Related Experiment Video
Updated: Nov 29, 2025
05:31
Transradial Access Chemoembolization for Hepatocellular Carcinoma Patients
Published on: September 20, 2020
5.9K
Candesartan-induced cholestatic hepatitis: a case report
Benito Hermida Pérez1, Marta Izquierdo Romero2, Rosa García López1
1Aparato Digestivo, Hospital Universitario de Cabueñes.
Revista Espanola De Enfermedades Digestivas
|November 23, 2020
Summary
A 55-year-old male developed cholestatic hepatitis after starting candesartan cilexetil. Discontinuation of the medication led to complete recovery, confirming drug-induced liver injury.
Area of Science:
- Hepatology
- Clinical Pharmacology
Background:
- Drug-induced liver injury (DILI) is a significant clinical concern.
- Cholestatic hepatitis can result from various etiologies, necessitating thorough investigation.
Observation:
- A 55-year-old male presented with symptoms of cholestatic hepatitis.
- Initial investigations excluded common causes of hepatitis.
- Liver biopsy results were consistent with toxic hepatitis.
Findings:
- The patient reported initiating candesartan cilexetil 3 weeks before symptom onset.
- Withdrawal of candesartan cilexetil resulted in progressive improvement of cholestasis.
- Liver biochemistry normalized within 6 months post-discontinuation.
Implications:
- This case highlights candesartan cilexetil as a potential cause of drug-induced cholestatic hepatitis.
- The CIOMS/RUCAM scale supported the diagnosis of probable drug-induced liver injury.
- Clinicians should consider candesartan in the differential diagnosis of unexplained cholestatic hepatitis.
Related Concept Videos
01:30Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors
2.1K
Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
2.1K
01:25Antihypertensive Drugs: Direct Renin Inhibitors
1.1K
The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
1.1K
01:22Dose-Response Relationship: Potency and Efficacy
6.0K
The potency of a drug is the measure of its ability to produce a biological response and can be compared by looking at the half-maximum effective concentration or EC50 values of different drugs. A lower EC50 value indicates higher potency of the drug. In the dose–response curve of two antihypertensive drugs, candesartan and irbesartan, a significant difference is observed in their EC50 values. A lower EC50 value for candesartan indicates that it is more potent than irbesartan, as it...
6.0K
01:08Effect of Hepatic Disease on Pharmacokinetics: Dose Adjustments Due to Hepatic Impairment
92
Hepatic impairment, characterized by decreased liver function, does not uniformly mandate adjustments in drug dosage. Whether dosage modifications are necessary depends on various factors related to the drug's metabolism and elimination pathways. If a drug is primarily excreted via the kidneys and bypasses significant hepatic processing, if it undergoes minimal metabolic transformation in the liver, or if it is volatile and primarily expelled through the lungs, dose adjustments may not be...
92
01:26Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
690
The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
690
01:28Antihypertensive Drugs: Potassium-Sparing Diuretics
2.0K
Liddle syndrome is a genetically inherited form of hypertension characterized by the overactivity of epithelial sodium channels in the nephron, the functional unit of the kidney. This heightened activity leads to increased sodium reabsorption and excessive excretion of potassium. To counteract this, potassium-sparing diuretics such as amiloride are used. They function by blocking these sodium channels, thereby reducing the influx of sodium into the epithelial cells and minimizing the loss of...
2.0K