Adverse Reactions Associated With Ticrynafen Use

There is evidence from knock-out mice that the extrahepatic vitamin K-dependent protein, matrix gla protein, is necessary to prevent arterial calcification. The aim of this study was to determine if a warfarin treatment regimen in rats, designed to cause extra-hepatic vitamin K deficiency, would also cause arterial calcification. Sprague-Dawley rats were treated from birth for 5-12 weeks with daily doses of warfarin and concurrent vitamin K1. This treatment causes an extrahepatic vitamin K deficiency without affecting the vitamin K-dependent blood clotting factors. At the end of treatment the rats were killed and the vascular system was examined for evidence of calcification. All treated animals showed extensive arterial calcification. The cerebral arteries and the veins and capillaries did not appear to be affected. It is likely that humans on long-term warfarin treatment have extrahepatic vitamin K deficiency and hence they are potentially at increased risk of developing arterial calcification.

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“…There have been isolated reports of renal stones associated with warfarin therapy in humans (McLain et al . 1980; Miller et al .…”

Section: Discussionmentioning

confidence: 99%

Warfarin exposure and calcification of the arterial system in the rat

Howe

Webster

2000

Int J Experimental Path

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“…5 The first group consists of drugs that induce metabolic abnormalities (e.g. hypercalciuria, 6,7 hypocitraturia, 8,9 hyperuricosuria, 10 and alteration of urine acidity 8,9 ) which subsequently provoke formation of metabolic calculi; e.g. Ca-containing stones and uric acid (UA) nephrolithiasis.…”

Section: Introductionmentioning

confidence: 99%

Kidney Stones and Ceftriaxone

Dursun¹,

Ötünçtemur

Özbek

2015

EMJ Urol

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Metabolic causes such as hypercalciuria, urinary tract infection, and obstruction are the most common aetiologies of urolithiasis, and drugs, although important in this regard, are rarely the cause of urolithiasis. Administration of one of these drugs, ceftriaxone (CTX), has been associated with biliary pseudolithiasis in adult and paediatric patients, and rarely may cause urolithiasis. Several factors, including drug concentration and incubation time, are very important for determining the degree of CTX/calcium (Ca) crystallisation in the urine. According to this data, CTX crystallisation was a dose and time-dependent reaction. It is particularly important to monitor patients on high-dose long-term CTX treatment with the urinary Ca to creatinine ratios, ultrasound sonography, and renal function testing, as these individuals may be at greater risk of large stones and renal damage. This type of screening may help prevent permanent complications in the future. This underlying review will help to educate readers on the pathophysiology and interaction between CTX and urolithiasis.

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The Effects of Eprosartan, an Angiotensin II AT₁ Receptor Antagonist, on Uric Acid Excretion in Patients with Mild to Moderate Essential Hypertension

Ilson

Martin

Boike

et al. 1998

The Journal of Clinical Pharma

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The effects of antihypertensive agents, including angiotensin II receptor antagonists, on urine uric acid excretion may have important clinical consequences. Therefore, the effects of single and repeated doses of eprosartan on uric acid excretion were evaluated in 57 male patients with mild-to-moderate essential hypertension in a double-blind, randomized, placebo-controlled, repeated dose, dose-rising, two-period, period-balanced, crossover study conducted in two parts. In part 1 (n = 33), the effects of eprosartan dose regimens of 50 mg, 100 mg, and 350 mg once daily and 150 mg every 12 hours on uric acid excretion were assessed. In part 2 (n = 24), the effects of eprosartan dose regimens of 600 mg, 800 mg, and 1,200 mg once daily on uric acid excretion were assessed. Eprosartan was well tolerated. There were no appreciable changes from predose values in fractional excretion of uric acid (FEua), urine uric acid excretion, urine uric acid to creatinine (Uua/Ucr) ratios, or serum uric acid concentrations after single or repeated doses of eprosartan. Mean Uua/Ucr ratios for eprosartan doses of 50 mg, 100 mg, or 350 mg daily or 150 mg every 12 hours were comparable to those for placebo. Mean FEua values and Uua/Ucr ratios for eprosartan doses of 600 mg, 800 mg, or 1,200 mg daily also were comparable to those for placebo. Single and repeated oral doses of eprosartan ranging from 50 mg to 1,200 mg daily had no effect on serum uric acid concentrations or urine uric acid excretion in patients with mild-to-moderate essential hypertension.

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Adverse Reactions Associated With Ticrynafen Use

Cited by 23 publications

References 5 publications

Warfarin exposure and calcification of the arterial system in the rat

Warfarin exposure and calcification of the arterial system in the rat

Kidney Stones and Ceftriaxone

The Effects of Eprosartan, an Angiotensin II AT₁ Receptor Antagonist, on Uric Acid Excretion in Patients with Mild to Moderate Essential Hypertension

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Adverse Reactions Associated With Ticrynafen Use

Cited by 23 publications

References 5 publications

Warfarin exposure and calcification of the arterial system in the rat

Warfarin exposure and calcification of the arterial system in the rat

Kidney Stones and Ceftriaxone

The Effects of Eprosartan, an Angiotensin II AT1 Receptor Antagonist, on Uric Acid Excretion in Patients with Mild to Moderate Essential Hypertension

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The Effects of Eprosartan, an Angiotensin II AT₁ Receptor Antagonist, on Uric Acid Excretion in Patients with Mild to Moderate Essential Hypertension