Related Experiment Video
Updated: Jul 11, 2026
08:56
Synthesis of a Borylated Ibuprofen Derivative Through Suzuki Cross-Coupling and Alkene Boracarboxylation Reactions
Published on: November 30, 2022
Ibuprofen-induced HUS.
N J Schoenmaker1, J J Weening, R T Krediet
1Department of Medicine, Academic Medical Center, University of Amsterdam, The Netherlands. niks50@hotmail.com
Clinical Nephrology
|October 6, 2007
Summary
Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause recurrent hemolytic uremic syndrome (HUS). A case report highlights ibuprofen as a potential trigger for HUS, emphasizing the need for prompt diagnosis and avoidance of drug re-exposure.
Area of Science:
- Nephrology
- Hematology
- Pharmacology
Background:
- Hemolytic uremic syndrome (HUS) is a triad of nonimmune hemolytic anemia, thrombocytopenia, and renal impairment.
- Drug-induced HUS is an emerging concern, with nonsteroidal anti-inflammatory drugs (NSAIDs) increasingly implicated.
- NSAIDs, commonly used analgesics, can paradoxically trigger severe HUS.
Observation:
- A 44-year-old woman presented with anemia and thrombocytopenia post-ibuprofen use.
- Diagnosis of HUS was established based on clinical presentation and laboratory findings.
- The patient's symptoms resolved following treatment with fresh-frozen plasma and plasma exchange.
Findings:
- Ibuprofen (NSAID) was identified as the sole potential cause of HUS in this patient.
- No other etiological factors for HUS were identified.
- Complete recovery was achieved after therapeutic interventions.
Implications:
- Early recognition of drug-induced HUS is crucial for effective management.
- Avoiding re-exposure to the causative NSAID is essential to prevent recurrent HUS.
- This case underscores the importance of considering NSAIDs in the differential diagnosis of HUS.
Related Concept Videos
01:21Drugs 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...
01:24Peptic Ulcer Disease II: Pathophysiology
Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...
01:28Acid 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...
01:30Peptic 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...
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...
01:25Peptic Ulcer Disease I: Introduction
Peptic ulcer disease (PUD) involves breaks in the gastrointestinal tract's mucosal lining, primarily in the stomach and duodenum, with less frequent occurrences in the lower esophagus or near the pylorus.Ulcers can be acute or chronic. Acute ulcers are short-lived with minimal inflammation and heal quickly after the irritant is removed. Chronic ulcers persist, may recur, and often cause scarring due to ongoing tissue damage. Superficial erosions affect only the mucosal layer and are called...
01:26Peptic 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 medication...
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 medication...