Understanding Stevens-Johnson Syndrome (SJS)
Stevens-Johnson syndrome is a rare, severe, and unpredictable disorder affecting the skin and mucous membranes [1.4.1, 1.5.7]. It is considered a medical emergency requiring hospitalization [1.4.1]. The condition is typically a hypersensitivity reaction to a medication, though infections can also be a trigger [1.4.1, 1.5.7]. An SJS reaction usually begins one to three days before a rash with flu-like symptoms, such as fever, a sore mouth and throat, fatigue, and burning eyes [1.4.1]. This is followed by a painful red or purple rash that spreads and forms blisters. The top layer of the affected skin then dies and sheds [1.4.1].
The Link Between Antibiotics and SJS
Drugs are the primary cause of SJS, and antibiotics are implicated in over a third of drug-induced cases [1.2.1, 1.2.2]. A 2023 meta-analysis confirmed that antibiotics are associated with approximately 28% of all SJS/TEN cases globally [1.7.1]. The reaction can occur while actively using the medication or up to two weeks after discontinuation [1.3.1].
High-Risk Antibiotic Classes
While numerous antibiotics have been linked to SJS, some classes carry a significantly higher risk. Research consistently identifies the following as the most frequent precipitants:
- Sulfonamides: This class, particularly trimethoprim-sulfamethoxazole, is consistently ranked as the highest risk for causing SJS [1.2.1, 1.2.2, 1.2.5]. A major meta-analysis found that sulfonamides were responsible for 32% of antibiotic-associated SJS/TEN cases [1.2.3, 1.2.7].
- Penicillins: This broad class of beta-lactam antibiotics, including amoxicillin and ampicillin, is the second most commonly implicated group [1.2.1]. Penicillins account for about 22% of antibiotic-related SJS/TEN cases [1.2.3, 1.2.7].
- Cephalosporins: Another class of beta-lactam antibiotics, such as ceftriaxone and cefuroxime, is also a well-documented cause [1.2.1, 1.2.2]. They are associated with around 11% of antibiotic-induced cases [1.2.3, 1.2.7].
- Fluoroquinolones: This class, including ciprofloxacin and levofloxacin, is also a known trigger, though less common than the above classes, accounting for about 4% of cases [1.2.3, 1.2.5].
- Macrolides: While still a risk, macrolides like azithromycin are among the least common antibiotic classes to cause SJS, associated with roughly 2% of cases [1.2.3, 1.2.5].
- Other Implicated Antibiotics: Other antibiotics such as vancomycin, doxycycline, and metronidazole have also been associated with SJS cases [1.2.2, 1.2.5].
Comparison of Medications Associated with SJS/TEN
While antibiotics are a major cause, they are not the only ones. Many other drug categories can trigger SJS/TEN. It is crucial to recognize the broader landscape of high-risk medications.
| Medication Category | Common Examples | Relative Risk Level |
|---|---|---|
| Antibiotics | Sulfonamides (e.g., trimethoprim-sulfamethoxazole), Penicillins, Cephalosporins [1.2.1, 1.3.2] | High |
| Anticonvulsants | Carbamazepine, Lamotrigine, Phenytoin, Phenobarbital [1.3.2, 1.3.5] | High |
| Anti-gout Medications | Allopurinol [1.3.1, 1.3.2] | High |
| NSAIDs | Oxicam-type (Piroxicam), Diclofenac [1.3.2, 1.3.7] | Moderate |
| Antiretrovirals | Nevirapine [1.3.1, 1.3.2] | High |
| Analgesics | Acetaminophen (Paracetamol) [1.3.1, 1.3.2] | Low to Moderate |
SJS vs. Toxic Epidermal Necrolysis (TEN)
SJS and Toxic Epidermal Necrolysis (TEN) are considered part of the same disease spectrum, differing mainly in severity [1.6.4, 1.6.5]. The classification is based on the percentage of body surface area (BSA) where the skin has detached:
- SJS: Skin detachment affects less than 10% of the BSA [1.6.4, 1.6.5].
- SJS/TEN Overlap: Skin detachment is between 10% and 30% of the BSA [1.6.2, 1.6.5].
- TEN: Skin detachment affects more than 30% of the BSA [1.6.4, 1.6.5].
The mortality rate for SJS is around 10%, while for TEN it can be 25-35% or higher [1.6.1, 1.6.3].
Diagnosis and Treatment
Diagnosis of SJS is made based on a physical examination of the rash and mucous membranes, medical history (especially recent drug use), and sometimes a skin biopsy to confirm full-thickness skin necrosis [1.4.2, 1.4.4].
Treatment is a medical emergency and must occur in a hospital, often in an intensive care or burn unit [1.5.1, 1.5.3]. The core components of treatment include:
- Cessation of the Culprit Drug: The first and most critical step is to immediately stop the medication suspected of causing the reaction [1.5.1, 1.5.3].
- Supportive Care: This is the mainstay of treatment and includes fluid and electrolyte replacement (often intravenously), nutritional support, and wound care with non-adhesive dressings to protect the raw, exposed skin [1.5.1, 1.5.3].
- Pain Management: The condition is extremely painful, and appropriate pain medication is essential [1.5.1].
- Infection Control: Prophylactic antibiotics are often avoided, but any secondary infections are treated promptly [1.5.2, 1.5.5].
- Specialized Care: An ophthalmologist must be consulted for eye involvement to prevent long-term complications like blindness [1.5.1, 1.4.2].
- Medications: Systemic therapies are controversial, but may include corticosteroids, intravenous immune globulin (IVIG), or cyclosporine to modulate the immune response [1.5.1, 1.5.2].
Conclusion
While Stevens-Johnson syndrome is rare, its severity underscores the importance of vigilant prescribing and patient awareness. Antibiotics, particularly sulfonamides and penicillins, are among the most common triggers for this life-threatening condition [1.2.1]. Early recognition of flu-like symptoms followed by a painful rash after starting a new medication is critical. Immediate withdrawal of the suspected drug and emergency supportive care are paramount to improving patient outcomes and reducing the risk of mortality and long-term complications.
For more information, you may consult authoritative sources such as the National Institutes of Health (NIH).
