Sweet Syndrome

Sweet syndrome is a skin disease in which the body’s immune system suddenly sends many neutrophils, which are a type of white blood cell, into the skin. These cells gather in the upper and middle layers of the skin and cause hot, red, painful raised patches or plaques. The rash usually comes on quickly over hours or a few days. The spots are very tender when you touch them. Many people also have fever, feel unwell, and have body aches and headaches. A skin biopsy shows a dense collection of neutrophils and swelling in the skin without true destruction of the blood vessel walls. Doctors call this pattern a “neutrophilic dermatosis,” and Sweet syndrome is the most common one in this group. The disease can also affect other parts of the body in some people, but skin is the main site. The diagnosis is based on the sudden painful rash, the biopsy pattern, and supporting signs like fever, high inflammatory markers in blood tests, and quick improvement with steroids. NCBI

Sweet syndrome may happen by itself with no clear trigger. It can also be linked to an infection, an inflammatory disease, pregnancy, a cancer (most often blood cancers), or a medicine. The immune system seems to over-react to signals from infections, cancers, or drugs. Chemicals in the immune system called cytokines, including interleukins and colony-stimulating factors, are thought to play an important role because they activate and attract neutrophils into the skin. NCBI

Types and variants

1) Classical (idiopathic) Sweet syndrome.
This is the most common type. It appears without a proven single cause. It may follow a recent infection like a cold or stomach bug, but many times there is no clear trigger. The rash is sudden, painful, and red, and fever is common. NCBI

2) Malignancy-associated Sweet syndrome.
In some people, Sweet syndrome is linked to a cancer. It is most often tied to blood cancers such as acute myeloid leukemia (AML), myelodysplastic syndrome (MDS), and chronic myeloid leukemia. It can happen before, at the same time as, or after the cancer is found. The skin looks similar, but patients may also have abnormal blood counts or other cancer clues. Treating the cancer often helps the skin disease go away. NCBI

3) Drug-induced Sweet syndrome.
Some medicines can trigger the same skin reaction. The best-known trigger is granulocyte colony-stimulating factor (G-CSF). Other reported medicines include certain antibiotics (like trimethoprim-sulfamethoxazole and minocycline), cancer drugs (like bortezomib and imatinib), immune drugs (like azathioprine), some blood-pressure medicines (like hydralazine and furosemide), and some NSAIDs. Stopping the drug and treating the inflammation usually leads to improvement. NCBIDermNet®

4) Pregnancy-associated Sweet syndrome.
Sweet syndrome can start during pregnancy. It often improves after delivery and does not usually harm the baby. NCBI

5) Neuro-Sweet disease (central nervous system involvement).
In rare cases, the same neutrophil-driven process also inflames the brain or spinal cord. People can have headaches, confusion, or other neurologic symptoms along with the typical skin lesions. Neurologic symptoms tend to respond well to steroids, and doctors use published criteria to make this diagnosis. PubMedPMC

6) Subcutaneous Sweet syndrome.
Here the neutrophilic inflammation extends into the fat under the skin. It makes deep, very tender nodules that can look like erythema nodosum. The biopsy pattern confirms the diagnosis. NCBI

7) Histiocytoid Sweet syndrome.
This variant shows immature myeloid cells that look like histiocytes on the microscope. It is more often linked with myelodysplastic syndrome, so doctors look carefully for a blood disorder when this pattern is seen. NCBIMedscape

8) Localized or special-site variants.
Lesions can appear on the face, neck, upper chest, arms, and sometimes the mouth or tongue. The look can vary and may include pustules or blisters in some cases. The key point is still the sudden, painful, red plaques with a neutrophilic biopsy. NCBIJomos

Causes

1. Recent upper respiratory infection.
   A sore throat or cold can come one to three weeks before the rash. The infection may kick the immune system into high gear and start the neutrophil rush to the skin. NCBI

2. Recent gastrointestinal infection.
   A stomach bug or diarrhea can be a trigger in the same way, by waking up the immune system and sending signals that attract neutrophils. NCBI

3. Inflammatory bowel disease (Crohn disease or ulcerative colitis).
   People with IBD can develop Sweet syndrome during flares because their immune system is highly active and inflammatory messengers are high. NCBI

4. Rheumatoid arthritis.
   Autoimmune joint disease raises inflammatory chemicals that can drive neutrophil activity in the skin. NCBI

5. Systemic lupus erythematosus.
   Lupus is an immune system disease that can set off neutrophilic skin inflammation in some patients. NCBI

6. Behçet disease.
   This disease features inflamed blood vessels and mucosal ulcers. It can overlap with neutrophilic skin problems and sometimes a pathergy response is shared. NCBI

7. Sjögren syndrome or autoimmune thyroiditis.
   Autoimmune conditions sometimes coexist and can be triggers through chronic immune activation. NCBI

8. Hematologic malignancies (especially AML and MDS).
   Sweet syndrome can be a sign of a blood cancer, and its presence should prompt careful blood counts and sometimes bone marrow testing. NCBI

9. Other blood cancers (CML, lymphoma, multiple myeloma).
   These cancers can also be triggers because malignant cells and their treatments affect cytokines and white cells. NCBI

10. Solid tumors (breast, colon, lung and others).
    Less often, a solid cancer is the driver, again through immune and cytokine signals. NCBI

11. Pregnancy.
    Hormone and immune shifts in pregnancy can start the process, and the skin disease often calms after delivery. NCBI

12. Granulocyte colony-stimulating factor (G-CSF).
    This drug boosts neutrophils and is the classic medicine trigger; it can lead to a sudden neutrophil surge in skin. NCBIMedical Journals

13. Trimethoprim-sulfamethoxazole and other antibiotics.
    Certain antibiotics have been reported as triggers, likely by causing an immune reaction that draws neutrophils to the skin. NCBI

14. Minocycline and nitrofurantoin.
    These antibiotics have also been linked to Sweet syndrome in reports. NCBI

15. Bortezomib and other cancer drugs.
    Some anti-cancer medicines can activate immune pathways and trigger lesions that resolve after the drug is stopped. NCBI

16. Imatinib and other targeted therapies or immunotherapies.
    Targeted drugs and checkpoint therapies have been implicated in case reports and can provoke neutrophilic skin inflammation. NCBI

17. Azathioprine.
    This immune drug can trigger Sweet syndrome in a paradoxical way, possibly through shifts in immune balance. NCBI

18. Hydralazine and furosemide.
    These common medicines have been reported as causes in some people. NCBI

19. Nonsteroidal anti-inflammatory drugs (some cases).
    A few NSAIDs, including diclofenac and celecoxib, appear in reports as triggers. NCBI

20. Vaccinations and other immune stimuli (rare).
    Very rarely, a vaccine or another strong immune trigger has preceded a flare in people who are prone to neutrophilic skin diseases. DermNet®

Symptoms and signs

1. Sudden, painful red plaques or nodules.
   Lesions rise quickly, feel hot and very tender, and can appear on the face, neck, upper chest, back, and arms. They may look like they have blisters or pustules on top, but they are usually solid inflammatory plaques underneath. NCBI

2. Fever.
   Many people have a temperature higher than 38°C, but a minority do not, especially in cancer-related or classical cases. NCBI

3. Severe skin tenderness.
   Even light touch or clothing can hurt because the inflamed skin is very sensitive.

4. Malaise and fatigue.
   People feel sick and tired because the whole body is inflamed.

5. Headache.
   Headaches are common during active skin flares and usually improve when inflammation settles. NCBI

6. Muscle aches and joint pains.
   Arthralgia and myalgia are frequent and reflect body-wide inflammation. NCBI

7. Swelling and a “puffy” look around lesions.
   Edema in the top layer of the skin makes borders look raised and sometimes “pseudovesicular.”

8. Eye irritation.
   Red, gritty, or painful eyes can occur due to conjunctivitis or inflammation on the white of the eye. Less often there is deeper eye inflammation. NCBI

9. Mouth or genital ulcers (uncommon).
   These happen rarely but are reported, especially when blood cancers are present. NCBI

10. Pathergy at sites of minor trauma (sometimes).
    New lesions can appear where the skin is pricked or bumped because the skin is hyper-reactive. NCBI

11. Warmth over lesions.
    Plaques feel warm because blood flow and inflammatory cells are increased in the skin.

12. Asymmetric distribution.
    Rash often affects one side more than the other and clusters on the upper limbs and trunk. NCBI

13. Swollen lymph nodes (in some cases).
    Nearby nodes can be reactive and tender due to inflammation.

14. Cough or shortness of breath when lungs are involved (rare).
    Neutrophils can rarely collect in lungs and cause inflammatory changes like alveolitis or pleural fluid. NCBI

15. Neurologic symptoms in neuro-Sweet disease (rare).
    Headache, confusion, or other neurologic signs occur when the brain is inflamed in this special variant and they usually improve with steroids. PMC

Diagnostic tests

A. Physical examination 

1. Full skin inspection.
   The doctor looks at the number, size, color, and borders of the plaques and nodules and notes how fast they appeared. The abrupt, painful, red plaques suggest Sweet syndrome. The doctor also checks for signs that point to look-alike conditions, like ulcers of pyoderma gangrenosum or the bruised look of vasculitis. NCBI

2. Palpation for tenderness and warmth.
   Gently pressing and feeling each lesion helps show how inflamed the skin is. Sweet plaques are usually very tender and warm.

3. Body temperature and vital signs.
   A thermometer reading of 38°C or higher supports the diagnosis and shows the systemic nature of the flare. NCBI

4. Eye examination at the slit lamp when eyes are irritated.
   An eye doctor can look for conjunctivitis, episcleritis, or deeper eye inflammation that sometimes occurs with Sweet syndrome. NCBI

5. Joint examination.
   The doctor checks for swollen or tender joints that match the timing of the rash because joint inflammation is common in this condition. NCBI

B. Manual or bedside tests 

6. Diascopy (glass slide blanching test).
   Pressing a clear slide on a plaque shows whether it blanches (turns pale). In Sweet syndrome, redness often lessens with pressure because blood is pooled in small vessels, but the swelling and tenderness remain.

7. Pathergy testing when appropriate.
   A tiny sterile prick on the skin is watched to see if an exaggerated tender red bump develops, which can happen in some neutrophilic disorders, including Sweet syndrome. A positive pathergy response supports a neutrophil-driven process. NCBI

8. Nikolsky sign check (expect negative).
   Gentle rubbing does not make the top layer of skin peel away in Sweet syndrome, which helps distinguish it from blistering diseases.

9. Lesion measurement and serial photography.
   Using a ruler and standardized photos helps track spread or improvement, which is important because lesions can grow over days and then fade after treatment.

C. Laboratory and pathological tests 

10. Complete blood count (CBC) with differential.
    Many patients have a high white blood cell count and a high neutrophil percentage. Abnormal low counts can raise concern for an underlying blood disorder and may lead to bone marrow testing. NCBI

11. Erythrocyte sedimentation rate (ESR).
    ESR is often elevated and reflects whole-body inflammation. Medscape

12. C-reactive protein (CRP).
    CRP is usually high during the active phase and helps monitor response to treatment. Medscape

13. Skin biopsy for histopathology (the key test).
    A small piece of a fresh, painful plaque is removed under local anesthesia. The microscope shows a dense sheet of neutrophils in the dermis with swelling and little or no true blood-vessel destruction. This pattern confirms the diagnosis when combined with the clinical picture. Direct immunofluorescence testing is usually not helpful. NCBIMedscape

14. Tissue cultures from biopsy if infection is a concern.
    Because some infections can look similar under the microscope, cultures of tissue or pus help exclude bacteria, fungi, and mycobacteria when needed. Medscape

15. Autoimmune screening tailored to the person.
    Tests such as ANA, rheumatoid factor, thyroid antibodies, or others are chosen when there are symptoms of associated autoimmune diseases, since these conditions commonly coexist. NCBI

16. Bone marrow examination when blood counts are abnormal or lesions are atypical.
    If the CBC suggests a cancer of the blood or if there are bullous or ulcerative lesions, a bone marrow study can help detect myelodysplastic syndrome or leukemia. Medscape

D. Electrodiagnostic tests

17. Electroencephalogram (EEG) in suspected neuro-Sweet disease.
    If there are neurologic symptoms like confusion or seizures, an EEG can help rule out other causes of brain dysfunction and support the evaluation of neuro-Sweet disease, which typically improves with steroids. PMC

18. Nerve conduction studies and electromyography (NCS/EMG) when neuropathy-like symptoms complicate the picture.
    These tests do not diagnose Sweet syndrome itself, but they can rule out other nerve problems in a patient with limb pain or weakness so the care team can focus on the skin-driven inflammation.

E. Imaging tests 

19. Chest X-ray or chest CT when there are chest symptoms or cancer risk.
    Imaging can look for lung inflammation, pleural fluid, or signs of a cancer that might be linked to the skin disease. Doctors only order these when the story fits, to avoid unnecessary scans. NCBI

20. Age-appropriate cancer screening and targeted imaging.
    Depending on age and symptoms, tests like mammogram, colonoscopy (not imaging but part of screening), abdominal ultrasound, or CT/MRI may be used to look for an underlying cancer or inflammatory disease that could be the trigger. The plan is individualized to the person. NCBI

Non-Pharmacological Treatments (therapies and others)

(Each item includes Description • Purpose • Mechanism in simple English)

1. Trigger review and removal
   Description: Go through recent infections, new drugs, vaccines, stresses, and illnesses with your clinician.
   Purpose: Find the spark that keeps calling neutrophils.
   Mechanism: Taking away the trigger turns down the alarm so inflammation settles.

2. Medication reconciliation
   Description: List every medicine and supplement started in the past 1–8 weeks.
   Purpose: Spot a drug-induced cause.
   Mechanism: Stopping the culprit removes the immune stimulus.

3. Treat the underlying disease
   Description: Screen for and manage blood disorders, autoimmune disease, IBD, or infections.
   Purpose: Control the root driver.
   Mechanism: When the underlying fire is controlled, the skin smoke clears.

4. Cool, moist compresses
   Description: Clean, cool, damp gauze to painful plaques.
   Purpose: Ease heat, pain, and swelling.
   Mechanism: Cooling shrinks blood vessels and calms nerve endings.

5. Gentle skin care
   Description: Fragrance-free cleanser, lukewarm showers, bland emollients.
   Purpose: Reduce stinging and barrier damage.
   Mechanism: Healthy barrier dampens inflammatory signals.

6. Protect from sun and heat
   Description: Broad-spectrum SPF, shade, light clothing.
   Purpose: Cut UV/heat-induced flares.
   Mechanism: Less UV stress means fewer danger signals to immune cells.

7. Avoid skin trauma (anti-pathergy)
   Description: Minimize scratching, tight straps, rough exfoliation.
   Purpose: Prevent new lesions at injury sites.
   Mechanism: Fewer micro-injuries → less neutrophil recruitment.

8. Infection control basics
   Description: Hand hygiene, dental care, treat strep/UTI promptly.
   Purpose: Reduce inflammatory triggers.
   Mechanism: Fewer infections → less immune activation.

9. Stress-reduction practices
   Description: Mindful breathing, CBT skills, yoga, prayer/meditation.
   Purpose: Lower stress-hormone spikes that can worsen flares.
   Mechanism: Calmer nervous system → quieter immune tone.

10. Sleep regularity
    Description: 7–9 hours, regular schedule, dark cool room.
    Purpose: Support immune balance.
    Mechanism: Good sleep reduces inflammatory cytokines.

11. Anti-inflammatory eating pattern
    Description: Vegetables, fruits, legumes, whole grains, oily fish, olive oil; low ultra-processed foods.
    Purpose: Provide nutrients that quiet inflammation.
    Mechanism: Omega-3s and polyphenols modulate neutrophil activity.

12. Hydration
    Description: Water spaced through the day.
    Purpose: Help temperature control and skin comfort.
    Mechanism: Adequate fluids support microcirculation and healing.

13. Weight- and glucose-care
    Description: Gentle activity as tolerated, glucose checks if on steroids.
    Purpose: Limit steroid side-effects.
    Mechanism: Better metabolic health → less systemic inflammation.

14. Smoking cessation
    Description: Quit plan, nicotine replacement, counseling.
    Purpose: Reduce flare risk and infection risk.
    Mechanism: Less oxidative stress → calmer skin immune cells.

15. Alcohol moderation
    Description: Keep within low-risk limits or avoid during flares.
    Purpose: Protect liver (important for many medicines).
    Mechanism: Less liver strain → safer drug metabolism.

16. Wound-care for eroded plaques
    Description: Saline cleanse, non-stick dressings, watch for infection.
    Purpose: Promote clean, moist healing.
    Mechanism: Good wound care prevents secondary infection.

17. Targeted physical rest
    Description: Pause activities that rub or overheat lesions; resume gently.
    Purpose: Reduce mechanical irritation.
    Mechanism: Less friction → less inflammatory signaling.

18. Ocular care when eyes are involved
    Description: Urgent ophthalmology, preservative-free tears, shields.
    Purpose: Protect vision.
    Mechanism: Moisture and protection reduce surface inflammation.

19. Vaccination review (with doctor)
    Description: Ensure routine vaccines are up to date before long immunosuppression.
    Purpose: Lower infection complications.
    Mechanism: Vaccines prevent triggers and protect during therapy.

20. Relapse-plan and diary
    Description: Note flares, foods, drugs, stress, cycles; keep an action plan.
    Purpose: Catch early signs and act quickly.
    Mechanism: Early cooling of the immune response shortens flares.

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Drug Treatments

(Evidence-based options; give typical adult dosing ranges. Always individualize with your clinician.)
(Each item: Drug Class • Dosage & Time • Purpose • Mechanism • Key Side Effects)

1. Prednisone / Prednisolone (systemic corticosteroid)
   Dosage & Time: ~0.5–1.0 mg/kg/day (commonly 30–60 mg daily) for 1–2 weeks, then taper over 2–6 weeks.
   Purpose: Rapid flare control.
   Mechanism: Strongly blocks cytokines (like IL-1/IL-6) and neutrophil migration.
   Key Side Effects: High sugar, mood change, insomnia, fluid retention, infection risk, BP rise, bone thinning with long use.

2. Colchicine (microtubule inhibitor)
   Dosage & Time: 0.6 mg twice daily (some use 0.6 mg 2–3×/day short-term).
   Purpose: Steroid-sparing control and relapse prevention.
   Mechanism: Dampens neutrophil movement and activation.
   Side Effects: GI upset/diarrhea; dose-adjust in kidney disease; drug interactions (CYP3A4/P-gp).

3. Potassium iodide / SSKI (anti-inflammatory iodide salt)
   Dosage & Time: ~300–900 mg/day in divided doses; short courses.
   Purpose: Quick lesion resolution in some patients.
   Mechanism: Modulates neutrophils; exact pathway unclear.
   Side Effects: Thyroid dysfunction, metallic taste, acneiform rash—use with thyroid monitoring.

4. Dapsone (sulfone; neutrophil modulator)
   Dosage & Time: 50–150 mg daily; check G6PD before starting.
   Purpose: Maintenance or steroid-sparing in recurrent disease.
   Mechanism: Reduces neutrophil-mediated tissue injury.
   Side Effects: Hemolysis (esp. if G6PD-deficient), methemoglobinemia, rash.

5. Indomethacin / NSAIDs (non-steroidal anti-inflammatory)
   Dosage & Time: Indomethacin 25–50 mg 3×/day with food; short term.
   Purpose: Pain and fever relief; sometimes adjunctive.
   Mechanism: Blocks prostaglandins (COX inhibition).
   Side Effects: Gastritis/ulcer, kidney strain, BP rise; avoid with anticoagulants or ulcers.

6. Cyclosporine (calcineurin inhibitor)
   Dosage & Time: ~2–4 mg/kg/day in divided doses.
   Purpose: For steroid-refractory or steroid-dependent cases.
   Mechanism: Lowers T-cell cytokines that amplify neutrophil recruitment.
   Side Effects: Kidney toxicity, hypertension, gum overgrowth, tremor; drug interactions.

7. Methotrexate (antimetabolite, immunomodulator)
   Dosage & Time: 10–25 mg weekly + folic acid; monitor labs.
   Purpose: Maintenance and steroid-sparing.
   Mechanism: Down-regulates immune cell proliferation and cytokines.
   Side Effects: Liver toxicity, cytopenias, mouth sores; avoid in pregnancy; alcohol caution.

8. Azathioprine (purine analog immunosuppressant)
   Dosage & Time: 1–2 mg/kg/day; TPMT/NUDT15 testing helpful.
   Purpose: Maintenance when others fail.
   Mechanism: Reduces lymphocyte activity that drives neutrophil signaling.
   Side Effects: Low blood counts, liver issues, infection risk.

9. Clofazimine (riminophenazine anti-inflammatory)
   Dosage & Time: 100–200 mg daily; specialist use.
   Purpose: Option in recalcitrant disease.
   Mechanism: Neutrophil and cytokine modulation.
   Side Effects: Skin discoloration (brown/red), GI upset.

10. Anakinra (IL-1 receptor antagonist; biologic)
    Dosage & Time: 100 mg subcutaneously daily (off-label).
    Purpose: Rapid help in steroid-refractory Sweet’s, especially when IL-1 driven.
    Mechanism: Blocks IL-1, a key alarm for neutrophils.
    Side Effects: Injection-site reactions, infection risk, neutropenia (monitor counts).

Other specialist options sometimes used: canakinumab (IL-1β inhibitor), TNF-α inhibitors (infliximab, adalimumab), tocilizumab (IL-6), JAK inhibitors—see “advanced” section below.

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Dietary Molecular Supplements

(Supportive only; none are proven cures for Sweet’s. Discuss with your clinician, check interactions, and pause if you flare.)

1. Omega-3 fish oil (EPA/DHA)
   Dose: 1–2 g/day combined EPA+DHA with food.
   Function: General anti-inflammatory support.
   Mechanism: Shifts cell mediators toward pro-resolving pathways.

2. Vitamin D3
   Dose: 1000–2000 IU/day (or as per blood level).
   Function: Immune tone support.
   Mechanism: Vitamin D modulates innate and adaptive immune signals.

3. Vitamin C
   Dose: 500–1000 mg/day.
   Function: Antioxidant and collagen support.
   Mechanism: Scavenges oxidative stress that fuels inflammation.

4. Zinc
   Dose: 15–30 mg elemental zinc/day for short courses.
   Function: Barrier and wound support.
   Mechanism: Aids skin healing and immune enzyme function.

5. Selenium
   Dose: 100–200 mcg/day (short-term).
   Function: Antioxidant enzyme cofactor.
   Mechanism: Supports glutathione peroxidase to reduce oxidative signals.

6. Curcumin (turmeric extract, ≥95% curcuminoids with pepperine or liposomal form)
   Dose: 500–1000 mg/day.
   Function: Inflammation modulation.
   Mechanism: Lowers NF-κB signaling; gentle cytokine balancing.

7. Quercetin
   Dose: 500–1000 mg/day.
   Function: Mast-cell and cytokine calming.
   Mechanism: Antioxidant flavonoid that dampens mediator release.

8. Green tea extract (EGCG)
   Dose: 300–400 mg EGCG/day with food.
   Function: Anti-oxidative support.
   Mechanism: Polyphenols that reduce inflammatory signaling.

9. N-Acetylcysteine (NAC)
   Dose: 600–1200 mg/day.
   Function: Glutathione replenishment.
   Mechanism: Boosts cellular antioxidant defenses.

10. Probiotic (lactobacillus/bifidobacterium blend)
    Dose: As directed (often 10–20 billion CFU/day).
    Function: Gut-immune axis support.
    Mechanism: Healthier microbiome can quiet systemic inflammation.

Cautions: Fish oil may thin blood (avoid before procedures). Green tea extract: rare liver issues—take with food and monitor. Zinc/selenium: do not exceed recommended durations. Supplements do not replace medical treatment.

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Advanced Immunomodulators

(For tough, relapsing Sweet’s under specialist care. There is no established “stem cell drug” for Sweet syndrome. These medicines target immune signals and can suppress, not “boost,” immunity.)

1. Canakinumab (IL-1β inhibitor)
   Dose: 150 mg SC every 4–8 weeks (specialist, off-label).
   Goal: Longer control when anakinra works but daily shots are hard.
   Mechanism: Neutralizes IL-1β, quieting neutrophil alarms.

2. Rilonacept (IL-1 trap)
   Dose: 320 mg SC loading, then 160 mg weekly.
   Goal: Steady IL-1 blockade.
   Mechanism: Acts like a sponge that soaks up IL-1.

3. Infliximab (TNF-α inhibitor)
   Dose: 5 mg/kg IV at weeks 0, 2, 6, then every 8 weeks.
   Goal: Control in steroid-refractory cases, esp. with IBD.
   Mechanism: Blocks TNF-α, a key pro-inflammatory cytokine.

4. Adalimumab (TNF-α inhibitor)
   Dose: 40 mg SC every 2 weeks.
   Goal: Maintenance control with self-injection.
   Mechanism: Inhibits TNF-α signaling.

5. Tocilizumab (IL-6 receptor inhibitor)
   Dose: 162 mg SC weekly/biweekly, or 8 mg/kg IV monthly.
   Goal: Tame systemic symptoms and stubborn plaques.
   Mechanism: Blocks IL-6 signaling that sustains neutrophil activity.

6. Ruxolitinib (JAK1/2 inhibitor)
   Dose: Commonly 5–10 mg orally twice daily (individualize).
   Goal: Control cytokine storms in select refractory cases.
   Mechanism: JAK-STAT pathway dampening across many cytokines.

Safety for all biologics/JAKi: Screen for TB, hepatitis, ensure vaccines are current, and monitor blood counts/liver tests. Discuss pregnancy plans.

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Procedures / “Surgeries

Sweet syndrome is almost always treated without surgery. The items below are procedures used for diagnosis or to handle complications/associated conditions.

1. Skin biopsy (punch or excisional)
   Procedure: Small skin sample under local anesthesia.
   Why: Confirm diagnosis (dense neutrophils, no vasculitis early), rule out infection or other rashes.

2. Removal of a trigger device or lesion
   Procedure: For example, remove an infected catheter or a suspicious skin tumor if linked.
   Why: Eliminates a trigger maintaining inflammation.

3. Surgical management of associated malignancy
   Procedure: Tumor resection as part of cancer care.
   Why: Treating the cancer often quiets Sweet’s.

4. Debridement of superinfected erosions (selected cases)
   Procedure: Careful removal of necrotic tissue if true infection occurs.
   Why: Promote healing and allow accurate wound care.

5. Ophthalmic procedures for severe ocular Sweet’s
   Procedure: Periocular or intraocular steroid injections or related eye procedures by an ophthalmologist.
   Why: Protect vision when eye inflammation threatens sight.

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Preventions

1. Keep an up-to-date medication list and avoid past culprits.

2. Report new drugs to your clinician if a rash starts within days to weeks.

3. Treat infections early (strep throat, UTI, dental issues).

4. Maintain regular cancer follow-up if you have or had a blood disorder.

5. Practice sun/heat protection for your skin.

6. Use gentle skin care to protect the barrier.

7. Keep a relapse diary (stress, cycles, medicines, infections).

8. Don’t scratch or pick; trim nails; use cool compresses.

9. Stop smoking and moderate alcohol.

10. Plan pregnancy and medicines with your clinician if you have a Sweet’s history.

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When to see doctors

• Immediately / urgent care: high fever with confusion; severe eye pain or vision change; rapidly spreading painful plaques; signs of infection (pus, foul smell, streaking redness); severe mouth/genital ulcers; shortness of breath or chest pain.

• Soon (24–72 hours): new tender red plaques with fever; new rash after starting a medicine; relapse while tapering steroids; if you have a blood disorder and develop a rash.

• Specialists: Dermatology (skin), Hematology/Oncology (blood cancer links), Rheumatology (autoimmune), Ophthalmology (eyes), Obstetrics (pregnancy).

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What to eat and what to avoid

1. Eat: Oily fish (salmon, sardine) 2×/week • Avoid: Deep-fried fast foods that spike inflammation.

2. Eat: Colorful vegetables and berries daily • Avoid: Sugary drinks and sweets most days.

3. Eat: Whole grains and legumes • Avoid: Refined white flour snacks.

4. Eat: Olive oil and nuts • Avoid: Trans-fat snacks and margarine.

5. Eat: Plain yogurt or kefir (if tolerated) • Avoid: Excess alcohol, especially with steroids.

6. Eat: Lean proteins (poultry, tofu, beans) • Avoid: Processed meats.

7. Eat: Spices like turmeric/ginger • Avoid: Excess salt (can worsen steroid fluid retention).

8. Eat: Plenty of water and herbal teas • Avoid: Energy drinks high in caffeine/sugar.

9. Eat: Citrus and kiwi for vitamin C • Avoid: Very spicy/acidic foods only if they irritate mouth ulcers.

10. Eat: Small, balanced meals when on steroids • Avoid: Huge late-night meals that worsen sleep and reflux.

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Frequently Asked Questions

1. Is Sweet syndrome contagious?
   No. It is an inflammatory reaction of your own immune system, not an infection.

2. Can antibiotics cure it?
   No. Antibiotics don’t treat Sweet’s itself (unless a separate infection exists). The mainstays are steroids and anti-inflammatory medicines.

3. How fast do steroids work?
   Many people feel better within 24–48 hours; plaques soften over several days. A slow taper helps prevent rebound.

4. Will it come back?
   Relapses can happen, especially if the trigger persists. Prevent by removing triggers, gentle maintenance medicines (like colchicine or dapsone in select cases), and a relapse plan.

5. Do I always need a biopsy?
   Often yes at first. It confirms the diagnosis and excludes infection or other diseases that look similar.

6. Can Sweet’s affect organs other than skin?
   Yes. It can involve eyes, joints, mouth, lungs, liver, and rarely other organs. Report new symptoms promptly.

7. Is it related to cancer?
   Sometimes. A subset is malignancy-associated (often with blood cancers). Your clinician may order blood tests or other screening based on your history.

8. What if I’m pregnant?
   Sweet’s can occur in pregnancy. Work closely with obstetrics and dermatology. Use pregnancy-safe options and the lowest effective steroid dose.

9. Can children get it?
   Yes, though less common. Pediatric specialists tailor doses and look hard for triggers.

10. Are biologics safe?
    They can be very helpful in hard cases, but they suppress immunity and need screening and monitoring.

11. What lab tests are typical?
    Doctors may check CBC (white cells), CRP/ESR (inflammation), and sometimes cultures to rule out infection.

12. How long does a flare last?
    Untreated, weeks. With steroids or targeted therapy, often days to a couple of weeks.

13. Can diet alone fix it?
    No. Diet can support recovery but does not replace medical treatment.

14. Why do lesions hurt so much?
    The plaques are packed with neutrophils and fluid, stretching the skin and stimulating pain nerves.

15. Will it leave scars?
    Usually no scarring, but temporary color changes can linger. Gentle skin care and sun protection help.

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

Last Updated: August 27, 2025.