Stevens-Johnson Syndrome (SJS)

Stevens-Johnson syndrome is a rare but very serious reaction that usually happens after the body is exposed to a trigger, most often a medicine. The reaction makes the top layer of the skin and the moist linings of the mouth, eyes, genitals, and airway very inflamed and fragile. Blisters can form. The skin can peel off in sheets. The person often has fever and feels very sick. Doctors group SJS together with another, larger-area version called toxic epidermal necrolysis (TEN). The amount of skin that peels off helps doctors tell the type: less than 10% of the body surface is SJS, 10–30% is SJS/TEN overlap, and more than 30% is TEN. All forms are emergencies and need hospital care. NCBIDermNet®

Stevens–Johnson syndrome (SJS) is a rare, severe allergic-type reaction that usually happens after starting a new medicine (sometimes after an infection). The immune system mistakenly attacks the skin and the thin, moist linings of the mouth, eyes, and genitals. The top layer of skin dies and peels, causing raw, painful areas—much like a burn. Doctors group SJS and toxic epidermal necrolysis (TEN) on the same spectrum. The difference is how much skin is involved: SJS is <10% of the body surface, TEN is >30%, and 10–30% is “overlap.” Early diagnosis, stopping the trigger drug, and expert supportive care save lives. FrontiersPMC

What is happening inside the body

Your immune system is built to protect you from germs. In SJS, the immune system is mistakenly activated against your own skin and mucous membranes, usually after a new drug is started. Special white blood cells (T cells) release “death signals” and toxic proteins that tell skin cells to die too quickly. This sudden wave of cell death makes the upper skin split from the lower skin, which creates blisters and raw, painful areas. Scientists have found several pathways that do this, including Fas/Fas-ligand and molecules such as granulysin, perforin, and granzyme. These pathways explain why skin loss can spread fast once the process starts. DermNet®

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Types

1. SJS – skin detachment under 10% of the body surface.

2. SJS/TEN overlap – skin detachment between 10% and 30%.

3. TEN – skin detachment over 30%.

All three share the same process and the same emergency nature. The label simply tells how widespread the skin loss is. NCBI

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Causes

Important note: in most people, a new medicine started in the past few days to 8 weeks is the main trigger. Stopping the culprit drug quickly is vital. Some infections can also trigger similar reactions, especially in children and teens. NCBI

1. Sulfonamide antibiotics (for example, trimethoprim-sulfamethoxazole) – one of the most common drug triggers worldwide. The reaction can appear within days to a few weeks of starting the antibiotic. NCBInhs.uk

2. Penicillin-family antibiotics – medicines like amoxicillin can rarely set off SJS in sensitive people. PMC

3. Cephalosporin antibiotics – related to penicillins; have been reported as triggers in some cases. NCBI

4. Quinolone antibiotics – drugs like ciprofloxacin are less common causes but are reported. NCBI

5. Allopurinol – used for gout; a well-known high-risk drug, especially at higher doses or in certain genetic backgrounds. NCBI

6. Carbamazepine – a seizure and nerve-pain drug; strong link in people carrying the HLA-B*15:02 gene (common in some Asian populations). Screening can prevent harm. NCBIPubMed

7. Lamotrigine – a mood and seizure medicine; risk is higher when the dose is raised too fast or with valproate. NCBI

8. Phenytoin – a seizure drug; part of the aromatic anticonvulsant group linked to SJS/TEN. NCBI

9. Phenobarbital – another anticonvulsant in the same high-risk family. NCBI

10. Oxicam-type NSAIDs (e.g., piroxicam, meloxicam) – a pain-killer group more clearly associated with SJS/TEN than other NSAIDs. NCBInhs.uk

11. Acetaminophen (paracetamol) – rarely a trigger, but listed in large reviews and case series. NCBI

12. Nevirapine – an antiretroviral; risk is higher in certain settings and at higher CD4 counts. NCBI

13. Minocycline – an antibiotic that has been reported as a cause in some patients. NCBI

14. Sulfasalazine – an anti-inflammatory used in bowel disease and arthritis; belongs to the sulfonamide family. nhs.uk

15. Iodinated contrast dyes – given for imaging scans; uncommon but recognized trigger. NCBI

16. Mycoplasma pneumoniae infection – can cause a related mucosal-predominant illness in children and teens and can overlap with SJS features. NCBIPMC

17. Herpesviruses and other viral infections – cytomegalovirus and others, rarely, have been linked. NCBI

18. Dengue and some other infections – rare associations have been reported. NCBI

19. Vaccinations (very rare) – SJS/TEN after vaccines is uncommon; when reported, other causes must be ruled out. NCBI

20. Genetic predisposition (HLA genes) – HLA-B15:02 with carbamazepine and HLA-B58:01 with allopurinol increase risk; testing is recommended in some populations and situations. files.cpicpgx.orgNCBI

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Common symptoms and signs

1. Fever and feeling very unwell – the body reacts like it has a bad flu, with high temperature, chills, and severe tiredness. DermNet®

2. Sore throat and trouble swallowing – the lining of the mouth and throat becomes inflamed and raw, making eating and drinking painful. DermNet®

3. Cough and runny nose – early “cold-like” symptoms often come a day or two before the skin changes. DermNet®

4. Sore, red, sticky eyes – the eyes can be very inflamed, light-sensitive, and painful; this needs eye-doctor care. DermNet®

5. Skin pain and tenderness – the skin hurts to touch even before blisters appear, which is a warning sign in drug rashes. DermNet®

6. Spreading red or purple spots – flat patches or target-like spots start on the trunk and spread quickly to the face and limbs. DermNet®

7. Flaccid blisters – soft blisters can form and then break, leaving raw areas. DermNet®

8. Skin peeling (detachment) – the top layer lifts off, sometimes in sheets, exposing wet, painful skin underneath. DermNet®

9. Positive Nikolsky sign – gentle rubbing of the skin causes the top layer to shear off; this is a bedside clue for doctors. DermNet®+1

10. Mouth ulcers and bleeding lips – the mouth lining breaks down, crusts form on the lips, and eating becomes hard. DermNet®

11. Genital pain and urinary problems – erosions can cause pain, stinging with urination, or trouble passing urine. DermNet®

12. Breathing problems – if the airway lining is involved, coughing and shortness of breath can develop. DermNet®

13. Diarrhea or belly pain – the gut lining can be affected in severe cases. DermNet®

14. Severe anxiety and distress – pain, appearance changes, and illness severity cause significant emotional stress. DermNet®

15. Dehydration and weight loss – fluid loss from the skin and poor oral intake can be rapid and dangerous without hospital support. DermNet®

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Diagnostic tests

A) Physical examination tests (what the clinician checks at the bedside)

1. Body surface area (BSA) estimate – the team maps how much skin is detached or likely to detach (for example, with the rule of nines). This number tells whether it is SJS, overlap, or TEN and guides the level of care. NCBI

2. Vital signs and general appearance – fever, fast heart rate, low blood pressure, and fast breathing tell how sick the person is and help triage to ICU or burn unit care. NCBI

3. Full skin and mucosal survey – doctors look carefully at the pattern of spots, blisters, raw areas, and all mucous membranes (eyes, mouth, genitals, anus). Finding two or more mucosal sites supports the diagnosis. DermNet®

4. Skin pain assessment – unusual skin tenderness out of proportion to the rash is a red flag for SJS/TEN rather than a simple drug rash. DermNet®

5. Daily progression charting – clinicians mark the borders of involved skin and measure changes each day to track spread or healing; this helps judge response to treatment and risk. DermNet®

6. Ophthalmology examination at the slit-lamp – an eye specialist checks the eye surface for erosions, ulcers, and scarring risk to protect vision early. DermNet®

B) Manual bedside signs and simple maneuvers

7. Nikolsky sign – very gentle side-to-side rubbing on red skin makes the top layer shear off. A positive sign supports SJS/TEN and helps tell it apart from many other rashes. DermNet®+1

8. Asboe-Hansen (blister-spread) sign – pressing on the top of a blister makes the fluid extend under nearby skin, showing how easily the top layer separates. This also supports the diagnosis. DermNet®

9. Capillary refill and skin turgor checks – a quick finger press on a nail or the skin checks circulation and hydration, which can be unstable when large skin areas are lost. (Clinical standard in acute dermatologic emergencies.)

10. Oral intake and swallow assessment – bedside checks for ability to drink and swallow safely; many patients need tube feeding or IV fluids because of mouth and throat pain. DermNet®

C) Laboratory and pathological tests

11. Skin biopsy (urgent, often with a rapid “frozen section”) – a tiny piece of skin is examined under the microscope. Typical findings are full-thickness death of the upper skin layer with little inflammation. This confirms the diagnosis and rules out look-alike diseases. NCBIDermNet®

12. Direct immunofluorescence (DIF) – a special stain on the biopsy looking for antibody deposits. In SJS/TEN it is usually negative, which helps separate it from autoimmune blistering diseases. NCBIDermNet®

13. Complete blood count (CBC) – can show anemia, low lymphocytes, sometimes low neutrophils; these numbers also feed into severity scores and infection risk plans. NCBIDermNet®

14. Electrolytes, kidney and liver tests – dehydration and organ strain are common; rising urea/creatinine or abnormal liver enzymes signal trouble and are part of severity scoring. NCBI

15. C-reactive protein (CRP) and other inflammatory markers – track the degree of inflammation and help monitor for infection superimposed on skin breakdown. (Common clinical practice in SJS/TEN care.)

16. Blood, wound, urine cultures – large raw surfaces invite infection; cultures guide targeted antibiotics if infection develops. DermNet®

17. Mycoplasma testing (PCR/serology) – in children and teens with marked mouth/eye symptoms and little skin rash, testing can detect M. pneumoniae, which can cause “MIRM,” a related entity with heavy mucositis. NCBIPMC

18. HIV test (with consent) – HIV increases the risk of severe drug reactions; knowing status guides care and medicine choices. (Epidemiologic risk discussed in SJS/TEN reviews.) NCBI

D) Electrodiagnostic and monitoring tests

19. Electrocardiogram (ECG) and continuous cardiac monitoring – severe illness, electrolyte shifts, and some drugs can affect the heart rhythm; ECG helps catch problems early. NCBI

20. Pulse oximetry (and, when needed, respiratory monitoring) – checks oxygen levels because airway and lung linings can be involved, and pneumonia or ARDS can occur. Chest care is a key part of management. DermNet®

E) Imaging tests (used when complications are suspected)

• Chest X-ray – looks for pneumonia or lung inflammation when cough, low oxygen, or breathing difficulty are present. NCBI

• CT chest (selectively) – used if doctors need a closer look at lung complications or to guide intensive care decisions. NCBI

Non-pharmacological (non-drug) treatments

(each item explains what it is, why it’s done, and how it helps)

1. Stop the culprit drug immediately.
   The very first treatment is to permanently stop the suspected trigger medicine(s). This removes the cause and prevents the reaction from “fueling” itself. Keep a list of all recent drugs (including OTC and herbal products) to help clinicians identify the likely culprit. Frontiers

2. Early transfer to an ICU/burn-capable unit.
   SJS behaves like a burn: patients need careful fluids, wound care, temperature control, and infection prevention. Specialized units have the protocols and equipment for this level of support, improving outcomes. PMC

3. Airway and breathing protection.
   Swelling and crusting can narrow the mouth, throat, and nose. Early airway assessment keeps breathing safe; oxygen, humidification, and (rarely) intubation may be required to prevent sudden airway compromise. PMC

4. Fluid and electrolyte resuscitation.
   Skin loss leaks fluid and salts. Teams replace these carefully and track urine output (goal commonly ~0.5–1 mL/kg/hour) to protect kidneys and maintain circulation. PMC

5. Thermoregulation (warm, neutral room).
   Without an intact skin barrier, people lose heat fast. A thermoneutral environment prevents shivering and extra stress on the body, supporting healing. PubMed

6. Wound care with non-adherent dressings.
   Loose, non-stick dressings protect raw skin, limit pain, and lower infection risk. Gentle handling avoids tearing fragile skin so re-epithelialization can proceed. PMC

7. Pain control and comfort.
   SJS is extremely painful. Proper, titrated analgesia (from acetaminophen to opioid infusions) reduces stress responses and helps patients drink, eat, and move—key to recovery. PMC

8. Infection surveillance (but no routine prophylactic antibiotics).
   Open skin invites infection, yet blanket antibiotics can select resistant organisms. Teams use sterile technique, screen for infection, and treat only when indicated. PMC

9. Early, high-protein nutrition (preferably enteral).
   SJS causes a hyper-metabolic, protein-wasting state. Early feeding—ideally by mouth or feeding tube—maintains calories and protein to rebuild skin and mucosa. Targets often include ~30–35 kcal/kg/day and ≥1.5–2 g protein/kg/day (adjusted individually and for kidney function). LippincottPMC

10. Eye care from day 1.
    An ophthalmology exam on admission is essential. Copious preservative-free lubricants, eyelid hygiene, and lysis of early adhesions prevent scarring that can permanently harm vision. PMC

11. Emergency amniotic membrane for severe eye involvement.
    When eyes are badly inflamed, amniotic membrane transplantation (AMT) placed in the first days can dramatically reduce scarring and long-term vision loss. PMC+1

12. Mouth and throat care.
    Saline rinses, topical anesthetics, and careful dental hygiene reduce pain and infection in the mouth, helping patients drink and meet nutritional goals. PMC

13. Genital/urinary care.
    Regular lubrication, gentle dilation protocols, and specialist input (gynecology/urology) prevent adhesions and strictures that can cause pain and sexual/urinary problems later. PMC

14. Blood clot prevention and mobilization.
    SJS/TEN patients have a high risk of deep-vein thrombosis. Early leg movement, compression devices, and—when safe—pharmacologic prophylaxis reduce that risk. PMC

15. Physical and occupational therapy.
    Early, guided movement maintains muscle strength and joint range; splints and exercises prevent contractures.

16. Psychological support.
    Acute pain, ICU care, and body-image changes are traumatic. Counseling and social work support improve coping and rehabilitation.

17. Gentle skin care and sun protection after healing.
    New skin is fragile and sun-sensitive for months. Emollients and sun protection lower itch, dryness, and discoloration risks.

18. Medication allergy documentation and medical ID.
    A written allergy plan, an updated medication list, and a medical alert card/bracelet help avoid accidental re-exposure.

19. Pharmacovigilance reporting & genetic counseling where relevant.
    Reporting the event helps public safety. In populations at risk (e.g., many Asian groups for certain drugs), clinicians may discuss HLA screening before future prescriptions (details below). NCBICPIC

20. Multidisciplinary teamwork + severity scoring (SCORTEN).
    Coordinated care among dermatology, critical care, ophthalmology, nutrition, rehab, and others—guided by SCORTEN—improves outcomes. PMC

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Drug treatments

Important: Doses below are typical ranges used in studies/clinical practice; individual dosing must be tailored by the treating team based on weight, organ function, and real-time status.

1. Systemic corticosteroids (e.g., IV methylprednisolone).
   Class: anti-inflammatory steroid. When: very early after diagnosis, in selected patients. Dose: common approaches include methylprednisolone 1–2 mg/kg/day IV; some centers use “pulse” 500–1000 mg/day for 3 days, then taper. Purpose/mechanism: dampens the overactive immune attack on skin/mucosa (reduces cytokines; limits keratinocyte death). Cautions/side effects: infection risk, high blood sugar, GI bleeding, delirium—teams co-manage with ulcer prophylaxis and glucose control. Evidence is mixed; benefits seem greater with early, short courses under expert supervision. Frontiers

2. Intravenous immunoglobulin (IVIG).
   Class: pooled antibodies (immunotherapy). When: early in moderate–severe disease, often with corticosteroids. Dose: many regimens, e.g., 0.4 g/kg/day for 3–5 days. Purpose/mechanism: may block Fas/FasL-mediated cell death; modulates immune signaling. Cautions: headache, clot risk, kidney strain; effectiveness as a single agent is inconsistent, but combined with steroids may reduce deaths in some analyses. PMC+1

3. Cyclosporine.
   Class: calcineurin inhibitor (T-cell blocker). When: early in the acute phase. Dose: 3–5 mg/kg/day in divided oral doses (dose-adjusted). Purpose/mechanism: directly suppresses cytotoxic T-cell activation driving skin death. Evidence: multiple meta-analyses suggest lower-than-predicted mortality versus supportive care alone. Cautions: kidney toxicity, high blood pressure, infection risk; careful monitoring is mandatory. Dove PressPMCFrontiers

4. Etanercept.
   Class: TNF-α inhibitor (biologic). When: early to moderate–severe SJS/TEN. Dose used in RCT: 25–50 mg subcutaneously twice weekly (weight-based) in one open-label randomized trial that showed faster skin healing and lower observed vs predicted mortality than steroids. Mechanism: blocks TNF-α and reduces granulysin, a key killer protein in SJS/TEN blisters. Cautions: infection risk; off-label for SJS/TEN and should be used by experienced teams only. JCI

5. Infliximab.
   Class: TNF-α inhibitor (biologic). When: selected severe cases when etanercept isn’t available/appropriate. Dose: often 5 mg/kg IV once (case-based). Purpose/mechanism: similar to etanercept—neutralizes TNF-α. Cautions: serious infection risk; evidence is limited to small series/case reports—specialist use only. The Hospitalist Blog

6. Topical ophthalmic corticosteroids (e.g., prednisolone acetate 1% drops).
   Class: anti-inflammatory eye drops. When: acute eye inflammation, under ophthalmologist supervision. Dose: commonly QID then taper. Purpose/mechanism: reduces conjunctival inflammation and scarring risk. Cautions: raise eye pressure, infection risk—short, guided courses only. PMC

7. Antimicrobial eye ointment (e.g., erythromycin) & lubricants.
   Class: topical antibiotic & artificial tears/gel. When: acutely to prevent secondary infection and keep surfaces moist. Dose: ointment BID–QID; preservative-free tears hourly/prn. Purpose/mechanism: protects damaged ocular surface and eyelids. Cautions: use non-preserved lubricants to avoid irritation; avoid sulfonamide eye meds if sulfa implicated. PMC

8. Enoxaparin (LMWH) for VTE prophylaxis.
   Class: anticoagulant. When: during hospitalization unless contraindicated. Dose: typical prophylaxis 40 mg SC daily (adjusted for weight/kidney function). Purpose/mechanism: prevents blood clots in a high-risk, immobilized state. Cautions: bleeding risk; not disease-modifying but reduces serious complications. PMC

9. Gastroprotection (e.g., proton pump inhibitors).
   Class: acid-suppressing drugs. When: if using high-dose steroids or at GI-bleed risk. Dose: standard once-daily dosing. Purpose: prevents steroid-related ulcers/bleeds. Cautions: long-term use risks—tailor duration.

10. Investigational immunomodulators (e.g., JAK inhibitors such as tofacitinib/baricitinib; IL-6 blockade such as tocilizumab).
    Class: targeted immune therapies. When: only in research or highly selected refractory cases. Purpose/mechanism: dampen specific inflammatory pathways implicated in SJS/TEN. Cautions: sparse evidence; may raise infection risk; not standard of care. (Evidence base for systemic agents overall remains mixed; cyclosporine and etanercept currently have the most encouraging signals.) PMC

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Dietary “molecular” supports

These do not treat SJS directly. They support healing in a hyper-metabolic, protein-losing state—principles borrowed from burn/critical-care nutrition and adapted by clinicians case-by-case.

1. Protein (whey/casein blends or high-protein diet).
   Aim for ≥1.5–2.0 g/kg/day protein unless kidney function limits intake; protein supplies amino acids to rebuild skin and mucosa. PMC

2. Calories (energy).
   Early enteral feeding targeting roughly 30–35 kcal/kg/day helps meet the energy cost of healing and prevents muscle breakdown. Lippincott

3. Vitamin C (ascorbic acid).
   Typical adjunct 500–1000 mg/day supports collagen formation and immune function in wound repair (avoid mega-doses in kidney disease).

4. Zinc.
   Common adjunct 15–40 mg elemental/day (short term) supports epithelialization; excess zinc can lower copper—use under dietitian oversight.

5. Vitamin A.
   Low-dose 5,000–10,000 IU/day (short term) supports epithelial and ocular surface health; avoid in pregnancy/liver disease.

6. Selenium.
   100–200 mcg/day supports antioxidant defenses; avoid stacking multiple selenium-containing products.

7. Omega-3 fatty acids (EPA/DHA).
   1–2 g/day EPA+DHA may help temper excessive inflammation and support nutrition in critical illness.

8. L-Arginine.
   3–6 g/day in immunonutrition formulas may support collagen deposition and wound strength (avoid in sepsis unless supervised).

9. L-Glutamine.
   0.2–0.4 g/kg/day (enteral) is sometimes used in burn/ICU nutrition to support gut integrity; evidence is mixed—clinician-guided. PubMed

10. Probiotics/yogurt (only if immunosuppression isn’t severe and clinician approves).
    May aid gut tolerance during tube feeds or antibiotics; product choice and timing should be individualized.

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Regenerative/stem-cell-type” adjuncts

There are no approved “immunity-booster” or stem-cell drugs for SJS. Below are adjuncts clinicians may use—mostly to rebuild the ocular surface. These do not replace emergency systemic care.

1. Autologous serum eye drops (ASED).
   Your own serum, diluted (often 20–50%) and used QID–hourly. It delivers growth factors that mimic natural tears and can help regenerate the ocular surface.

2. Platelet-rich plasma (PRP) eye drops.
   Drops prepared from your own platelets, used QID–hourly short-term; rich in growth factors that may support epithelial healing.

3. Amniotic membrane devices (e.g., PROKERA) and amniotic extracts.
   A biologic “bandage” placed on the eye in the acute phase to calm inflammation and support regeneration (strongest evidence is for the membrane itself). PMC

4. Topical cyclosporine (0.05–0.1% eye drops).
   An anti-inflammatory drop BID long-term to calm chronic ocular surface inflammation after SJS/TEN.

5. Topical tacrolimus (0.03–0.1% ointment to lids/conjunctiva, specialist-supervised).
   Helps reduce lid margin keratinization and inflammation that abrade the cornea.

6. Cenegermin (recombinant human nerve growth factor) for neurotrophic keratopathy.
   20 mcg/mL every 2 hours while awake x 8 weeks in selected cases with corneal anesthesia; supports corneal nerve and epithelial recovery (specialist use).

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Surgeries

1. Emergency amniotic membrane transplantation (AMT) to the eyes.
   Procedure: a thin amniotic sheet is placed over the ocular surface (often like a large contact lens or sutured). Why: to sharply lower scarring, symblepharon, and long-term vision loss when performed in the first days of illness. PMC+1

2. Symblepharon lysis with rings/conformers.
   Procedure: gentle separation of early adhesions between eyelid and eyeball, plus placement of rings to keep spaces open. Why: prevents permanent shortening of the fornices that limits eye movement and vision. PMC

3. Mucous membrane grafting (MMG) to eyelid margins/conjunctiva.
   Procedure: small grafts from inner lip/cheek replace scarred tissue. Why: smooths rough, keratinized lid margins that scratch the cornea and helps restore a healthy ocular surface. PMC

4. Limbal stem-cell transplantation (e.g., KLAL, CLET, SLET).
   Procedure: transplants limbal stem cells (from donor or the patient’s other eye/relatives) to repopulate corneal surface stem cells. Why: treats limbal stem cell deficiency causing chronic pain, non-healing defects, and vision loss after SJS/TEN. Outcomes vary and require long-term immunosuppression with some techniques. BioMed Central

5. Boston keratoprosthesis (KPro) for end-stage corneal blindness.
   Procedure: an artificial cornea is implanted when standard grafts are unlikely to succeed. Why: sometimes the only path to useful vision, though complication rates are higher in SJS than in other diseases; careful lifelong follow-up is essential. PubMed+1

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Ways to prevent SJS

1. Never re-expose to the culprit drug.
   Once you’ve had SJS/TEN from a medicine, you should avoid it for life and avoid close chemical “cousins” unless a specialist explicitly says otherwise. Keep the drug allergy in every health record.

2. Use genetic (HLA) screening before certain drugs in at-risk groups.
   – Carbamazepine/oxcarbazepine: screen HLA-B*15:02 in people of Asian ancestry (Han Chinese, Thai, Vietnamese, Indian, Malay, Filipino, etc.). Consider HLA-A*31:01 across diverse groups to reduce broader CBZ hypersensitivity (e.g., DRESS/MPE).
   – Allopurinol: screen HLA-B*58:01 in Southeast Asians and African American patients (and consider in other high-prevalence groups) before starting. If positive, use alternatives. NCBIPMCduke.testcatalog.org

3. “Start low, go slow” with new high-risk medicines.
   Gradual dose titration and early check-ins can reveal intolerance before a severe reaction occurs.

4. Avoid self-medicating with high-risk drugs.
   Do not borrow antiepileptics, gout drugs, or strong antibiotics. Always involve a clinician.

5. Keep a detailed medicine list and a medical alert ID.
   Share it with every clinician, dentist, and pharmacist.

6. Report past reactions during every hospital or clinic intake.
   Reduces accidental exposure during admissions or procedures.

7. Ask about safer alternatives.
   Example: if allopurinol is risky, a clinician may consider febuxostat or non-drug strategies, depending on individual risks.

8. Treat infections promptly and appropriately.
   Certain infections (e.g., Mycoplasma pneumoniae in children/teens) can trigger SJS; early care reduces complications. PMC

9. One-new-drug-at-a-time rule when possible.
   Helps identify a culprit quickly if a reaction starts.

10. Enroll in pharmacovigilance/registry programs when offered.
    This strengthens safety data and improves future prevention.

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When to see a doctor—right away

• Immediately (Emergency/ER): fever plus a new, painful rash; blisters, skin peeling, sore/ulcerated mouth, red painful eyes, trouble swallowing, breathing, or urinating; faintness, confusion, or signs of infection (chills, pus, bad smell from wounds).

• Urgently (within 24–48 hours): any suspected drug rash that’s spreading, any eye discomfort/redness after a drug rash, or new mouth/genital ulcers.

• Routine follow-up: ophthalmology after discharge, wound and nutrition reviews, and careful review of all future prescriptions.

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What to eat and what to avoid

What to eat: soft, high-protein, high-calorie foods that are easy to swallow—smoothies with milk/yogurt and whey powder; blended soups with lentils/eggs/chicken; mashed potatoes with olive oil; soft fruits; scrambled eggs; rice porridge with tofu or fish; oral nutrition shakes if prescribed. Keep sipping fluids all day (water, oral rehydration solutions, milk). Aim for adequate calories and ≥1.5–2 g/kg/day protein unless your team advises otherwise. PMC

What to avoid (especially while mucosa is raw): sharp, crunchy, or spicy/acidic foods (chips, chili, citrus, vinegar), very hot drinks (heat hurts raw tissues), alcohol, and tobacco (both slow healing). If you’re on cyclosporine or other immunosuppressants, avoid grapefruit and St. John’s wort due to interactions; check every supplement or herbal product with your team first.

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Frequently asked questions (FAQs)

1) Is SJS always caused by drugs?
Most cases are medication-related, but infections—especially Mycoplasma pneumoniae in younger people—can do it too. Your team will look for both. PMC

2) Which medicines are the usual triggers?
Common culprits include allopurinol, aromatic antiepileptics (carbamazepine, phenytoin, lamotrigine), certain antibiotics (sulfonamides, some penicillins), and some NSAIDs. Many others are possible. Never stop a chronic medicine without medical advice; instead, get urgent evaluation. PMCJAMA Network

3) How soon after starting a drug can SJS appear?
Often 1–3 weeks after the new drug, but it can be sooner with re-exposure. That recent “new start” history is a key clue.

4) What is SCORTEN and why does it matter?
It’s a bedside scoring tool using simple clinical/lab factors to estimate death risk and guide intensity of care; higher scores need higher-level support. PMC

5) Do steroids help or harm?
Evidence is mixed, but early, short, carefully monitored steroid courses can help in selected patients; prolonged high-dose use increases infection and bleeding risks. Decisions are individualized. Frontiers

6) Is IVIG a “cure”?
No. As a supporting therapy it may help when combined with steroids in some analyses, but results vary; supportive care is always the foundation. PMC

7) Which treatment has the best evidence right now?
Signals are strongest for cyclosporine and etanercept in reducing deaths/faster healing compared with predicted outcomes, though high-quality randomized trials remain limited. PMC

8) Why is eye care so urgent?
Eye damage can happen in the first 24–48 hours and lead to lifelong pain and vision loss. Early ophthalmology plus amniotic membrane when indicated can be vision-saving. PMC

9) Will I have scars?
Skin usually re-epithelializes with minimal scarring, but pigment changes are common. Eyes, mouth, and genitals are at higher risk of scarring—hence the intensive early care. PMC

10) Can SJS happen again?
Yes—if you take the same or a related drug. That’s why lifelong avoidance, documented allergies, and genetic screening (when appropriate) matter. NCBI

11) Should family members be tested?
For some drugs, HLA testing is relevant mainly to the person who will take the medicine. In certain ethnic groups with high-risk alleles, relatives may also be considered for screening before exposure to high-risk drugs. Your prescriber will advise. CPIC

12) How long does recovery take?
Skin can re-cover in 2–3 weeks; eye and mucosal healing take longer. Fatigue and sensitivity may last months.

13) Is there a special SJS diet?
No specific “SJS diet,” but high-protein, high-calorie nutrition tailored to you speeds healing. A clinical dietitian is part of best-practice care. PMC

14) Are “stem cell” pills or shots available?
No. “Stem cell drugs” for SJS don’t exist. Some surgical approaches use stem-cell tissues (limbal transplants) for damaged corneas; these are operations, not pills. BioMed Central

15) What follow-up do I need?
Dermatology (skin healing, pigment care), ophthalmology (to preserve vision), primary care (med list, vaccines, nutrition), dentistry/ENT/gyne-urology as needed, and counseling/rehab.

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: August 26, 2025.

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