Long-term treatment with angiotensin II type 1 receptor antagonist, CV-11974, restores β-catenin mRNA expression in volume-overloaded rabbit hearts

2002 ◽  
Vol 17 (1) ◽  
pp. 36-41 ◽  
Author(s):  
Makoto Itoh ◽  
Y. Takeishi ◽  
Shigekazu Nakada ◽  
Takuya Miyamoto ◽  
Yuichi Tsunoda ◽  
...  
2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Simone Janett ◽  
Pietro Camozzi ◽  
Gabriëlla G. A. M. Peeters ◽  
Sebastiano A. G. Lava ◽  
Giacomo D. Simonetti ◽  
...  

In 2006, hypomagnesemia was first described as a complication of proton-pump inhibitors. To address this issue, we systematically reviewed the literature. Hypomagnesemia, mostly associated with hypocalcemic hypoparathyroidism and hypokalemia, was reported in 64 individuals on long-term proton-pump inhibitors. Hypomagnesemia recurred following replacement of one proton-pump inhibitor with another but not with a histamine type-2 receptor antagonist. The association between proton-pump inhibitors and magnesium metabolism was addressed in 14 case-control, cross-sectional studies. An association was found in 11 of them: 6 reports found that the use of proton-pump inhibitors is associated per se with a tendency towards hypomagnesemia, 2 found that this tendency is more pronounced in patients concurrently treated with diuretics, carboplatin, or cisplatin, and 2 found a relevant tendency to hypomagnesemia in patients with poor renal function. Finally, findings likely reflecting decreased intestinal magnesium uptake were observed on treatment with proton-pump inhibitors. Three studies did not disclose any relationship between magnesium metabolism and treatment with histamine type-2 receptor antagonists. In conclusion, proton-pump inhibitors may cause hypomagnesemia. In these cases, switching to a histamine type-2 receptor antagonist is advised.


Author(s):  
Brenden N. Moeun ◽  
Si Da Ling ◽  
Marco Gasparrini ◽  
Alissa K. Rutman ◽  
Sarita Negi ◽  
...  

2011 ◽  
Vol 50 (10) ◽  
pp. 1294-1295 ◽  
Author(s):  
Jens Greve ◽  
Thomas K. Hoffmann ◽  
Patrick Schuler ◽  
Stephan Lang ◽  
Adam Chaker ◽  
...  

Author(s):  
Abdulmaged Traish ◽  
Karim Sultan Haider ◽  
Gheorghe Doros ◽  
Ahmad Haider

AbstractBackgroundDutasteride has been successfully used in treatment of lower urinary tract symptoms (LUTS) secondary to benign prostatic hyperplasia (BPH). However, dutasteride inhibits 5α-reductase type 1 and type 2 enzymes and may compromises glucocorticoids and androgen metabolism and alters metabolic function resulting in undesirable metabolic and sexual adverse side effects.AimThe aim of this study was to investigate the long-term adverse effects of dutasteride therapy in men with BPH on: i) blood glucose, ii) glycated hemoglobin (HbAMethodsA retrospective registry study, with a cohort of 230 men aged between 47 and 68 years (mean 57.78 ± 4.81) were treated with dutasteride (0.5 mg/day) for LUTS, secondary to BPH. A second cohort of 230 men aged between 52 and 72 years (mean 62.62 ± 4.65) were treated with tamsulosin (0.4 mg). All men were followed up for 36–42 months. At intervals of 3–6 months, and at each visit, plasma glucose, HbAResultsLong-term treatment with dutasteride therapy is associated with significant improvements in LUTS, as assessed by reduction in prostate volume, IPSS and prostate specific antigen (PSA). Long-term dutasteride therapy, however, resulted in increased blood glucose, HbAConclusionOur findings suggest that long-term dutasteride therapy produces worsening of ED, reduced T levels and increased glucose, HbA


Life Sciences ◽  
2000 ◽  
Vol 66 (22) ◽  
pp. 2213-2219 ◽  
Author(s):  
Tiziana Rubino ◽  
Paola Massi ◽  
Daniela Viganò ◽  
Domenica Fuzio ◽  
Daniela Parolaro

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