Proton pump inhibitor use significantly increases the risk of cryptogenic liver abscess: a population-based study

Y-P Wang1, C-J Liu, T-J Chen

  • 1Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.

Abstract

Insights

Proton pump inhibitor use increases the risk of liver abscess. This study found a significant association between proton pump inhibitor therapy and cryptogenic liver abscess development.

Area of Science:

  • Gastroenterology
  • Hepatology
  • Infectious Diseases

Background:

  • Proton pump inhibitors (PPIs) elevate gastric pH, potentially compromising defenses against ingested pathogens.
  • This mechanism may facilitate the intestinal overgrowth of virulent Klebsiella pneumoniae, leading to liver abscess.

Purpose of the Study:

  • To investigate the association between proton pump inhibitor (PPI) use and cryptogenic liver abscess in Taiwan.
  • To quantify the risk of liver abscess associated with PPIs.

Main Methods:

  • A population-based case-control study was conducted using Taiwan's National Health Insurance Research Database.
  • Data from 958 adult liver abscess cases and 3832 matched controls (2000-2010) were analyzed.
  • Conditional logistic regression estimated adjusted odds ratios (ORs) for PPI use prior to liver abscess.

Main Results:

  • Current PPI use (within 30 days) showed an adjusted OR of 4.7 for cryptogenic liver abscess.
  • Recent PPI use (within 31-90 days) had an adjusted OR of 2.9.
  • A dose-response relationship was observed, with PPIs exceeding 60 cumulative defined daily doses showing the highest OR (6.5).

Conclusions:

  • Proton pump inhibitor therapy within the 90 days preceding the study period was significantly associated with an increased risk of cryptogenic liver abscess.
  • These findings highlight a potential iatrogenic risk associated with PPI use.

Related Concept Videos

Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors01:13

Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors

Peptic ulcers, often induced by H. pylori infections or NSAID usage, arise from disruptions in the delicate balance of gastric acid production. Peptic ulcers stem from heightened gastric acid levels due to H. pylori infections or NSAID use. The protective mucus layer diminishes in the presence of these factors, allowing gastric acid to erode the stomach lining and form ulcers.
Gastric acid, a potent cocktail of hydrogen and chloride ions, is produced in specialized parietal cells within the...
1.4K
Drugs for Treatment of Constipation-Predominant IBS01:21

Drugs for Treatment of Constipation-Predominant IBS

Pharmacological therapies for IBS-C are designed to alleviate abdominal discomfort and enhance bowel function. In patients with IBS-C, fiber supplements may help soften stools and decrease straining, but may also lead to increased gas production and bloating. Osmotic laxatives like milk of magnesia are frequently used to soften stools and increase stool frequency in IBS-C patients. In addition, two drugs approved for use in severe IBS-C adult cases are linaclotide (Linzess) and lubiprostone...
1.3K
Acid Suppressive Drugs for Peptic Ulcer Disease: Antacids01:31

Acid Suppressive Drugs for Peptic Ulcer Disease: Antacids

In the complex environment of the gastric lumen, excessive acid secretion can lead to the formation or worsening of ulcers within the delicate mucosal layer. Antacids, such as sodium bicarbonate and calcium carbonate, provide relief by neutralizing this acid, transforming it into harmless salt and water. This neutralization process raises the gastric pH from a highly acidic level of 1 to a more basic 3-4, reducing the acidity within the stomach.
However, this neutralization reaction between...
1.0K
Peptic Ulcer Disease I: Introduction01:30

Peptic Ulcer Disease I: Introduction

Peptic Ulcer Disease (PUD) is characterized by mucosal excavation in the esophagus, stomach, pylorus, or duodenum. It can manifest as acute or chronic based on the extent and duration of mucosal involvement.
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
1.1K
Peptic Ulcer Disease IV: Management01:26

Peptic Ulcer Disease IV: Management

Medical treatment strategies for peptic ulcers encompass various methods. The primary goal of treatment is to diminish gastric acidity and strengthen mucosal defense mechanisms.
The therapeutic approach involves ensuring adequate rest, implementing drug therapy, promoting smoking cessation, making dietary modifications, and emphasizing long-term follow-up care.
Pharmacological management
The prevailing therapy for peptic ulcers involves a combination of managing the patient's current...
690
Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists01:28

Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists

Histamine H2 receptors, which are intricately located on the basolateral membrane of parietal cells, play a crucial role in modulating gastric acid secretion. When released from enterochromaffin-like cells, histamine engages H2 receptors, initiating the cyclic AMP (cAMP) pathway. In this pathway, adenylyl cyclase converts ATP into cAMP, elevating intracellular cAMP levels. The activation of protein kinase A follows, stimulating the proton pump. This stimulation prompts the secretion of hydrogen...
1.3K