Related Experiment Video
Updated: Aug 12, 2026
10:27
Recognition of Epidermal Transglutaminase by IgA and Tissue Transglutaminase 2 Antibodies in a Rare Case of Rhesus Dermatitis
Published on: December 15, 2011
Infantile Henoch-Schönlein purpura
Christina T Wong1, John W Harrington
1Department of Pediatrics, New York Medical College, Valhalla, New York, United States of America.
Emergency Medicine Australasia : EMA
|July 2, 2004
Summary
Infantile Henoch-Schönlein purpura (HSP) presents differently than in older children, with unique symptoms and prognoses. Physicians should consider this rare condition in infants with generalized purpura, arthritis, and fever.
Area of Science:
- Pediatrics
- Immunology
- Dermatology
Background:
- Henoch-Schönlein purpura (HSP) is a common vasculitis in childhood.
- Classic HSP presentation involves palpable purpura, arthritis, abdominal pain, and renal disease.
- Infantile HSP is rare and may present with atypical symptoms.
Observation:
- An infant presented with generalized palpable purpura, arthritis, and fever.
- The clinical presentation was atypical for classic childhood HSP.
- This case highlights the variability of HSP in very young children.
Findings:
- Infantile HSP exhibits distinct clinical manifestations compared to school-aged children.
- Prognostic differences exist between infantile and older childhood HSP.
- Generalized purpura, arthritis, and fever in infants can be indicative of HSP.
Implications:
- Increased physician awareness of infantile HSP is crucial for timely diagnosis.
- Considering infantile HSP in the differential diagnosis improves patient outcomes.
- Recognizing atypical presentations in infants is key for appropriate management.
Related Concept Videos
01:23Rheumatic Heart Disease I: Introduction
Rheumatic heart disease or RHD is a chronic condition that results from rheumatic fever, causing permanent damage to the heart valves.Etiology and Risk FactorsIt primarily arises from rheumatic fever, an inflammatory disease that can develop after untreated or inadequately treated group A streptococcal (GAS) pharyngitis. Streptococcus spreads through direct contact with oral or respiratory secretions. While the bacteria are the causative agents, factors like malnutrition, overcrowding, poor...
01:27Acute Pyelonephritis I: Introduction
Pyelonephritis is a bacterial infection that primarily affects the renal parenchyma and collecting system, including the renal pelvis, tubules, and interstitial tissue of one or both kidneys. It can be classified as either acute—a sudden, severe infection—or chronic, which refers to long-term or recurrent kidney infections.The primary cause of acute pyelonephritis (APN) is bacterial infection, with Escherichia coli accounting for approximately 70-80% of cases. Other bacteria, such as Proteus,...
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...
01:20Inflammatory Bowel Disease II: Ulcerative Colitis
Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal BarrierA...
01:25Jaundice
Jaundice, or icterus, is the yellow discoloration of the skin, sclerae, and mucous membranes. It happens when plasma bilirubin levels rise above 2.5-3 mg/dL, leading to bilirubin deposition in tissue.Bilirubin is a byproduct of hemoglobin degradation. In macrophages, hemoglobin breaks down into globin and heme. Globin is converted into amino acids, while heme is turned into biliverdin by heme oxygenase, which is then reduced to unconjugated bilirubin by biliverdin reductase.Unconjugated...
01:19Hypersensitivity Reactions: Immune-Complex Reactions
Type III hypersensitivity reactions occur when antigen–antibody complexes form and activate the complement system. Normally, these complexes help the clearance of antigens by phagocytes and red blood cells. However, when large numbers of immune complexes are present, they can deposit in tissues—particularly in the walls of blood vessels—leading to inflammation and tissue injury. These deposits trigger complement activation and neutrophil recruitment, resulting in serum sickness, a systemic...