Prosthetic Replacement of the Ocular Surface Ecosystem as Treatment for Ocular Surface Disease in Patients with a History of Stevens–Johnson Syndrome/Toxic Epidermal Necrolysis

OBJECTIVE: To describe a patient who developed toxic epidermal necrolysis (TEN) possibly secondary to lamotrigine use. CASE SUMMARY: A 74-year-old white man with a history of probable complex partial seizures was admitted to the neurology service for a prolonged postictal state. His antiepileptic regimen was changed while he was in the hospital to include lamotrigine. After 19 days of hospitalization and 14 days of lamotrigine therapy, the patient became febrile. The next day he developed a rash which progressed within 4 days to TEN, diagnosed by skin biopsy. All suspected drugs were discontinued, including lamotrigine. The patient was treated with hydrotherapy in the burn unit. His symptoms improved and he was discharged from the hospital 26 days after the rash developed. DISCUSSION: During lamotrigine's premarketing clinical trials, the manufacturer reported several cases of Stevens-Johnson syndrome and TEN. There are several published case reports of lamotrigine-induced severe skin reactions. All of these reports included patients being treated with both valproic acid and lamotrigine. Our patient was exposed to phenytoin, carbamazepine, clindamycin, and lamotrigine, but not valproic acid. The patient reported prior use of phenytoin with no skin rash. Carbamazepine was the antiepileptic drug the patient was maintained on prior to his hospital admission, and the symptoms of TEN resolved while he was still receiving carbamazepine. The patient received only two doses of clindamycin, which makes this agent an unlikely cause of TEN. CONCLUSIONS: Because of the temporal relationship of the onset of the patient's rash and several drugs that are known to cause severe rashes, it is not certain which drug was the definite culprit. However, based on the evidence from the literature, lamotrigine appears to be the causative agent.

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Meropenem-induced Stevens-Johnson syndrome/toxic epidermal necrolysis in a patient with known type IV penicillin hypersensitivity

BMJ Case Reports ◽

10.1136/bcr-2019-230144 ◽

2019 ◽

Vol 12 (8) ◽

pp. e230144 ◽

Cited By ~ 3

Author(s):

Muhammad Sameed ◽

Christine Nwaiser ◽

Prashant Bhandari ◽

Sarah A Schmalzle

Keyword(s):

Toxic Epidermal Necrolysis ◽

Cross Reactivity ◽

Delayed Hypersensitivity ◽

Stevens Johnson Syndrome ◽

Hypersensitivity Reactions ◽

Beta Lactam ◽

Type Iv ◽

Johnson Syndrome ◽

Life Threatening ◽

History Of

Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are considered variants of a disease continuum that results in a life-threatening exfoliative mucocutaneous disease. These are categorised as type IV cell-mediated delayed hypersensitivity reactions, and antibiotics are often implicated as a cause. Penicillins and other beta-lactam antibiotics are known to cause both immediate and delayed hypersensitivity reactions. While immediate IgE-mediated cross-reactivity between penicillins and carbapenems is well studied, less information on the risk of type IV delayed cell-mediated cross-reactivity between the two is available. We present a case of meropenem-induced SJS in a patient with documented history of SJS from amoxicillin. There are few cases of cross-reactivity with carbapenems reported in the literature, but based on the potential for life-threatening reaction, it is likely prudent to avoid the use of any beta-lactams in a patient with a history of SJS, TEN or any other severe cutaneous adverse reactions to another beta-lactam antibiotic.

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Drugs causing severe ocular surface involvements in Japanese patients with Stevens–Johnson syndrome/toxic epidermal necrolysis

Allergology International ◽

10.1016/j.alit.2015.05.002 ◽

2015 ◽

Vol 64 (4) ◽

pp. 379-381 ◽

Cited By ~ 10

Author(s):

Nahoko Kaniwa ◽

Mayumi Ueta ◽

Ryosuke Nakamura ◽

Yoshimi Okamoto-Uchida ◽

Emiko Sugiyama ◽

...

Keyword(s):

Toxic Epidermal Necrolysis ◽

Ocular Surface ◽

Japanese Patients ◽

Stevens Johnson Syndrome ◽

Johnson Syndrome

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Prosthetic Replacement of the Ocular Surface Ecosystem Scleral Lens Therapy for Patients With Ocular Symptoms of Chronic Stevens-Johnson Syndrome

American Journal of Ophthalmology ◽

10.1016/j.ajo.2014.03.012 ◽

2014 ◽

Vol 158 (1) ◽

pp. 49-54 ◽

Cited By ~ 29

Author(s):

Martin Heur ◽

Dianne Bach ◽

Christos Theophanous ◽

Gloria B. Chiu

Keyword(s):

Ocular Surface ◽

Stevens Johnson Syndrome ◽

Prosthetic Replacement ◽

Ocular Symptoms ◽

Johnson Syndrome

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Phenytoin induced toxic epidermal necrolysis: a case report

International Journal of Basic & Clinical Pharmacology ◽

10.18203/2319-2003.ijbcp20192219 ◽

2019 ◽

Vol 8 (6) ◽

pp. 1448

Author(s):

Sandipan Barkakaty ◽

Girish K.

Keyword(s):

Oral Cavity ◽

Toxic Epidermal Necrolysis ◽

Past History ◽

Clinical History ◽

The Body ◽

Stevens Johnson Syndrome ◽

Medicine Department ◽

Johnson Syndrome ◽

History Of ◽

Emergency Medicine Department

Stevens Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN), are severe idiosyncratic reactions characterized by fever and mucocutaneous lesions leading to necrosis and sloughing of the epidermis. The usage of anticonvulsants like carbamazepine, phenytoin, lamotrigine, phenobarbital are associated with high risk for occurrence of TEN. We present a case of toxic epidermal necrolysis in a 30 year old female probably induced by phenytoin. A 30 year old female was admitted to the emergency medicine department of KIMS hospital, Bengaluru. Lesions over the lips and oral cavity, multiple fluid filled blisters were present diffusely all over the body. Patient had a past history of oral cavity lesions with injection phenytoin. Patient is a known epileptic of over 12 years and was on treatment. Patient had a seizure attack 3 days back and visited nearby hospital and did not inform the doctor of her allergy to phenytoin. Patient was given inj phenytoin after which she developed oral lesions and also presented with fluid filled bullae all over the body. A diagnosis of toxic epidermal necrolysis was made based on clinical history and Scoreten score and was treated with betadine wash, fluconazole and antibiotics .The lesions improved significantly with the above management and patient recovered enough to be discharged from the hospital after 5 days. Severe and serious reactions such as toxic epidermal necrolysis can be caused by commonly used drugs like phenytoin.

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Pathogenesis of Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis With Severe Ocular Complications

Frontiers in Medicine ◽

10.3389/fmed.2021.651247 ◽

2021 ◽

Vol 8 ◽

Author(s):

Mayumi Ueta

Keyword(s):

Toxic Epidermal Necrolysis ◽

Ocular Surface ◽

Acute Stage ◽

Stevens Johnson Syndrome ◽

Prostaglandin E ◽

Ocular Complications ◽

Chronic Stage ◽

Snp Association ◽

Johnson Syndrome ◽

Burn Units

Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) is an acute inflammatory vesiculobullous reaction of the mucosa of the ocular surface, oral cavity, and genitals, and of the skin. Severe ocular complications (SOC) are observed in about half of SJS/TEN patients diagnosed by dermatologists and in burn units. Ophthalmologists treat SOC, and they tend to encounter the patients not only in the acute stage, but also in the chronic stage. Our investigation of the pathogenesis of SJS/TEN with SOC led us to suspect that abnormal innate mucosal immunity contributes to the ocular surface inflammation seen in SJS/TEN with SOC. We confirmed that cold medicines such as NSAIDs and multi-ingredient cold medications are the main causative drugs for SJS/TEN with SOC. Single nucleotide polymorphism (SNP) association analysis of cold medicine-related SJS/TEN with SOC showed that the Toll-like receptor 3 (TLR3)-, the prostaglandin-E receptor 3 (PTGER3)-, and the IKZF1 gene were significantly associated with SNPs and that these genes could regulate mucocutaneous inflammation including that of the ocular surface. We also examined the tear cytokines of SJS/TEN with SOC in the chronic stage and found that IL-8, IL-6, IFN-γ, RANTES, eotaxin, and MIP-1β were significantly upregulated in SJS/TEN with SOC in the chronic stage. Only IP-10 was significantly downregulated in SJS/TEN with SOC in the chronic stage. This mini-review summarizes the pathological mechanisms that we identified as underlying the development of SJS/TEN with SOC.

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