Restoration of endothelial function after repaired coarctation of the aorta--a case report

According to current literature, there is no clinical report regarding coronary spasm in the presence of aortic coarctation. There are no cases in which endothelial function was restored after the repair of aortic coarctation. A 29-year-old woman with aortic coarctation and acute myocardial infarction due to coronary spasm experienced restoration of endothelial function after the repair of aortic coarctation. This case may increase knowledge of the mechanism of coronary damage in human coronary arteries not only with a coarcted aorta but also with hypertensive heart.     

Glucagon acutely inhibits but chronically activates Na(+)/H(+) antiporter 3 activity in OKP cells.

BACKGROUND: We previously found that the Na(+)/H(+) exchanger 3 (NHE3) is localized in the apical membrane of the rat renal proximal tubule and thick ascending limb of Henle. In the present study, we examined the direct effect of glucagon on the opossum kidney P (OKP) cell Na(+)/H(+) antiporter, encoded by NHE3. METHODS: Na(+)/H(+) antiporter activity was measured as the rate of cell pH recovery from an acid load using 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein. Northern blot and Western blot analyses were performed using OKP NHE3 cDNA and anti-OKP-NHE3 antibodies. RESULTS: Glucagon (1 ng/ml) acutely (1 h) inhibited, but chronically (24 h) activated NHE3 activity in OKP cells. These effects were blocked by either KT5720 or RpcAMP [protein kinase A (PKA) inhibitors], and mimicked by 10(-4) M dibutyryl-cAMP. Both NHE3 mRNA and protein abundance increased with the 24-hour incubation in glucagon or dibutyryl-cAMP. Cycloheximide did not prevent a significant increase in NHE3 activity at 24 h. We therefore examined NHE3 protein abundance in the surface membrane by the biotinylation method. cAMP or glucagon significantly increased NHE3 protein abundance in the surface membrane when incubated with cycloheximide for 24 h. CONCLUSIONS: Glucagon acutely inhibits but chronically activates NHE3 activity in OKP cells via a PKA-dependent pathway. Both protein-synthesis-dependent and -independent mechanisms play important roles in the chronic activation of NHE3.     

Extreme hyperbilirubinemia induced by endoscopic injection sclerotherapy in a patient with esophageal varices and thalassemia: Report of a case

We describe herein the case of a 57-year-old man with thalassemia who developed acute liver failure after undergoing endoscopic injection sclerotherapy (EIS) to control hemorrhage from a ruptured esophageal varix. The patient, who had been comfirmed as having liver cirrhosis due to chronic hepatitis C with thalassemia in 1989, was admitted to our department to undergo EIS for esophageal varices, at which time his serum total bilirubin level was 5.5 mg/dl. As a small amount of hematemesis occurred just after a percutaneous transhepatic portography was performed, emergency EIS was carried out, following which the serum total bilirubin level markedly increased, mainly with a direct fraction, until it reached 70 mg/dl. The patient eventually died from acute liver failure with extreme hyperbilrubinemia on the 27th day after experiencing hematemesis despite all treatment. This unfortunate case demonstrates that sclerotherapy could be an inappropriate method of treatment for patients with hemolytic disease.     

Detection of Gangliosides as N-Glycolylneuraminic Acid-specific Tumor-associated Hanganutziu-Deicher Antigen in Human Retinoblastoma Cells

Gangliosides were shown to bear the tumor-associated N -glycolylneuraminic acid (NeuGc)-specific Hanganutziu-Deicher (HD) antigen expressed in human retinoblastoma cells. HD antigenie gangliosides were detected by thin-layer chromatography/enzyme-immunostaining using affinity-purified chicken antibody against GM3 containing NeuGc and horseradish peroxidase-conjugated anti-chicken IgG. One to four species of the antigenic gangliosides were detected from all of 4 cell lines, Y79, WERI-Rb1, TOTL1, and YK, as well as freshly cultured retinoblastoma cells and isolated tumor tissue. All cases contained GMS(NeuGc) as an HD antigen. No HD antigenic ganglioside was detected in normal retinal tissues by the same procedure.     

Is the Volume of the Parathyroid Gland a Predictor of Maxacalcitol Response in Advanced Secondary Hyperparathyroidism?

We evaluated the relationship between the volume of parathyroid glands estimated by ultrasonography (US) and response of 22-oxa calcitriol (Maxacalcitol, OCT) in patients with secondary hyperparathyroidism (2HPT) to evaluate whether the volume can be a predictor of the OCT response. Eleven institutes participated in this study. Ninety-four patients with advanced 2HPT were enrolled. The volume of the parathyroid glands were estimated by US before and 6 months after OCT treatment. The response of OCT treatment was classified into three groups (Group A: i-PTH < 300 pg/mL; Group B: 300 pg/mL < or = i-PTH < 500 pg/mL; Group C: i-PTH > or = 500 pg/mL). Forty-eight patients were in Group A, 28 patients in Group B, and 18 patients in Group C. The PTH levels at the beginning and 6 months were 458.3-199.1 pg/mL (P < 0.0001) in Group A, 524.6-403.2 pg/mL (P = 0.007) in Group B and 736.7-613.6 pg/mL (ns) in Group C, respectively. The volume of the largest gland in Group B was significantly larger than that in Group A (96.2 vs. 343.2 mm3: P < 0.001). Clinical factors affecting response of OCT was evaluated by logistic regression analysis and only the volume of the largest gland was a significant factor. In the patients whose volume was less than 300 mm3, the OCT response was significantly effective. We conclude that the glandular volume of the largest parathyroid gland estimated by US can be a useful factor to predict the OCT response in patients with moderate or severe renal HPT.     

Late stent malapposition with marked positive vascular remodeling observed only at the site of drug-eluting stents after multivessel coronary stenting

A 74-year-old woman presented with effort-induced chest pain. Diagnostic coronary angiography revealed three-vessel disease. A successful angioplasty was performed with two sirolimus-eluting stents placed in the left anterior descending artery (LAD) and left circumflex artery (LCX). The right coronary artery (RCA) was treated with a bare-metal stent. Follow-up angiography and intravascular ultrasound (IVUS) assessment were performed 8 months later, which showed late stent malapposition (LSM) with marked positive vascular remodeling around the drug-eluting stents (DES) in both LAD and LCX lesions, but there was no evidence of ectatic area around the BMS in the RCA lesion. Compared with the baseline IVUS, a significant increase in external elastic membrane (EEM) cross-sectional area was found. Twenty-seven months later, we performed repeat follow-up angiography. Intravascular ultrasound still showed vessel malapposition. A previous report showed that aneurysmal dilatation of the stented segment with severe localized hypersensitivity reaction could be a potential cause of late thrombosis after DES implantation. If LSM is related to hypersensitivity of the DES, it may have a potential risk of adverse events. Although there is a paucity of data regarding malapposition as the cause of adverse events, careful long-term follow-up of patients with vessel enlargement after DES placement is recommended.