Dilantin® is an anti-epileptic drug; or, as it is also known: an anticonvulsant.

Its particular purpose is to assist in the control of epileptic seizures.

Dilantin® works by slowing down the specific brain-impulses that can cause epileptic seizures.

Stevens-Johnson Syndrome

The use of Dilantin® has been linked to Stevens-Johnson Syndrome (SJS): a potentially-life-threatening condition that can result in skin-cell death, and may result in the epidermis separating from the dermis.

Furthermore, SJS can lead to the development of scar-tissue within the eyelids, which may cause impaired vision.

Within the U.S., around 300 new cases of SJS are diagnosed on a yearly basis.

Its mortality rate is approximately 5 percent.

Purple Glove Syndrome

Purple Glove Syndrome (PGS) is a disease of the skin that has also been linked to the usage of Dilantin®.

It can cause the patient's limbs to become swollen and painful, and may lead to amputation in rare cases.

PGS is generally reported amongst elderly patients, and chiefly those who have been prescribed large, multiple intravenous doses of the epilepsy drug phenytoin.

Dilantin®, Phenytoin & Pregnancy

According to the FDA:

Prenatal exposure to phenytoin may increase the risks for congenital malformations and other adverse developmental outcomes.

Increased frequencies of major malformations (such as orofacial clefts and cardiac defects), minor anomalies (dysmorphic facial features, nail and digit hypoplasia), growth abnormalities (including microcephaly), and mental deficiency have been reported among children born to epileptic women who took phenytoin alone or in combination with other antiepileptic drugs during pregnancy.

There have also been several reported cases of malignancies, including neuroblastoma, in children whose mothers received phenytoin during pregnancy.

The overall incidence of malformations for children of epileptic women treated with antiepileptic drugs (phenytoin and/or others) during pregnancy is about 10%, or two- to three-fold that in the general population.

However, the relative contributions of antiepileptic drugs and other factors associated with epilepsy to this increased risk are uncertain and in most cases it has not been possible to attribute specific developmental abnormalities to particular antiepileptic drugs.

Toxic Epidermal Necrolysis Syndrome or TENS

SJS is potentially viewed as part of a group of conditions that includes Eruthema Multiforme, Toxic Epidermal Necrolysis and Stevens-Johnson Synrdome.  Toxic Epidermal Necrolysis Syndrome, TENS, is often viewed as an extremely severe type of Stevens Johnson Syndrome.  TENS includes blisters that can cover the entire body and even internal organs, and sometimes the skin can shed in large sheets. 

TENS is often fatal, with some estimates at about 40%.

Erythema Multiforme is a less severe form of Stevens Johnson Syndrome in the opinion of many doctors.  The skin lesions in this disease are less severe. 

If you or a loved one have been diagnosed with SJS, TENS, or Erythema Multiforme due to the side effects of Dilantin®, Bextra®, Celebrex®, Daypro®, Lamectal®, or any other drug - including over the counter medications and supplements -  we sould like to speak with you immediately.  

If You Have Been Injured by Dilantin®

Have you or a loved one been injured after taking Dilantin®?

For a free evaluation of your potential claim, call 1-888-446-8087, or fill out an intake form on this website by clicking on "Can We Help You?" on the upper right hand corner of the home page.

Let us help you receive the potential compensation you need and deserve.    Do not delay, as your legal rights may be lost if you wait. 

Never stop or alter your medications unless you first speak with your licensed physician;  always follow closely your physician's advice. 

WIKIPEDIA ON STEVENS-JOHNSON SYNDROME:

We thank Wikipedia for the information below and encourage you to support their work.  Please see main article, Discussion Tab, Contributors List, and additional information on this article here:

http://en.wikipedia.org/wiki/Stevens%E2%80%93Johnson_syndrome

Some technical data and other information below is included to help you find this website.  The main article on this subject at wikipedia.org has more information and potentially an updated article on this subject.  

Stevens–Johnson syndrome

From Wikipedia, the free encyclopedia

Stevens–Johnson syndrome

Classification and external resources
ICD-10
L51.1
ICD-9
695.13
OMIM
 608579
 DiseasesDB
 4450
 MedlinePlus
 000851
 eMedicine
emerg/555 derm/405
MeSH
D013262

Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN)[1] are two forms of a life-threatening skin condition, in which cell death causes the epidermis to separate from the dermis. The syndrome is thought to be a hypersensitivity complex that affects the skin and the mucous membranes. Although the majority of cases are idiopathic (without a known cause), the main class of known causes is medication, followed by infections and, rarely, cancers.
 

Classification
 
There is agreement in the medical literature that Stevens–Johnson syndrome (SJS) can be considered a milder form of toxic epidermal necrolysis (TEN). These conditions were first recognised in 1922.[2]
 
Both diseases can be mistaken for erythema multiforme. Erythema multiforme is sometimes caused by a reaction to a medication but is more often a type III hypersensitivity reaction to an infection (caused most often by Herpes simplex) and is relatively benign. Although both SJS and TEN can also be caused by infections, they are most often adverse effects of medications. Their consequences are potentially more dangerous than those of erythema multiforme.
 
Signs and symptoms
 
Conjunctivitis (inflammation of eye and eyelid) in SJS
SJS usually begins with fever, sore throat, and fatigue, which is misdiagnosed and usually treated with antibiotics. Ulcers and other lesions begin to appear in the mucous membranes, almost always in the mouth and lips but also in the genital and anal regions. Those in the mouth are usually extremely painful and reduce the patient's ability to eat or drink. Conjunctivitis of the eyes occurs in about 30% of children who develop SJS. A rash of round lesions about an inch across arises on the face, trunk, arms and legs, and soles of the feet, but usually not the scalp.[3]
 
Pathology

Micrograph showing full thickness epidermal necrosis with a basket weave-like stratum corneum and separation of the dermis and epidermis. Skin biopsy. H&E stain.
SJS, like toxic epidermal necrolysis and erythema multiforme, are characterized by confluent epidermal necrosis with minimal associated inflammation. The acuity is apparent from the (normal) basket weave-like pattern of the stratum corneum.
 
 Causes
 
SJS is thought to arise from a disorder of the immune system.[3] The immune reaction can be triggered by infections, drugs, or medications. In some groups, drug reaction may be aggravated by genetic factors.
 
 Infections
 
SJS can be caused by infections. It usually follows common infections such as herpes simplex virus, influenza, mumps, cat-scratch fever, histoplasmosis, Epstein-Barr virus, mycoplasma pneumoniae, or similar.
 
 Medication/drugs
 
See also: List of SJS inducing substances
 
Although Stevens–Johnson Syndrome can be caused by viral infections, malignancies, or severe allergic reactions to medication, the leading cause appears to be the use of antibiotics and sulfa drugs.
 
SJS can be caused by adverse effects of drugs allopurinol (a.k.a. Aloprim), Zyloprim, Dilantin, Depakote, Levaquin, diclofenac, etravirine, isotretinoin (a.k.a. Accutane), fluconazole,[4] valdecoxib, sitagliptin, oseltamivir, penicillins, barbiturates, sulfonamides, phenytoin, azithromycin, oxcarbazepine, zonisamide, modafinil,[5] lamotrigine, nevirapine, pyrimethamine, ibuprofen,[6] ethosuximide, carbamazepine, nystatin, and gout medications.[7][8]
 
Medications that have traditionally been known to lead to SJS, erythema multiforme and toxic epidermal necrolysis include sulfonamides (antibiotics), penicillins (antibiotics), barbiturates (sedatives), lamotrigine, and phenytoin (e.g. Dilantin) (anticonvulsants). Combining lamotrigine with sodium valproate increases the risk of SJS.
 
Non-steroidal anti-inflammatory drugs are a rare cause of SJS in adults; the risk is higher for older patients, women and those initiating treatment.[2] Typically, the symptoms of drug-induced SJS arise within a week of starting the medication. People with systemic lupus erythematosus or HIV infections are more susceptible to drug-induced SJS.[3]
 
SJS may also be caused by cocaine use.[9]
 
 Genetics
 
In some East Asian populations studied (Han Chinese and Thai), carbamazepine- and phenytoin-induced SJS is strongly associated with HLA-B*1502 (HLA-B75), an HLA-B serotype of the broader serotype HLA-B15.[10][11][12] A study in Europe suggested that the gene marker is only relevant for East Asians.[13][14]
 
Based on the Asian findings, similar studies in Europe showed 61% of allopurinol-induced SJS/TEN patients carried the HLA-B58 (phenotype frequency of the B*5801 allele in Europeans is typically 3%). One study concluded: "Even when HLA-B alleles behave as strong risk factors, as for allopurinol, they are neither sufficient nor necessary to explain the disease."[15]
 
 Treatment
 
SJS constitutes a dermatological emergency. All medications should be discontinued, particularly those known to cause SJS reactions. Patients with documented mycoplasma infections can be treated with oral macrolide or oral doxycycline.[3]
 
Initially, treatment is similar to that for patients with thermal burns, and continued care can only be supportive (e.g. intravenous fluids and nasogastric or parenteral feeding) and symptomatic (e.g., analgesic mouth rinse for mouth ulcer). Dermatologists and surgeons tend to disagree about whether the skin should be debrided.[3]
 
Beyond this kind of supportive care, there is no accepted treatment for SJS. Treatment with corticosteroids is controversial. Early retrospective studies suggested that corticosteroids increased hospital stays and complication rates. There are no randomized trials of corticosteroids for SJS, and it can be managed successfully without them.[3]
 
Other agents have been used, including cyclophosphamide and cyclosporine, but none has exhibited much therapeutic success. Intravenous immunoglobulin (IVIG) treatment has shown some promise in reducing the length of the reaction and improving symptoms. Other common supportive measures include the use of topical pain anesthetics and antiseptics, maintaining a warm environment, and intravenous analgesics. An ophthalmologist should be consulted immediately, as SJS frequently causes the formation of scar tissue inside the eyelids, leading to corneal vascularization, impaired vision and a host of other ocular problems.
 
 Prognosis
 
SJS proper (with less than 10% of body surface area involved) has a mortality rate of around 5%. The risk for death can be estimated using the SCORTEN scale, which takes a number of prognostic indicators into account.[9] Other outcomes include organ damage/failure, cornea scratching, and blindness.
 
 Epidemiology
 
Stevens–Johnson syndrome is a rare condition, with a reported incidence of around 2.6[3] to 6.1[2] cases per million people per year. In the United States, there are about 300 new diagnoses per year. The condition is more common in adults than in children. Women are affected more often than men, with cases occurring at a two to one (2:1) ratio.[2]
 
 History
 
Stevens-Johnson Syndrome is named for Albert Mason Stevens and Frank Chambliss Johnson, American pediatricians who in 1922 jointly published a description of the disorder in the American Journal of Diseases of Children.[16][17][18][19]
 
 Notable cases
 Padma Lakshmi, actress, model, television personality, and cookbook writer;[20]
 Tessa Keller of MTV show Laguna Beach;[21]
 Sabrina Brierton Johnson, whose family unsuccessfully sued the manufacturer of Children's Motrin, Johnson & Johnson, after a case of SJS blinded her.[22]
 Manute Bol, former professional basketball player and member of NBA's Washington Bullets, Golden State Warriors, Philadelphia 76ers, and Miami Heat, who died from complications.[23]
 

 References
 
1.^ Merck Manual: Stevens-Johnson syndrome
 2.^ a b c d Ward, K. E.; Archambault, R.; Mersfelder, T. L. (2010). "Severe adverse skin reactions to nonsteroidal antiinflammatory drugs: A review of the literature". American Journal of Health-System Pharmacy 67 (3): 206–213. doi:10.2146/ajhp080603. PMID 20101062. edit
 3.^ a b c d e f g Tigchelaar H, Kannikeswaran N and Kamat D (December 1, 2008). "Stevens-Johnson Syndrome: An Intriguing Diagnosis". Consultant for Pediatricians.
 4.^ Medsafe Data Sheet March 8, 2005. Accessed April 26, 2007.
 5.^ US FDA 2007 Safety Alerts for Drugs, Biologics, Medical Devices, and Dietary Supplements
 6.^ Raksha MP, Marfatia YS (2008). "Clinical study of cutaneous drug eruptions in 200 patients". Indian J Dermatol Venereol Leprol 74 (1): 80. doi:10.4103/0378-6323.38431. PMID 18193504.
 7.^ Fagot J, Mockenhaupt M, Bouwes-Bavinck J, Naldi L, Viboud C, Roujeau J (2001). "Nevirapine and the risk of Stevens–Johnson syndrome or toxic epidermal necrolysis". AIDS 15 (14): 1843–8. doi:10.1097/00002030-200109280-00014. PMID 11579247.
 8.^ Devi K, George S, Criton S, Suja V, Sridevi P (1 September 2005). "Carbamazepine--the commonest cause of toxic epidermal necrolysis and Stevens–Johnson syndrome: a study of 7 years". Indian J Dermatol Venereol Leprol 71 (5): 325–8. doi:10.4103/0378-6323.16782. PMID 16394456.
 9.^ a b Stevens–Johnson Syndrome - emerg/555 at eMedicine
 10.^ Chung WH, Hung SI, Hong HS, et al. (April 2004). "Medical genetics: a marker for Stevens–Johnson syndrome". Nature 428 (6982): 486. doi:10.1038/428486a. PMID 15057820.
 11.^ Locharernkul C, Loplumlert J, Limotai C, et al. (July 2008). "Carbamazepine and phenytoin induced Stevens–Johnson syndrome is associated with HLA-B*1502 allele in Thai population". Epilepsia 49 (12): 2087. doi:10.1111/j.1528-1167.2008.01719.x. PMID 18637831.
 12.^ Man CB, Kwan P, Baum L, et al. (May 2007). "Association between HLA-B*1502 allele and antiepileptic drug-induced cutaneous reactions in Han Chinese". Epilepsia 48 (5): 1015–8. doi:10.1111/j.1528-1167.2007.01022.x. PMID 17509004.
 13.^ Alfirevic A, Jorgensen AL, Williamson PR, Chadwick DW, Park BK, Pirmohamed M (September 2006). "HLA-B locus in Caucasian patients with carbamazepine hypersensitivity". Pharmacogenomics 7 (6): 813–8. doi:10.2217/14622416.7.6.813. PMID 16981842.
 14.^ Lonjou C, Thomas L, Borot N, et al. (2006). "A marker for Stevens–Johnson syndrome ...: ethnicity matters". Pharmacogenomics J. 6 (4): 265–8. doi:10.1038/sj.tpj.6500356. PMID 16415921.
 15.^ Lonjou C, Borot N, Sekula P, et al. (February 2008). "A European study of HLA-B in Stevens–Johnson syndrome and toxic epidermal necrolysis related to five high-risk drugs". Pharmacogenet. Genomics 18 (2): 99–107. doi:10.1097/FPC.0b013e3282f3ef9c. PMID 18192896.
 16.^ Stevens–Johnson syndrome at Who Named It?
 17.^ Stevens AM, Johnson FC (1922). "A new eruptive fever associated with stomatitis and ophthalmia; report of two cases in children". Am J Dis Child 24: 526–533.
 18.^ Stevens–Johnson syndrome - Definitions from Dictionary.com
 19.^ American Medical Association (1922). American journal of diseases of children. American Medical Association. pp. 526–. Retrieved 5 June 2010.
 20.^ Jess Cartner-Morley, "Beautiful and Damned", The Guardian, 8 April 2006
 21.^ Source: Daly, Melissa. "My Friend Ditched Me!" Seventeen Magazine Dec. 2006: 102
 22.^ Jury finds for J&J in Motrin suit
 23.^ FanHouse Staff (19). "Manute Bol Dies at Age 47". Fanhouse. Retrieved 20 June 2010.
 
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