Can antibiotics make your skin peel

Can antibiotics make your skin peel?Yes, they can. But don’t worry—it’s not a big deal.

If you’re on antibiotics, and you start to notice that your skin is peeling or flaking off in small pieces, there are several possible causes for this. In this guide, we review the aspects of: Can antibiotics make your skin peel, toxic epidermal necrolysis, skin peeling medication reaction, and what infections cause skin peeling.

First of all, if you’re taking an antibiotic that causes acne, it’s possible that the medication is causing a reaction in your body that’s causing your skin to shed. This is called “acne exfoliation syndrome,” and it’s most common in people with cystic acne who have been prescribed isotretinoin (Accutane). If you’ve been taking Accutane and haven’t noticed any changes in your skin, don’t worry! Your body may just be reacting differently to the medication than other people.Another reason could be an allergic reaction to the antibiotic itself. If this happens to you, call your doctor immediately so they can switch out your antibiotic for one that won’t trigger an allergic reaction.It’s also possible that there is another underlying cause for this happening—for example, if you have cold sores or other herpes-related outbreaks on your face, it could be caused by the virus itself rather.

What Are the Most Common Side Effects of Antibiotics?

All medications have side effects, including antibiotics. Antibiotics are medications that treat infections by killing bacteria or other organisms or slowing their growth. An antibiotic side effect occurs as an unwanted reaction that occurs in addition to the desirable therapeutic action of the antibiotic you are taking.

Side effects of antibiotics can range from mild allergic reactions to severe and debilitating adverse events. When used appropriately, most antibiotics are relatively safe with few side effects. However, some side effects may interfere with your ability to finish the medication. In these cases, you should contact your doctor.

Common side effects with antibiotics include:

• Mild skin rash or other allergic reactions
• Soft stools, short-term diarrhea
• Upset stomach, nausea
• Loss of appetite
• Fungal (yeast) vaginal infections or oral thrush 

More severe antibiotic side effects include:

• Severe allergic reaction that results in difficulty breathing, facial swelling (lips, tongue, throat, face)
• Severe watery or bloody diarrhea; Clostridium difficile infection
• Stomach cramps
• Yeast infections in the mouth or vagina (white discharge and severe itching in the vagina or mouth sores or white patches in your mouth or on your tongue)

These side effects are extremely variable; however, there are some common side effects that may occur within larger antibiotic drug classes, as described in Table 1. Long term side effects of antibiotics can occur, but are infrequent.

Should I Stop My Antibiotic If I’m Having a Side Effect?

If you are experiencing a bothersome or serious antibiotic side effect, you should contact your health care provider to discuss your symptoms. The outcomes may include:

• Staying on the same antibiotic and managing the side effect
• Adjusting the dose
• Switching to a different antibiotic

In most cases, all antibiotic treatment should be finished unless your healthcare prover tells you otherwise. Stopping antibiotics early may allow the infection to worsen and may lead to antibiotic resistance, making the antibiotic less effective. Even if the infection appears to have cleared up before all of the medication is gone, finish your treatment unless your doctor tells you to stop.

Antibiotic Allergies

Antibiotic allergies or hypersensitivity reactions are some of the most common side effects of antibiotics leading to emergency room admission.¹ Always tell your doctor of any previous allergic reaction to any medication, including antibiotics. Mild allergic reactions may only result in a skin rash or itch. A more severe allergic reaction, called anaphylaxis, is a life-threatening medical emergency that requires immediate medical attention.

Anaphylactic reactions due to antibiotics may include:

• Shortness of breath
• Wheezing
• Severe nausea/vomiting
• Lightheadedness, dizziness
• Fast heart rate
• Swelling of the face, lips or tongue
• Shock

Immediately call 911 for medical help if any of these symptoms should appear after taking an antibiotic.

Are Antibiotics Effective for a Cold, Flu or COVID?

Antibiotics are used to kill bacterial infections; they are not effective against viral infections, such as a cold, the flu, COVID. They also do not work against fungal infections, like ringworm or vaginal yeast infections.

You should avoid demanding an antibiotic from your healthcare provider when you have a viral infection as it will not cure your infection and might make it worse. In addition, this adds to the problem of antibiotic resistance, and it costs you money you do not need to spend. Your doctor can offer symptomatic treatment to ease your viral infection, or prescribe specific anti-viral medications if appropriate.

If you eventually need an antibiotic because of a secondary bacterial infection that might occur later, your doctor will prescribe it then.

List of Antibiotics and Their Side Effects

There are several side effects that are common to most antibiotics, regardless of class or drug. These side effects may include:

• antibiotic-associated diarrhea
• yeast infections (vaginal, oral)
• anaphylaxis
• serious allergic skin reactions, other allergic reactions
• complications from intravenous (IV) use of antibiotics (phlebitis)

What are the side effects of antibiotics? The most common antibiotic classes and drug members are listed in Table 1, along with the most commonly reported antibiotic side effects (list are not comprehensive). 

Table 1: Common Antibiotic Side Effects*

Common Antibiotic Classes	Antibiotic Class Members	Most Common Class Side Effects	Additional Clinical Comments
List of penicillins, penicillinase- resistant penicillins, and other penicillin-type drugs	penicillinamoxicillin (Amoxil)amoxicillin and clavulanate (Augmentin)ampicillinpiperacillin and tazobactam (Zosyn)nafcillin oxacillin	skin rashdiarrheastomach painnausea and vomitingdrug feverhypersensitivity (allergic) reactions	If bloody stools, an extreme watery diarrhea, stools with pus, anaphylaxis (a severe allergy), urgent stomach pain, severe skin reaction, or fever occur contact health care provider immediately.Antibiotics may cause life-threatening pseudomembranous colitis and Clostridium difficile infection.
List of cephalosporins	cephalexin (Keflex)cefaclor  cefadroxil (Duricef)cefazolin cefepime (Maxipime)cefotaxime (Claforan)ceftaroline (Teflaro)cefuroxime (Ceftin, Zinacef)cefdinircefiximeceftriaxone	rashdiarrheanausea and vomiting (rare)hypersensitivity (allergic) reactionsserum sicknessvaginal candidiasis (yeast infection)	Cross-hypersensitivity may occur in patients with documented penicillin allergy; may be more common with first generation cephalosporins due to structural similarities.In one prospective study2, the rate of cross-reactivity among subjects with a positive penicillin skin test was 6%; however rates up to 10% have been reported.If you have a history of penicillin allergy, your doctor may recommend penicillin skin testing if a cephalosporin is required.
List of monobactams	aztreonam (Azactam, Cayston)The monobactams have a unique structure and are different from other beta-lactam antibiotics (eg, penicillins, cephalosporins, cephamycins). Cayston (aztreonam) inhalation is used in people who have cystic fibrosis and a certain bacteria in their lungs. This helps to improve their breathing symptoms.	Aztreonam (Azactam, IV)nausea, vomitingdiarrhearashvaginal itching or dischargepain, bruising, swelling, or irritation where the medicine was injectedAztreonam (Cayston, inhalation)cough, wheezingnasal congestion, throat painfeverchest discomfortstomach pain and vomiting	While cross-reactivity of aztreonam (Azactam) with other beta-lactam antibiotics is rare,  use with caution to any patient with a history of hypersensitivity to beta-lactams (eg, penicillins, cephalosporins, and/or carbapenems).6,8 Treatment with aztreonam can result in hypersensitivity reactions in patients with or without prior exposure.
List of aminoglycosides	amikacin (Amikin, Arikayce)gentamicin (Garamycin)neomycintobramycin (Bethkis, Tobi)plazomicin (Zemdri)paromomycin (Humatin)	renal (kidney) toxicityototoxicity (hearing loss)dizzinessnausea and vomitingnystagmus (involuntary eye movement)Long-term aminoglycosides or multiple treatment periods may lead to greater risk for ototoxicity (hearing damage, loss) and renal (kidney) toxicity.	Aminoglycosides are often reserved for times when less toxic antibiotics cannot be used or are ineffective.Aminoglycosides are not well absorbed by mouth, and are usually given by injection. Some products are given by inhalation for lung infection.Neomycin is given by mouth for its effects in the intestine, although it can be absorbed and toxic reactions may occur.
List of carbapenems	meropenem (Merrem)ertapenem (Invanz)imipenem and cilastatin (Primaxin)	diarrheanausea and vomitingheadacherashhepatic (liver) toxicityeosinophilia (high levels of a type of white blood cell)	Hypersensitivity reactions reported with meropenem and imipenem in patients with penicillin allergy.
List of antituberculosis agents	dapsoneethambutol (Myambutol)isoniazidpyrazinamiderifabutin (Mycobutin)rifampin (Rifadin, Rimactane)isoniazid, pyrazinamide, and rifampin (Rifater)isoniazid and rifampin (Rifamate)	diarrheanausea and vomitinganorexiahemolytic anemialiver toxicityheadacheperipheral neuropathydizzinessreddish-orange body fluids (with rifampin, rifabutin only)	Sides effects vary among agents, check each individually.Vitamin B6 (pyridoxine) may be taken to help prevent peripheral neuropathy with isoniazid.
List of glycopeptides	telavancin (Vibativ)vancomycin (Vancocin, Firvanq)oritavancin (Orbactiv, Kimyrsa)dalbavancin (Dalvance)	vancomycin: “red man syndrome” (RMS) – flushing, hypotension, itching with IV use; phlebitistelavancin: taste alteration, nausea/vomiting, headache, dizziness	IV infusion of vancomycin over 60 minutes may help to prevent RMS.Other cases of RMS due to other antibiotics have been reported, including: rifampin, cefepime, teicoplanin, ciprofloxacin, and amphotericin B.7
List of macrolide antibiotics	azithromycin (Azithromycin, Z Pak)clarithromycin (Biaxin)erythromycin (E.E.S., EryPed, Ery-Tab, Erythrocin)fidaxomicin (Dificid)	abdominal paindiarrheaappetite lossnausea and vomitingtaste alterations (clarithromycin)	High rate of gastrointestinal (stomach) side effects.Do not crush, chew, break, open enteric-coated or delayed-release pills.
List of sulfonamides (antibiotic)	sulfacetamide sodium topical (Klaron, Ovace)sulfadiazine (generic)sulfamethoxazole  and trimethoprim (Bactrim, Co-trimoxazole, Septa, SMZ-TMP)	nausea and vomitingdiarrheaanorexia (appetite loss)abdominal (stomach pain)rashheadachedizzinessphotosensitivityAvoid prolonged sunlight exposure; use sunscreen, and wear protective clothing.	Sulfonamide allergic reactions have been reported in roughly 1.5% to 3% of the general population. Learn more about sulfa allergies here.May lead to severe skin reactions: Stevens Johnson Syndrome, Toxic Epidermal Necrolysis.
List of tetracyclines	tetracycline (Achromycin V)doxycycline (Doryx, Oracea, Monodox Vibramycin)eravacycline (Xerava)minocycline (Solodyn, Minocin)omadacycline (Nuzyra)sarecycline (Seysara)	nausea and vomitingdiarrheaanorexiaabdominal (stomach) paintooth discoloration in children < 8 yearsliver toxicityphotosenstivityAvoid prolonged sunlight exposure, use sunscreen, wear protective clothing.	The development of bacterial resistance has limited the effectiveness of this class of drugs, although they may still be used in human and animal medicine.
List of fluoroquinolones (quinolones)	delafloxacin (Baxdela)ciprofloxacin (Cipro)ciprofloxacin extended-release (Cipro XR)gemifloxacin (Factive)levofloxacin (Levaquin)moxifloxacin (Avelox)ofloxacin (generic)	nausea and vomitingdiarrheaabdominal (stomach) painheadachelethargyinsomnia (difficulty sleeping)photosensitivity (can be severe)	Due to a risk for serious adverse reactions, doctors may withhold use of this class unless absolutely required for more serious or unresponsive infections.Avoid prolonged sunlight exposure; use sunscreen, wear protective clothing.See FDA alerts and boxed warnings for fluoroquinolones: tendon rupture, tendonitis, peripheral neuropathy, aggravation of myasthenia gravis, aortic aneurysm or dissection, low blood sugar, mental status changes.
List of lincomycin derivatives	clindamycin (Cleocin)lincomycin (Lincocin)	pseudomembranous colitis (may be severe and life-threatening)diarrheanausea and vomitingrashallergiesjaundice (clindamycin)	If severe diarrhea during treatment or for up to 8 weeks after treatment consult health care provider immediately, may be pseudomembranous colitis (C. difficile); consider use of less toxic agents.
Miscellaneous antibiotics	metronidazole (Flagyl)	metallic tastenausea and vomitingdizzinessheadachevaginal yeast infections	Avoid alcohol use and or propylene glycol use during treatment and for up to 3 days after treatment stopped.Combined use with alcohol may lead to cramps, nausea/vomiting, flushing, headache; may discolor urine red-brown.

*This is not a complete list of common antibiotics or side effects that may occur. For a complete list of side effects, please refer to the individual drug monographs.

Side Effects

Allergic Reactions, Anaphylaxis: Allergic reactions account for the most common type of side effect with antibiotics.

• Previous research showed that 142,000 emergency department visits per year were due to antibiotic adverse events, and approximately 80% of these events were due to allergic reactions.
• Allergic reactions can typically only be prevented by avoiding the drug, although desensitization may be possible in certain circumstances for patients who have no other antibiotic options.¹
• Skin testing may be recommended for some instances of a reported penicillin allergy, when other drug classes are not optimal.²
• Anaphylaxis is the most serious type of allergic reaction and can be life-threatening.

Antibiotic-associated diarrhea: Antibiotic-associated diarrhea occurs in patients receiving antibiotics.

• About 5% to 25% of patients may develop antibiotic-associated diarrhea at any one time. The diarrhea occurs due to eradication of the normal gut flora by the antibiotic and results in an overgrowth of infectious bacteria, such as Clostridium difficile.
• If the diarrhea is severe, bloody, contains pus, or is accompanied by stomach cramps, fever or vomiting, a physician should be contacted.
• The most common antibiotics implicated in antibiotic-associated diarrhea are amoxicillin-clavulanate, ampicillin, and cefixime; however, other antibiotics may lead to this side effect, including cephalosporins, fluoroquinolones (e.g., side effects of Cipro antibiotic), azithromycin (e.g., Azithromycin, Z Pak), clarithromycin (Biaxin), erythromycin, and tetracycline.³
• Probiotics such as Saccharomyces boulardii (Florastor) have been shown to be effective in helping to prevent antibiotic-associated diarrhea in children and adults.⁵

Vaginal yeast infections or oral thrush (candida species): Antibiotics may also change the normal flora balance in the vagina, often leading to an overgrowth of fungal species.

• Candida albicans is a common fungus normally present in small amounts in the vagina, mouth, gastrointestinal tract and on the skin and does not normally cause disease or symptoms. However, the fungus may take over when there is limited competition from bacteria due to antibiotic treatment.
• Thrush may appear as white patches in the mouth or on the tongue, and vaginal yeast infections produce a white discharge and intense itching. 

Stevens Johnson Syndrome (SJS), Toxic Epidermal Necrolysis (TEN): Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are rare but serious allergic reactions to substances, often medications, that result in severe skin and mucous membrane disorders.

• Antibiotics such as sulfonamides, penicillins, cephalosporins, and fluoroquinolones may result in SJS and TEN.
• SJS and TEN can both cause rash, skin peeling, and sores on the mucous membranes and may be life-threatening.⁴ 

Injection site reactions or phlebitis: A reaction to an antibiotic can occur if the antibiotic is given intravenously (IV) into a vein.

• Injections site reactions and phlebitis (vein inflammation) can occur. The vein and area with the IV needle may be red, swollen and hot. An infection may or may not be present.
• Typically, the needle must be removed and reinserted elsewhere to help clear the injection site reaction.

Antibiotics are among the most commonly prescribed medications in the US. However, many side effects may not be reported. Always consult your doctor or healthcare specialist for medical advice.

toxic epidermal necrolysis

Toxic epidermal necrolysis (TEN) is a potentially life-threatening dermatologic disorder characterized by widespread erythema, necrosis, and bullous detachment of the epidermis and mucous membranes, resulting in exfoliation and possible sepsis and/or death. Mucous membrane involvement can result in gastrointestinal hemorrhage, respiratory failure, ocular abnormalities, and genitourinary complications.

TEN is most commonly drug induced. However, the disorder occasionally has other potential etiologies, including infection including COVID-19, [1, 2]  malignancy, and vaccinations, including following COVID-19 vaccination.  TEN is idiosyncratic, and its occurrence is not easily predicted.

Some authors believe that Stevens-Johnson syndrome (SJS; also known as erythema multiforme major) is a manifestation of the same process involved in TEN, with the latter involving more extensive necrotic epidermal detachment. TEN involves more than 30% of the body surface, whereas SJS involves less than 10%.

A classification system, based largely on the extent of epidermal detachment and morphology of the skin lesions, aids in differentiating opposite spectrums of the same disease entity. This system comprises the following:

TEN with spots is defined as widespread, irregularly shaped erythematous or purpuric macules with blistering that occurs on all or part of the macule. Blisters become more confluent and result in detachment of the epidermis and erosions on greater than 30% of the body surface area. Mucosal surfaces are usually involved.

TEN without spots is defined as widespread, large areas of erythema with no discrete lesions. Epidermal detachment is greater than 10% of the body surface area. Mucosal surfaces are usually involved.

Overlap Stevens-Johnson syndrome and TEN (SJS-TEN) is characterized by widespread, irregularly shaped erythematous or purpuric macules with blistering that occurs on all or part of the macule. Blisters become confluent and result in detachment of the epidermis and erosions on 10-29% of the body surface area.

TEN is a clinical diagnosis, confirmed by histopathologic analysis of lesional skin. The mainstay of treatment is supportive care until the epithelium regenerates. Early transfer of patients to a burn or intensive care unit has been shown to reduce the risk of infection, mortality rate, and length of hospitalization.

Historical background

Alan Lyell provided an early description of TEN in 1956, describing the condition as “an eruption resembling scalding of the skin.” This dermatologic condition is characterized by extensive epidermal loss suggestive of severe scalding. In that same year, Lang and Walker reported a case of TEN. The disorder was originally described by Debre et al in 1939 in French as l’erythrodermie bulleuses avec epidermolyse.

Lyell later reclassified the conditions of 2 of his patients as having staphylococcal scalded skin syndrome, which is due to Staphylococcus aureus infection rather than to a probable drug hypersensitivity-type reaction. Histopathologic analysis of the skin remains the main tool for discrimination between the two conditions.

Patient education

Patients who have had TEN must be counseled regarding the likely causative medication or agent, and they must be advised to avoid these medications and those of the same or similar classes in the future. Cross-reactivity may occur with agents that chemically resemble the causative agent. Patients must call a pharmacist whenever they start a new prescription.

The patient should be educated on any medical treatment that is still necessary and on sun protection to prevent post-inflammatory hyperpigmentation. There are several long-term complications in patients surviving TEN and the patient should be educated on the prognosis and the need for follow-up. At discharge, patients should be asked to complete the General Health Questionnaire-12 and scores of 2 or greater should trigger a referral to a psychiatrist or psychologist. Information on available support groups should be given to the patient.

Genetic factors are suspected in drug-induced blistering disorders, and blood relatives of the patient also should not use the suspected drug.

For patient education information, see the Skin, Hair, and Nails Center, as well as Life-Threatening Skin Rashes.

Pathophysiology

The pathophysiology of TEN has not been fully elucidated; however, various theories have received wide acceptance. TEN is believed to be an immune-related cytotoxic reaction aimed at destroying keratinocytes that express a foreign antigen.

TEN mimics a hypersensitivity reaction, with its characteristic delayed reaction to an initial exposure and an increasingly rapid reaction with repeated exposure.

The widespread epidermolysis and blistering of TEN results from keratinocyte apoptosis—an organized series of biochemical reactions leading to cell changes and cell death. However, the number of inflammatory T cells in the skin of patients with TEN is variable and perhaps too low to explain the widespread destruction.

There is evidence supporting several immunopathologic pathways leading to keratinocyte apoptosis in TEN, including the following:

Release of destructive proteins (perforin and granzyme B) from cytotoxic T lymphocytes (CTLs) generated from an interaction with cells expressing major histocompatability complex (MHC) class I

Overproduction of T cell– and/or macrophage-derived cytokines (interferon-γ [INF-γ], tumor necrosis factor-α [TNF-α], and various interleukins) [14, 15]

Drug-induced secretion of granulysin from CTLs, natural killer cells, and natural killer T cells

Precisely how the inciting agent triggers the proposed pathways is yet to be elucidated.

Etiology

TEN can be induced by drugs or infection or can be idiopathic. Medications are the major precipitating cause. Numerous medications have been implicated, including antibiotics, antiepileptic drugs, nonsteroidal anti-inflammatory drugs (NSAIDs), ampicillin, allopurinol, corticosteroids (topical and systemic), and the antiretroviral drugs nevirapine and abacavir. [18, 19]  TEN usually occurs during the first course of therapy with a drug (ie, without sensitization).

Antibacterial drugs associated with TEN include the following:

Anticonvulsants associated with TEN include the following:

TEN in patients taking anticonvulsants has most often been reported within 2 months of starting the drug. However, some cases associated with long-term use have been reported.

NSAIDs associated with TEN include the following:

With allopurinol, risk is not constant over time. Patients have a 5.5 relative risk. However, during the first 2 months of therapy, the relative risk is 52, and the long-term therapy risk is 0.5.

No laboratory test is able to confirm a specific drug etiology. A causal link is suggested when TEN occurs during the first 4 weeks of medication therapy, usually between 1 and 3 weeks. Drugs with longer half-lives and those with circulating active metabolites may result in more fulminant disease.

Infectious agents (ie, Mycoplasma pneumoniae, herpes virus, hepatitis A), immunizations (eg, meningococcal vaccine), and bone marrow or solid organ transplantation have also been associated with TEN.

Epidemiology

In the United States, the annual frequency of TEN is reported to be 0.22-1.23 cases per 100,000 population. In the HIV-positive population, the incidence of TEN increases to 1 case per thousand per year.

Worldwide, the average annual incidence of TEN is 0.4-1.3 cases per million population. In 1992, the cumulative incidence of TEN and SJS in Germany was 1.9 cases per million population. A French survey of dermatologists and health care facilities reported an annual incidence of 1 case per million population.

Race-, sex-, and age-related demographics

A genetic predilection toward carbamazepine-induced TEN has been observed in HLA-B*1502–positive patients in mainland southeast Asian people from China to India. The US Food and Drug Administration recommends screening for the HLA-B*1502 allele before initiating carbamazepine in patients of Asian ancestry.  The HLA-B*58:01 allele is associated with allopurinol-induced TEN in Han Chinese people. HLA-A*66:01, HLA-B*44:03, and HLA-C*12:03 have been associated with cold medicine-TEN with severe ocular complications in patients who had taken cold medicines in the 1-14 days prior to onset of the disease. The HLA-B*44:03 (odds ratio, 5.50) and HLA-C*12:03 (OR, 8.79) alleles were associated with a less-robust tisk of cold medicine-TEN only in European patients.

Registration databases from Tawain, Thailand, Japan, Malaysia, Singapore, Hong Kong, the Philippines, and mainland China (Fujian) identified that from 1998-2017, greater than 50% of cases of SJS/TENS involved carbamazepine, allopurinol, phenytoin, lamotrigine, and sulfamethoxazole.  Oxacarbazepine, sulfasalazine, COX-II inhibitors, and strontium ranelate (not approved by the Food and Drug Administration but used in more than 70 countries as a treatment option for postmenopausal osteoporosis) have been identified as potential new causes of SJS/TENS in Asian patients.  Other medications known to cause SJS/TENS such as oseltamavir, terbinafine, and sorafenib, were not associated with any cases in Asian patients enrolled in these databases.

For unclear reasons, TEN appears to have a predilection for females. The female-to-male ratio is 1.5:1.

TEN may occur in all age groups; however, the mean age of patients with TEN is reported to be between 46 and 63 years. Infection is more commonly implicated as an etiology in children, whereas medication exposure is more common in adults. Elderly persons may be at greater risk because of their tendency to use multiple medications.

skin peeling medication reaction

Stevens-Johnson syndrome and toxic epidermal necrolysis are two forms of the same life-threatening skin disorder that cause rash, skin peeling, and sores on the mucous membranes.

(See also Overview of Hypersensitivity and Reactive Skin Disorders Overview of Hypersensitivity and Reactive Skin Disorders The immune system plays a vital role in maintaining the health of all the tissues of the body. The immune system reacts to invaders, such as microorganisms, foreign substances, or cancer cells… read more .)

Stevens-Johnson syndrome and toxic epidermal necrolysis are commonly caused by drugs or infections.

Typical symptoms for both diseases include peeling skin, fever, body aches, a flat red rash, and blisters and sores on the mucous membranes.

Affected people are typically hospitalized in a burn unit and given fluids and sometimes drugs, and all suspected drugs are stopped.

Skin peeling is the hallmark of these conditions. The skin peeling involves the entire top layer of the skin (the epidermis), which sometimes peels off in sheets from large areas of the body ( see Structure and Function of the Skin Structure and Function of the Skin The skin is the body’s largest organ. It serves many important functions, including Protecting the body against trauma Regulating body temperature Maintaining water and electrolyte balance Sensing… read more ).

Stevens-Johnson syndrome causes only small areas of peeling skin (affecting less than 10% of the body).

Toxic epidermal necrolysis causes large areas of peeling skin (affecting over 30% of the body).

Involvement of 15 to 30% of body surface area is considered overlap of Stevens-Johnson syndrome and toxic epidermal necrolysis.

In both forms, blistering of the mucous membranes typically occurs in the mouth, eyes, and vagina and sometimes in the digestive, respiratory, and urinary tracts.

Both disorders can be life threatening.

About half the cases of Stevens-Johnson syndrome and nearly all the cases of toxic epidermal necrolysis are caused by a reaction to a drug, most often sulfa and other antibiotics; antiseizure drugs, such as phenytoin and carbamazepine; and certain other drugs, such as piroxicam or allopurinol. Some cases are caused by a bacterial infection, vaccination, or graft-versus-host disease Graft-versus-host disease Transfusions are given to increase the blood’s ability to carry oxygen, restore the amount of blood in the body (blood volume), and correct clotting problems. Transfusions are usually safe,… read more . Sometimes, a cause cannot be identified. In children with Stevens-Johnson syndrome, an infection is the most likely cause.

These disorders occur in all age groups. These disorders are more likely to occur in people with an abnormal immune system, such as those with a bone marrow transplant, systemic lupus erythematosus Systemic Lupus Erythematosus (SLE) Systemic lupus erythematosus is a chronic autoimmune inflammatory connective tissue disorder that can involve joints, kidneys, skin, mucous membranes, and blood vessel walls. Problems in the… read more , other chronic joint and connective tissue diseases, or with human immunodeficiency virus (HIV) infection Human Immunodeficiency Virus (HIV) Infection Human immunodeficiency virus (HIV) infection is a viral infection that progressively destroys certain white blood cells and is treated with antiretroviral medications. If untreated, it can cause… read more (particularly when people also have pneumonia caused by Pneumocystis jirovecii). The tendency to develop one of these disorders can run in families.

Symptoms of SJS and TEN

Stevens-Johnson syndrome and toxic epidermal necrolysis usually begin with fever, headache, cough, keratoconjunctivitis (inflammation of the conjunctiva and the cornea in the eyes), and body aches. If caused by a drug, these symptoms usually appear 1 to 3 weeks after the start of the drug. Then the skin changes begin, with a flat red rash on the face, neck, and trunk, often spreading later to the rest of the body in an irregular pattern. The areas of rash enlarge and spread, often forming blisters in their center. The skin of the blisters is very loose and easy to rub off, often with just a gentle touch or pull, and the blisters peel off over a period of 1 to 3 days. The affected areas are painful, and the person feels very ill with chills and fever. In some people, the hair and nails fall out. The palms and soles may be affected.

In both disorders, sores appear on the mucous membranes lining the mouth, throat, anus, genitals, and eyes. The damage to the lining of the mouth makes eating difficult, and closing the mouth may be painful, so the person may drool. The eyes may become very painful and swell and become so crusted that they seal shut. The corneas can become scarred. The opening through which urine passes (urethra) may also be affected, making urination difficult and painful. Sometimes the mucous membranes of the digestive and respiratory tracts are involved, resulting in diarrhea and cough, pneumonia, and difficulty breathing.

The extensive skin loss in toxic epidermal necrolysis is similar to a severe burn and is equally life threatening. People are very ill and may be unable to eat or open their eyes. Huge amounts of fluids and salts can seep from the large, raw, damaged areas. People who have this disorder are very susceptible to organ failure. They are also at risk of infection at the sites of damaged, exposed tissues. Such infections are the most common cause of death in people with this disorder.

Diagnosis of SJS and TEN

Doctors can usually diagnose Stevens-Johnson syndrome and toxic epidermal necrolysis by the appearance of the affected skin and mucous membranes, by their symptoms (pain rather than itching), by how quickly the skin manifestations progress, and by how much of the skin is affected.

A sample of skin may be removed and examined under a microscope (called a skin biopsy Biopsy Doctors can identify many skin disorders simply by looking at the skin. A full skin examination includes examination of the scalp, nails, and mucous membranes. Sometimes the doctor uses a hand-held… read more ).

Prognosis for SJS and TEN

In toxic epidermal necrolysis, the death rate can be as high as 25% in adults and can be even higher in older adults with very severe blistering. The death rate in children is estimated to be under 10%.

In Stevens-Johnson syndrome, the death rate is about 5%.

Treatment of SJS and TEN

Treatment in a burn center or intensive care unit

Possibly cyclosporine, corticosteroids, plasmapheresis, immune globulin, or immunosuppressants

People with Stevens-Johnson syndrome or toxic epidermal necrolysis are hospitalized. Any drugs suspected of causing either disorder are immediately discontinued. When possible, people are treated in a burn center or intensive care unit and given scrupulous care to avoid infection (see Severe burns Severe burns Burns are injuries to tissue that result from heat, electricity, radiation, or chemicals. Burns cause varying degrees of pain, blisters, swelling, and skin loss. Small, shallow burns may need… read more ). If the person survives, the skin grows back on its own, and, unlike burns, skin grafts are not needed. Fluids and salts, which are lost through the damaged skin, are replaced by vein (intravenously).

Use of drugs to treat these disorders is controversial because, although there are theoretical reasons why certain drugs might be helpful, none have clearly been shown to improve survival. Cyclosporine may lessen the duration of active blistering and peeling and possibly increase the survival rate. Some doctors believe that giving large doses of corticosteroids within the first few days is beneficial, whereas others believe they should not be used because they might increase the risk of serious infection. If infection develops, doctors give antibiotics immediately.

Doctors may do a plasmapheresis Apheresis In apheresis, blood is removed from a person and then returned after substances are removed from it. Apheresis can be used to Obtain healthy blood components from a donor to transfuse to a person… read more . During this procedure, the person’s blood is removed, and the plasma is separated from the blood and discarded. This procedure removes certain harmful substances from the blood, possibly including drugs and antibodies (immune system proteins) that could be causing either disorder. After the substances are removed, the blood cells are returned to the person.

Doctors may give intravenous human immune globulin to treat toxic epidermal necrolysis. This substance may help prevent further damage to skin cells.

Drugs called immunosuppressants may be given. Immunosuppressants weaken (suppress) the immune system and help keep it from attacking the body’s own tissues. Tumor necrosis factor (TNF)–inhibiting drugs are a type of immunosuppressant. TNF inhibitors, such as infliximab and etanercept, are given to people with Stevens-Johnson syndrome or toxic epidermal necrolysis to help suppress the immune process that is causing inflammation.

what infections cause skin peeling

Dry, flaky, peeling skin doesn’t feel great, and it can look even worse. If you’re dealing with peeling skin, Dr. Taylor Dickerson of U.S. Dermatology Partners in Tyler, Texas, says, “The good news about peeling skin is that it’s not often a warning sign of anything serious. In many cases, skin peeling is a response to chronic skin disorders, a mild side effect of a medication, or a symptom related to allergies or other adverse responses. Typically, skin peeling can be addressed with mild, over-the-counter products. In rare cases, skin peeling can be a sign of something more serious, so it’s important to consult with a dermatologist to pinpoint the underlying causes of skin peeling. This allows your dermatologist to recommend the best treatment options to renew your skin’s health and appearance.” Keep reading to hear more about common causes of skin peeling from Dr. Dickerson.

Reason 1 – Allergic Response

When it comes to common causes of skin peeling, Dr. Dickerson says, “Allergic reactions to products that directly touch the skin like environmental irritants, metals, skincare products, cleansers, and other elements are possibly the most common causes of skin peeling. Allergic response to foods and medications as well as seasonal allergies can also lead to skin peeling.”

Reason 2 – Infections

Infection is another common cause of peeling skin. Any type of infection can lead to skin peeling, but it’s most often a symptom of skin infections caused by staphylococcus (staph infections). Skin peeling is also linked to fungal skin infections like athlete’s foot, jock itch, and ringworm. Systemic infections like scarlet fever may also lead to skin peeling.

Reason 3 – Immune Disorders

Immune disorders can lead to skin peeling. Specifically, this occurs as a symptom of Pemphigus, an autoimmune disorder that causes the body to attack cells in the outer layers of the skin.

Reason 4 – Idiopathic Disorders

Several idiopathic disorders can lead to skin peeling. Kawasaki disease, a condition that most often impacts children under the age of five, causes rashes and peeling skin. Additionally, acral peeling skin syndrome, a rare skin disorder, causes the outer layers of the skin to peel. This peeling is painless, but it can negatively impact the appearance of the skin and cause itching and irritation that adversely affects the look and feel of the skin.

Reason 5 – Cancer & Treatments for Cancer

According to Dr. Dickerson, “Cancer, specifically Non-Hodgkin Lymphoma, and cancer treatments are often linked to skin conditions, including skin peeling. As part of your comprehensive cancer treatment plan, you should consult with a dermatologist to keep skin healthy and address symptoms as soon as they arise.”

Reason 6 – Chronic Skin Conditions

Many chronic skin conditions cause skin thickening, flaking, and peeling. Specifically, those who struggle with skin conditions like eczema (atopic dermatitis), contact dermatitis, seborrheic dermatitis, psoriasis, rosacea, and acne-prone skin are likely to experience skin peeling. Managing all symptoms of chronic skin conditions, including skin peeling, and taking steps to prevent flare-ups in these skin conditions is essential.

Reason 7 – Skin Type

When it comes to skin types prone to skin peeling, Dr. Dickerson says, “Those with dry, acne-prone, or sensitive skin are much more likely to experience skin peeling. This can be especially true when using new skincare products, so make sure to consult with a dermatologist before making changes to your routine. For dry skin, pay attention and adjust your skincare routine during the fall and winter months when skin tends toward dryness.”

Reason 8 – Medication Side Effects

Certain medications have skin health side effects, including peeling. In most cases, peeling skin is a mild symptom that will clear up on its own after you complete medication use. If you are going to be using a medication for the long term, you may need to talk to your doctor about different treatment options and work with a dermatologist to address side effects until your skin heals. There is a more severe skin peeling condition that can arise as a symptom of certain medications. According to Dr. Dickerson, “While skin peeling related to medications typically clears up and causes minimal adverse effect to skin health, there is a rare condition called Stevens-Johnson Syndrome that may also occur when taking some medication. This adverse drug reaction starts with symptoms common to the flu, including fever and chills. From there, there is redness and blistering of the skin, which leads to skin peeling. If you believe you’re suffering from Stevens-Johnson Syndrome, you should seek emergency medical attention immediately.”

Reason 9 – Burns & Sunburn

Two of the most common causes of skin peeling are burns and sunburns. After the skin is burned by heat, chemicals, or the sun, it reddens, blisters, and peels. Following a burn, keep skin moisturized with deep-hydrating products like aloe vera to promote faster, more comfortable healing. As the skin peels, avoid the urge to scratch or scrub. Instead, gently wash the skin and use soft cleansing cloths to remove peeling skin without causing irritation or wounds that increase the risk of infection. Additionally, protect the skin from further sun damage with sunscreen. ALASTIN Skincare Silkshield All Mineral Sunscreen SPF 30 with TriHex Technology offers optimal protection against sun damage while also hydrating and healing burned skin.

Reason 10 – Using Certain Skincare Products & Treatments

According to Dr. Dickerson, “It’s important to choose your skincare products carefully. Products that contain drying ingredients like alcohol, retinols, exfoliants, and acids can all irritate the skin, leading to peeling. You can minimize the risk of peeling skin by spot-testing any new skincare products. Apply the product to the skin in a small area. Then, wait for a few days to a week. Observe any changes in skin health. If you notice irritation or peeling, discontinue use of this product.” To minimize the risk of peeling skin, you can also consult with a dermatologist before adding any new skincare products to your daily routine.

Consult Your Dermatologist

If your skin is peeling and you need additional support addressing this symptom, you want to talk about updating your skincare routine, or you’re interested in a dermatologic procedure, the U.S. Dermatology Partners team is here to support your skin health goals. Getting started is quick and easy, simply take a few moments to fill out our online scheduling form. Then, a dermatology team member will call to finalize the details of your visit.