Pioglitazone reduces urinary albumin excretion in renin-angiotensin system inhibitor-treated type 2 diabetic patients with hypertension and microalbuminuria: the APRIME study.

BACKGROUND: The aim of his study was to compare the efficacy of pioglitazone with metformin on the reduction of albuminuria in type 2 diabetic patients with hypertension and microalbuminuria treated with renin-angiotensin system inhibitors (RAS-Is). METHODS: The open-label, randomized trial was performed in type 2 diabetic patients with hypertension and microalbuminuria. On the basis of the treatment with RAS-Is, 68 patients with microalbuminuria received either pioglitazone (15-30 mg/day; n = 32) or metformin (500-750 mg/day; n = 31) for 52 weeks. Urinary albumin-to-creatinine ratio (UACR) was measured every 12 weeks. RESULTS: After 52 weeks of treatment, the changes in the log-UACR from baseline were -8.3% in the pioglitazone group and +4.2% in the metformin group (p = 0.01), with similar glycemic and blood pressure changes. CONCLUSION: The combination of pioglitazone and RAS-Is showed therapeutic benefit in the reduction of urinary albumin excretion for type 2 diabetic patients with hypertension and microalbuminuria.

Regression of cardiac hypertrophy in type 2 diabetes with hypertension by candesartan.

This study was designed to compare the effect of candesartan on cardiac left ventricular mass in Japanese patients with that of amlodipine. A total of 40 type 2 diabetic patients with hypertension and left ventricular hypertrophy (LVH) were randomly assigned to receive candesartan (n=20) or amlodipine (n=20). The two treatments when administered for 6 months significantly reduced systolic and diastolic blood pressures (BPs) to a comparable extent. Notably, candesartan significantly reduced left ventricular mass index (LVMI: from 131.5+/-4.5 to 112.1+/-5.9g/m(2), P=0.0009, M+/-S.E.M.), LV posterior wall thickness (PWTd: from 10.3+/-0.3 to 9.1+/-0.3mm, P=0.0052) and interventricular septal thickness (IVSTd: from 10.7+/-0.4 to 9.3+/-0.4mm, P=0.0019) as determined by echocardiography in diastole, but amlodipine treatment did not. LVMI, PWTd and IVSTd were decreased more significantly by the treatment with candesartan than by that with amlodipine (P=0.020, 0.031 and 0.043). The present study thus revealed that candesartan effectively induced regression of LVH in type 2 diabetic patients with hypertension due to effects beyond reduction in BP.

A case of type 2 diabetes with a large abscess of the gastric wall successfully treated with a glycemic control and systemic antibiotics.

A case of type 2 diabetic patient, a 67-year-old woman, with a large abscess of the gastric wall which seemed to be a primary lesion is described for the first time. Fortunately, patient was successfully treated with both the maintenance of a good glycemic control and systemic antibiotics without laparotomy or drainage. Thus, a tight glycemic control and awareness of this disease should be reemphasized, and this may improve the prognosis of this rare and fatal one, even a poorly-controlled diabetes.

Effects of the prostanoids on the proliferation or hypertrophy of cultured murine aortic smooth muscle cells.

Effects of the prostanoids on the growth of cultured aortic vascular smooth muscle cells (VSMCs) were examined using mice lacking prostanoid receptors. Proliferation of VSMCs was assessed by measuring [(3)H]-thymidine incorporation and the cell number, and their hypertrophy by [(14)C]-leucine incorporation and protein content. In VSMCs from wild-type mice, expressions of mRNAs for the EP(4) and TP were most abundant, followed by those for the IP, EP(3) and FP, when examined by competitive reverse transcriptase-PCR. Those for the EP(1), EP(2) and DP, however, could not be detected. AE1-329, an EP(4) agonist, and cicaprost, an IP agonist, inhibited platelet derived growth factor (PDGF)-induced proliferation of VSMCs from wild-type mice; these inhibitory effects disappeared completely in VSMCs from EP(4)(-/-) and IP(-/-) mice, respectively. In accordance with these effects, AE1-329 and cicaprost stimulated cAMP production in VSMCs from wild-type mice, which were absent in VSMCs from EP(4)(-/-) and IP(-/-) mice, respectively. Effects of PGE(2) on cell proliferation and adenylate cyclase were almost similar with those of AE1-329 in VSMCs from wild-type mice, which disappeared in VSMCs from EP(4)(-/-) mice. PGD(2) inhibited PDGF-induced proliferation of VSMCs from both wild-type and DP(-/-) mice to a similar extent. This action of PGD(2) was also observed in VSMCs from EP4(-/-) and IP(-/-) mice. In VSMCs from wild-type mice, I-BOP, a TP agonist, showed potentiation of PDGF-induced hypertrophy. I-BOP failed to show this action in VSMCs from TP(-/-) mice. The specific agonists for the EP(1), EP(2) or EP(3), and PGF(2)alpha showed little effect on the growth of VSMCs. These results show that PGE(2), PGI(2) and TXA(2) modulate PDGF-induced proliferation or hypertrophy of VSMCs via the EP(4), IP and TP, respectively, and that the inhibitory effect of PGD(2) on PDGF-induced proliferation is not mediated by the DP, EP(4) or IP.