One and a half ventricle repair for Ebstein’s anomaly

The surgical strategy for patients having Ebstein’s anomaly and hypoplastic right ventricle is controversial. An 11-year-old boy patient having such condition, with estimated end-diastolic volume index of the atrialized and functional right ventricle being 70% of normally expected values, underwent biventricular repair. Immediately after the surgery, however, he developed right heart failure with the central venous pressure of 11 mmHg. He consequently underwent additional bidirectional cavopulmonary anastomosis, thereby converting the biventricular repair into one and a half ventricle repair. He recovered uneventfully and is doing well 2 years after the surgery.     

Intraoperative angiographic assessment of graft patency during extracranial-intracranial bypass procedures

The use of intraoperative angiography to monitor graft patency was retrospectively reviewed in extracranial-intracranial bypass procedures. Forty-two patients underwent 43 extracranial-intracranial bypass procedures with the use of intraoperative angiography. Superficial temporal artery (STA)-middle cerebral artery (MCA) bypass was performed in 41 patients (42 procedures) with ischemic cerebrovascular diseases, and vertebral artery-MCA bypass using radial artery graft for intentional ligation of the common carotid artery in one patient with nasopharyngeal carcinoma. Intraoperative angiography provided high-quality subtraction images in every case. There were no complications due to angiography. Graft occlusion was observed intraoperatively in three cases, but an additional procedure reopened the occluded graft in all three cases. Graft patency rate was 100% after surgery. Outcome was excellent in 40 patients and good in one patient who underwent STA-MCA bypass. Intraoperative angiography provides useful information regarding graft patency during bypass surgery. Intraoperative assessment prior to wound closure allows for the recognition and correction of technical failure and decreases the risk of postoperative complications.     

Combination of Obesity with Hyperglycemia is a Risk Factor for the Presence of Vertebral Fractures in Type 2 Diabetic Men

Although patients with type 2 diabetes show no bone mineral density (BMD) reduction, fracture risks are known to increase. It is unclear why the patients have an increased risk of fracture despite sufficient BMD. We investigated the relationships of body mass index (BMI), HbA_1c, and urinary C-peptide (uC-peptide) versus BMD, bone metabolic markers, serum adiponectin, and prevalent vertebral fracture (VF). A total of 163 Japanese type 2 diabetic men were consecutively recruited, and radiographic and biochemical data were collected. BMI was positively correlated with BMD at the whole body, lumbar spine, and femoral neck (P < 0.05) and negatively correlated with osteocalcin and urinary N-terminal cross-linked telopeptide of type-I collagen (uNTX) (P < 0.01). HbA_1c was negatively correlated with osteocalcin (P < 0.01) but not BMD at any site. Subjects were classified into four groups based on BMI and HbA_1c (group LL BMI < 24 and HbA_1c < 9, group LH BMI < 24 and HbA_1c ≧ 9, group HL BMI ≧ 24 and HbA_1c < 9, group HH BMI ≧ 24 and HbA_1c ≧ 9). Serum adiponectin, osteocalcin, and uNTX were lower and the incidence of VF was higher despite sufficient BMD in the HH group. Multivariate logistic regression analysis adjusted for age, duration of diabetes, uC-peptide, and estimated glomerular filtration rate showed that the HH group was associated with the presence of a VF and multiple VFs (odds ratio [OR] = 3.056, 95% confidence interval [CI] 1.031–9.056, P = 0.0439, and OR = 5.415, 95% CI 1.126–26.040, P = 0.0350, respectively). Combination of obesity with hyperglycemia was a risk factor for VF despite sufficient BMD in diabetic men.     

Repair of an Abdominal Aortic Aneurysm with a Remarkably Dilated Meandering Artery: Report of a Case

A 73-year-old man on dialysis for chronic renal dysfunction was referred to our hospital for surgical treatment of an abdominal aortic aneurysm (AAA). Preoperative angiography showed a remarkably developed meandering artery branching from the inferior mesenteric artery (IMA). The superior mesenteric and celiac arteries were occluded at the origin, and all blood flow to the abdominal organs was apparently supplied by collateral circulation from the IMA. Considering the risk of mesenteric ischemia after aortic clamping in conjunction during surgery, we used a perfusion catheter with a 12-F balloon to create a shunt to the IMA from the subclavian artery. The operation was successful and the patient recovered uneventfully. We describe this surgical procedure for its effectiveness in preventing postoperative mesenteric ischemia in a rare case of an AAA with complex branching lesions.     

The sinusoidal pressure during ischemia-reperfusion injury in perfused mouse liver pretreated with or without L-NAME

BACKGROUND: Hepatic ischemia-reperfusion (I/R) is accompanied by liver weight gain and ascites formation possibly caused by an increase in the sinusoidal pressure, a determinant of hepatic transvascular fluid movement. However, changes in the sinusoidal pressure during hepatic I/R in mice are not known. It is also controversial whether nitric oxide (NO) exerts a beneficial or detrimental effect on hepatic I/R injury. We determined the changes in hepatic sinusoidal pressure and liver weight, and the effect of a NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME) on I/R injury of isolated mouse liver. MATERIALS AND METHODS: Isolated liver from 20 male outbred ddY mice was perfused portally with diluted blood (Hct 3%). After pretreatment with L-NAME (100 microm) or D-NAME (100 microm), ischemia was induced at room temperature by occlusion of the inflow line of the portal vein for 1 h followed by 1-h reperfusion in a recirculating manner. The sinusoidal pressure was assessed by the double vascular occlusion pressure (Pdo), and pre- and postsinusoidal resistance was determined. Liver injury was assessed by blood levels of alanine aminotransferase (ALT). RESULTS: In the d-NAME group (n=7), immediately after reperfusion, the portal pressure increased by 2.8 +/- 0.1 (SE) mmHg, which was accompanied by an increase in Pdo of 1.5 +/- 0.1 mmHg, indicating increases in pre- and postsinusoidal resistance to a similar degree. Then, presinusoidal, but not postsinusoidal, resistance sustained increased until 60 min after reperfusion. Liver weight increased to 0.14 +/- 0.04 g/g liver after reperfusion, followed by a gradual return to baseline. Blood ALT levels increased at 60 min after reperfusion. There were no significant differences in changes in the variables between the D- and L-NAME (n=7) groups. In the time-matched non- I/R control group (n=6), no changes in variables were observed for 2 h. CONCLUSIONS: Mouse hepatic I/R causes marginal liver weight gain associated with a small and transient increase in the sinusoidal pressure, and nitric oxide does not play any significant roles in this injury.     

Lumbar posterolateral fusion inhibits sensory nerve ingrowth into punctured lumbar intervertebral discs and upregulation of CGRP immunoreactive DRG neuron innervating punctured discs in rats

Degeneration of lumbar intervertebral discs is thought to be a cause of low back pain. Studies have found that a cause of discogenic low back pain is intervertebral disc inflammation and axonal growth of afferent fibers innervating the disc. Lumbar spine fusion for chronic discogenic low back pain is considered an effective procedure. However, no study has investigated the mechanism of pain relief. We did this by applying Fluoro-Gold (FG) to the ventral aspect of the L4–L5 intervertebral discs of 40 rats. We exposed the nucleus pulposus to the annulus fibrosus in a disc punctured model. Rats were divided into 4 groups. Group A: Punctured intervertebral disc with sham posterolateral fusion (PLF) (n = 10), Group B: Punctured intervertebral disc with PLF (n = 15), Group C: Normal intervertebral disc (no puncture) with PLF (n = 10), and Group D: Normal disc (no disc puncture) with sham PLF (n = 5). Four weeks after surgery, bilateral L1–L5 dorsal root ganglia (DRGs) were stained with growth-associated protein 43 (GAP43), a marker of axonal growth, and calcitonin gene-related peptide (CGRP), a neuropeptide marker of pain. Bone union was evaluated using X-ray imaging. Of the FG-labeled neurons, the proportions of GAP43- and CGRP-immunoreactive (IR) neurons in Group A were significantly higher than in Group D (P < 0.05). The proportions of GAP43- and CGRP-IR neurons in bone union rats in Group B were significantly lower than in nonunion rats in Group B and in the rats in Group A (P < 0.05). No significant differences in GAP43- and CGRP-IR neurons were observed between bone union and nonunion rats in Group C and the rats in Group D (P > 0.05). PLF is strongly related to the downregulation of GAP43 and CGRP expression. Therefore, PLF may suppress the increase of inflammatory neuropeptides and the process of axonal growth. Moreover, these results may explain, in part, the mechanism of pain relief following lumbar spinal fusion for chronic discogenic low back pain in humans.     

Current status of hip bone densitometry in Japan: a nationwide survey

Hip fracture greatly impairs quality of life in patients with osteoporosis. Measurement of bone mineral density (BMD) in the hip, which is closely related to fracture risk, is therefore diagnostically important. Furthermore, since in some elderly individuals lumbar BMD may be overestimated because of vertebral fracture or spondylosis deformans, measurement of hip BMD is also important. However, hip BMD is unlikely to be measured as often as lumbar BMD in Japan. A questionnaire survey was conducted to determine how many institutions measure hip BMD. A total of 861 institutions responded to the survey, 596 (69%) of which performed hip bone densitometry. The number of such institutions per million population was calculated to be 4.7. Measurement of hip BMD was more frequent in university hospitals than in general hospitals, clinics, and non-medical institutions. Furthermore, 298 (51%) of 590 institutions measured hip BMD in more than 75% of all bone densitometry examinees. This is the first report on the current status of utilization of hip bone densitometry in Japan.     

Voriconazole-associated salt-losing nephropathy

A 74-year-old man was diagnosed with nephrotic syndrome due to focal segmental glomerulosclerosis, and steroid therapy was initiated. Subsequently, he was affected by deep mycosis, and hence, voriconazole (VRCZ) was administered. On the 16th day, he was transferred to our hospital because of somnolence and malaise. His systolic blood pressure was approximately 80 mmHg, and he showed decreased skin turgor, indicating volume depletion. Laboratory analysis revealed hyponatremia and liver dysfunction. Discontinuation of VRCZ and drip infusion of normal saline improved the consciousness disorder, hyponatremia, and liver dysfunction. The levels of antidiuretic hormone (ADH) and plasma renin activity were elevated. This patient showed high excreted urine sodium, despite volume depletion and low serum osmolality. Therefore, this patient was diagnosed with salt-losing nephropathy (SLN). SLN should be considered for treatment of VRCZ-associated hyponatremia, together with syndrome of inappropriate secretion of ADH.     

Hypermethylation of MCAM gene is associated with advanced tumor stage in prostate cancer

BACKGROUND: DNA methylation has emerged as a promising biomarker for prostate cancer detection. In this report, we screened 36 candidate genes generated by a bioinformatic analysis of the human genome, and found that the melanoma cell adhesion molecule (MCAM) was an excellent candidate for cancer-specific methylation in prostate cancer. METHODS: Direct sequencing of bisulfite-treated genomic DNA, conventional methylation-specific PCR (MSP), real-time quantitative methylation-specific PCR, immunohistochemistry, colony formation assay, and statistical analysis. RESULTS: We found that the melanoma cell adhesion molecule (MCAM) gene promoter was specifically methylated in prostate cancer cell lines and primary prostate cancer (PCa) but not in non-neoplastic prostate (BPH) tissues by direct sequencing of bisulfite-treated genomic DNA and conventional methylation-specific PCR (MSP). Further analysis with quantitative MSP showed greater hypermethylation of the MCAM promoter (80%, 70/88) in primary prostate cancer compared to 12.5% (3/24) in BPH. Prostatic intraepithelial neoplasias (PIN), potential precursors of prostate carcinoma, showed an intermediate methylation rate of 23% (7/30). We further observed that MCAM promoter methylation was directly correlated with tumor stage (pT3+pT4) (P = 0.001) and Gleason score (P = 0.018) in primary prostate carcinoma. CONCLUSIONS: Our results suggest that MCAM promoter hypermethylation deserves further attention as a potential diagnostic prostatic DNA marker in human prostate cancer.