: Sixtyfive patients (47 men and 18 women) with CRF who followed LPD (0.69 g/kg/day) for more than 3 months were recruited in this study. Compliance with the diet therapy was strictly assessed by the patients' dietary records, subsequent interviews regarding the status of daily dietary intake and estimated protein intakes calculated from urinary nitrogen excretion by 24hour urine collections. The changes of glomerular filtration rate (GFR), serum creatinine (Cr), blood urea nitrogen (BUN), the reciprocal of serum creatinine (1/Cr), scores of Medical Outcomes Study 36Item ShortForm Health Survey (SF36), scales of Profile of Mood States (POMS), scores of selfefficacy and social support were investigated. Results: Decline rate of GFR, elevation of Cr and BUN and reduction in 1/Cr were significantly lower in compliant patients than in noncompliant patients (p<0.05). There were no differences in SF36 scores between compliant and noncompliant patients. The POMS scales of depression/dejection were high in female noncompliant patients compared to other groups of patients (p<0.05). Selfefficacy score was higher in compliant patients than in noncompliant patients (p<0.05). Social support scores were significantly higher in male compliant patients than in others (p<0.05), and both emotional support and behavioral support showed interaction with both gender and compliance with diet therapy (p<0.05). Conclusion: LPD therapy is effective in suppressing the progression of CRF when it is welladhered to. There are no correlations of this diet therapy to healthrelated QOL. Social support and high selfefficacy for men and high selfefficacy for women are associated with improvement of the compliance with LPD therapy, leading to good therapeutic effects.
Symptomatic hypermagnesemia is rare and can be induced by exogenous magnesiumcontaining cathartics or antacids. We report a patient with hypermagnesemia. The patient was treated with continuous hemodiafiltration (CHDF); however, he died on the 4th hospital day. Hypermagnesemia is not easily detected because the magnesium level is not examined during routine investigations, and many physicians are relatively unfamiliar with hypermagnesemia. Hypermagnesemia should be considered in elderly patients presenting with hypotension, bradycardia, hyporeflexia, or respiratory depression, and particularly in patients with abnormal renal function or small bowel hypomotility. Magnesiumcontaining cathartics or antacids should be used more carefully in the elderly.
A 56yearold mentally retarded Japanese woman (intelligence quotient: 49) was admitted to our hospital with the chief complaints of headache, dizziness, vomiting, and lower limb paralysis. Laboratory tests showed severe hypokalemia, metabolic alkalosis, hypomagnesemia, and hypocalciuria. These findings suggested a diagnosis of Gitelman's syndrome (GS). We examined the thiazidesensitive NaCl cotransporter (TSC) gene for the mutations that can be responsible for Gitelman's syndrome, and confirmed the diagnosis. After potassium and magnesium supplementation, her paralysis improved dramatically. The marriage of her parents was consanguineous. She had nine siblings (all with mental retardation), among whom five had died of unknown causes during childhood. Familial mental retardation has never been detected before in Gitelman's syndrome. Here we report a rare case of Gitelman's syndrome with familial mental retardation.
A 71yearold Japanese woman who was seropositive for Tlymphotropic virus type1 (HTLV1) developed primary Burkitt lymphoma of the uterus. CT showed marked enlargement of the uterine body. Chromosomal abnormalities were detected in biopsied cells, and most showed the t (8; 14) (q24; q32) translocation. Fluorescence in situ hybridization (FISH) with a dualcolor stain for IgH/CMYC fusion showed 99% positively. Biopsies from abdominal operation were diagnosed as Burkitt lymphoma. Treatment was started with intensive chemotherapy according to a protocol for Burkitt lymphoma and matureB cell leukemia. Two regimens were done with four courses with rituximab. Treatment response was fast, with a documented and lasting first complete remission on CT and laboratory markers after the 4 cycle treatment.