Relationship between serum albumin level before initiating haemodialysis and angiographic severity of coronary atherosclerosis in end-stage renal disease patients.

BACKGROUND: In patients with chronic kidney disease (CKD), although strong associations have been observed between malnutrition and atherosclerosis, the relationship between serum albumin concentration and angiographic changes of coronary artery disease (CAD) remains poorly explored. The goal of the present study was, in patients with CKD, to clarify the relationship between the angiographic severity of CAD and serum albumin concentration reflecting either inflammation or nutrition or both. METHODS: In this study, 100 end-stage renal disease (ESRD) patients were enrolled, who commenced long-term dialysis therapy at our hospital and underwent coronary angiography within 3 months of the first haemodialysis (HD) session. Mean age was 63+/-11 years, 20% of the subjects were female and 62% had diabetes. Severity of CAD was evaluated in terms of (i) number of vessels exhibiting CAD (>or=75% stenosis) and (ii) Gensini score (GS). Clinical characteristics and laboratory findings were recorded at initiation of long-term HD therapy. We then evaluated a possible association with the presence and degree of CAD. RESULTS: Sixty-four patients exhibited signs of CAD. Forty-one among them (64%) had multivessel disease. On univariate logistic regression analysis, age, diabetes and hypoalbuminaemia were significantly associated with multivessel CAD. Univariate linear regression analysis demonstrated a positive correlation of age and diabetes with GS, and an inverse correlation of BMI and serum albumin level with GS. Stepwise regression analysis showed age and serum albumin level to be independently associated with multivessel CAD and GS. The ROC curves demonstrated best cut-off levels of age and albumin for predicting multivessel CAD to be 70 years and 3.15 g/dl, respectively. CONCLUSION: Hypoalbuminaemia at the initiation of dialysis is an important predictor of advanced CAD, particularly in male and in diabetic patients. It may reflect mainly a state of inflammation. However, malnutrition as a confounding factor cannot be entirely excluded.     

Concurrent presence of metabolic syndrome in obstructive sleep apnea syndrome exacerbates the cardiovascular risk: a sleep clinic cohort study.

This cross-sectional study was conducted to examine whether the obstructive sleep apnea syndrome (OSAS) is associated with elevation of the pulse wave velocity (PWV) and increase in the plasma levels of C-reactive protein (CRP), both of which are known markers of cardiovascular risk, and also to determine if the concurrent presence of the metabolic syndrome might exacerbate this elevation in the levels of these cardiovascular risk markers in subjects with OSAS. With these objectives, the PWV and serum CRP were measured in 184 subjects attending a sleep clinic. It was found that the PWV and CRP were higher in the subjects with OSAS (n=94) than in those without OSAS (n=90). Furthermore, among the subjects with OSAS, the PWV and CRP were higher in those with the concurrent presence of the metabolic syndrome (n= 41; PWV=1,562+/-19 cm/s; CRP=1.8+/-0.2 mg/l) than in those without metabolic syndrome (n=53; PWV=1,432+/-21 cm/s; CRP=1.2+/-0.1 mg/l) (p<0.05). A general linear model analysis demonstrated that OSAS and metabolic syndrome were independently associated with elevated PWV and increase of the plasma levels of CRP. OSAS appears to be associated with increased cardiovascular risk, as reflected by both elevated PWV and increase of the plasma CRP. The concurrent presence of metabolic syndrome may exacerbate this increase in cardiovascular risk in subjects with OSAS. Therefore, the concurrent presence of metabolic syndrome may constitute an additive cardiovascular risk factor in subjects with OSAS.     

Prefrontal cerebral activity during a simple “rock, paper, scissors” task measured by the noninvasive near-infrared spectroscopy method

We conducted a noninvasive near-infrared spectroscopy (NIRS) study using the game of rock, paper, scissors (RPS) as a simple neurocognitive task for the prefrontal cortex (PFC) in 15 healthy volunteers. We employed an opposite “to lose” RPS task coupled with a normal “to win” RPS task, since the former requires inhibition of behavior, one of the most important functions of the prefrontal cortex. During the NIRS examination, subjects had to present one of the three RPS hands in response to hands displayed randomly on a computer screen every 1.5 s, and were required to show hands that lose to the computer, or that beat the computer. We measured the relative concentrations of oxyhemoglobin (oxy-Hb) using the prefrontal probes of the NIRS system during the tasks. The increases in oxy-Hb during the “to win” RPS task were small, but were quite large and laterally dominant during the “to lose” RPS task. The difference between the two tasks might have been due to the participants’ cognitive conflict with losing on the RPS. We conclude that losing is better than winning on the RPS as a sensitive indicator in the NIRS examination of PFC.     

Hepatic infarction with portal thrombosis

A case of hepatic infarction with portal thrombosis is reported. A 63-year-old woman with liver cirrhosis and esophageal varices was admitted for treatment of the esophagel varices. Endoscopic variceal ligation (EVL) and endoscopic injection sclerotherapy (EIS) were performed. Two months later, she experienced right hypochondralgia and right flank pain. Serum transaminase levels were suddenly elevated, and computed tomography scans of the liver showed multiple small nodular lesions. Her condition worsened, and she died of hepatic failure. Autopsy revealed splenic and portal vein thrombosis, multiple hepatic infarction, and evidence of chronic pancreatitis. We believe that liver cirrhosis and chronic pancreatitis were the main risk factors for the portal thrombosis, and the treatment for esophageal varices appeared to have triggered the thrombosis. The hepatic infarction was caused by the portal thrombosis.     

The role of magnetic resonance cholangiopancreatography (MRCP) after resection of the pancreas

Magnetic resonance cholangiopancreatography (MRCP) was performed in 35 patients to evaluate the feasibility of its use as a postsurgical imaging technique after resection of the pancreas. The surgical procedures performed were: pancreatoduodenectomy in 22 patients, segmental pancreatectomy in 1, distal pancreatectomy in 7, and pyroluspreserving pancreatoduodenectomy in 5. The pancreatic duct was shown in its entirety in 24 of the 35 patients (68.6%) and was partially visualized in 8 patients (22.9%), but the intrahepatic and extrahepatic bile ducts were visualized completely in all patients. Furthermore, MRCP was able to demonstrate lesions in 3 of 6 patients who had shown clinical evidence of recurrence. The visualization of the pancreatic and bile duct system was satisfactory despite anatomical changes brought about by resection of the pancreas. Thus, we conclude that MRCP is an appropriate follow-up screening test for patients with suspected abnormalities of the biliary and pancreatic duct system.     

Reduced levels of MMP-2 and TIMP-1 in dyssegmental dysplasia.

Matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) were measured in a mild case of dyssegmental dysplasia. X-ray pictures of a female baby born vaginally at 39 weeks of gestation showed short, bent, dumbbell-shaped long bones of the limbs and profound dyssegmental ossification in the spine, findings characteristic of dyssegmental dysplasia. When the levels of MMP-1, MMP-2, MMP-9, TIMP-1, and TIMP-2 were measured, the levels of MMP-2 and TIMP-1 were significantly reduced. This case might provide a clue to disclose the etiology of dyssegmental dysplasia.     

Experimental study on the pathogenesis of acute ulceration in obstructive jaundice--with reference to gastric mucosal blood flow

We prepared obstructive jaundice models in rats in order to study the mechanism of acute ulceration in obstructive jaundice centering on impediments to gastric wall blood flow and changes in gastric mucosal NA and PGE2 when the rats were subjected to water immersion restraint stress. The results were: In the obstructive jaundice 2 weeks group, when subjected to water immersion restraint stress, gastric mucosal NA reached a dried up stage from the incipient stage, causing gastric mucosal impediments at the same time, showing a significant decrease of gastric mucosal PGE2. Intragastric pH was at a similar level of excessive acidity in all groups; gastric acid is believed to be a secondary factor promoting ulceration. Gastric mucosal PGE2 showed a significant decrease coinciding with the increase in ulceration index, being a possible factor of ulceration; it is also presumed to regulate gastric wall blood flow alternatively with gastric mucosal NA. Pre-treatment with PGE2 prior to loading stress resulted in a decrease in gastric wall blood flow being significantly controlled. The administration of PGE2 brought about an improvement in gastric wall blood flow and a consequent increase in gastric mucosal NA, being judged effective for acute ulceration in obstructive jaundice.