The Health Info Of Steven Johnson Syndrome

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Stevens–Johnson syndrome

 
Stevens–Johnson syndrome
Classification and external resources

Man with Stevens–Johnson syndrome
ICD10 L51.1
ICD9 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

Mucosal desquamation in a person with Stevens-Johnson syndrome

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

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.
  • OTHER INFO
  • Stevens-Johnson Syndrome is an immune complex hypersensitivity reaction that can be caused from an infection or immune response to drugs. The symptoms of SJS are life altering.It is a severe expression of a simple rash known as erythema multiforme. SJS is also known as erythema multiforme major. It affects all ages and genders including pediatric populations. The most severe form of SJS is toxic epidermal necrolysis (TENS). SJS occurs twice as often in men as in women. Most cases of SJS appear in children and young adults under age 30.

    Females with SJS are twice as likely as males to develop TENS, and have an even higher chance if taking a category of drugs known as NSAIDs, non-steroidal anti-inflammatory drugs.

    If you or a loved one has been diagnosed by a doctor with the condition know as Stevens-Johnson Syndrome call our Law Firm at 1-800-862-1260. Stevens-Johnson Syndrome can be a potentially deadly skin disease that usually results from a drug reaction. Another form of this disease is called Toxic Epidermal Necrolysis. This condition can also be the result of a negative drug-related reaction. These conditions have been linked to adverse drug reactions. Some of the drugs are “over the counter” some are prescription. The results and consequences of this condition can be extremely painful and potentially deadly. Our Law Firm can help you determine if your condition was caused by the negligence of one of the drug manufactures. Call us today at 1-800-862-1260.

    Common Symptoms of Stevens-Johnson Syndrome / Toxic Epidermal Necrolysis:

    Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis can start with non-specific symptoms such as cough, aching, headaches, and feverishness. This may be followed by a red rash across the face and the trunk of the body, which can continue to spread to other parts of the body. The rash can form into blisters, and these blisters can form in areas such as the eyes, mouth and vaginal area. The mucous membranes can become inflamed, and with Toxic Epidermal Necrolysis layers of the skin can also come away with ease and often the skin peels away in sheets. The hair and nails can also come away in some cases, and sufferers can become cold and feverish.

    With Toxic Epidermal Necrolysis the most common cause of death is infection, which can enter through the exposed areas. This disease can leave the skin looking as though it has been burned, and areas where skin has flayed away can seep copiously and quickly become infected.

    Both Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis can start with non-specific symptoms such as:

    • Coughing
    • Aching
    • Headaches
    • Feverishness
    • Vomiting
    • Diarrhoea

    This is usually followed by a red rash across the face and the trunk of the body, which can continue to spread to other parts of the body. Blisters then form across the body in places such as the nose, mouth, eyes, and genital areas, and the mucous membrane becomes inflamed. With some people the nails and hair begin to come out as well. In the case of Toxic Epidermal Necrolysis patients, the skin can start to come away in sheets leaving exposed flesh that could be likened to serious burning and is very susceptible to infection. Both of these disease variations are potentially deadly. In drug related cases, the symptoms for both diseases can take one or two weeks to manifest from the first time the patient takes the drug.

    Drugs that have been linked to Stevens-Johnson Syndrome include:

    • NSAIDS (non-steroid anti-inflammatory drugs),
    • Allopurinol,
    • Phenytoin,
    • Carbamazepine,
    • Barbiturates,
    • Anticonvulsants,
    • Sulfa Antibiotics,
    • Children’s Motrin,
    • Advil,
    • Children’s Advil,
    • Cox-2 Inhibitor

    In some cases, the condition is caused by a bacterial infection. However, in many cases there is no known cause for the onset of Stevens-Johnson Syndrome or Toxic Epidermal Necrolysis. These skin diseases can cause massive pain, suffering and anxiety. People that have taken or are taking medications such as the ones mentioned above are urged to familiarize themselves with the symptoms of SJS (Stevens-Johnson Syndrome) and Toxic Epidermal Necrolysis (TEN). This will enable you to seek immediate medical attention should the need arise, and early initiation of treatment can make a big difference to the seriousness of the disease as this can stop any secondary infections. The aim of this website page is to help educate and informed the public about the symptoms, causes and treatment of SJS and TEN, and also to offer advice with regards to possible legal options of those affected by these diseases.

    As stated above Stevens-Johnson Syndrome is a potentially deadly skin disease that usually results from a negative drug reaction. Another form of the disease is called Toxic Epidermal Necrolysis, and again this usually results from a drug-related reaction. Both forms of the disease can be deadly as well as very painful and distressing. In most cases, these disorders are caused by a reaction to a drug, and one drug that has come under fire lately is the cox-2 inhibitor Bextra, which is already linked to these disorders.

    There are other drugs that have been linked to Stevens-Johnson Syndrome, and these include some other NSAIDS (non-steroid anti-inflammatory drugs), Allopurinol, Phenytoin, Carbamazepine, barbiturates, anticonvulsants, and sulfa antibiotics. The condition can sometimes – although not very often – be attributed to a bacterial infection, and in some cases there is no known cause for the onset of Stevens-Johnson Syndrome or Toxic Epidermal Necrolysis. However, the most common cause is through drug related reaction.

    Stevens-Johnson Syndrome can affect any age group. However, it occurs most commonly in older people, and this could be because older people tend to use more of the drugs associated with the disease and are therefore collectively more at risk from the disease. People that have AIDS are also at an increased risk of contracting Stevens-Johnson Syndrome or Toxic Epidermal Necrolysis. Those in the higher risk groups are urged to remain vigilant for any signs of these skin diseases, and are also advised to remain well informed about the symptoms that could indicate the presence or onset of Stevens-Johnson Syndrome or Toxic Epidermal Necrolysis.

    Most Common Treatments for this Condition:

    Those individuals suffering from SJS or TEN are treated in hospital, and if the cause of the problem is drug related then the drugs are stopped with immediate effect. Surviving patients are treated intravenously to replace any lost fluids, and the skin is left to re-grow on its own. However, the chances of survival can be hit and miss depending on the level of damage and the degree of infection incurred by the patient.

    It is vital that those taking drugs that could result in these skin diseases are vigilant and can identify the danger signs associated with these problems. Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis can be deadly, and the earlier the symptoms are recognized the faster treatment can be initiated. Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis are very serious, potentially deadly conditions and have to be treated accordingly. Firstly, the cause of the condition has to be identified if possible. So, if the cause if drug related, doctors can stop the drug immediately. In the case of a new infection on top of the condition or a bacterial infection, doctors may use a suitable antibiotic. In severe cases, the patient is treated in a burns unit. Patients have to be treated in meticulously hygienic environments to alleviate the risk of further infection, which could result in death. In cases where the patients has lost a lot of fluid through seeping areas where the skin has come away, intravenous fluid replacement may be required. The hos

  • The only way to get rid of this disease is to eliminate the source of the problem. Anything, the atmosphere, the drugs or the medicines that are causing this disease have to be changed so that it may not aggravate the problem. The immunity of the system suffers a great setback. Anyone who does not have a strong immunity is bound to suffer from more severe complexities than those who do. Treatment process is similar to the burn therapy process as the condition of the skin almost becomes the same. There is fluid loss, the nerves in the location do not respond and the skin starts to peel causing great trauma.

    Treatment involves providing the patient with high levels of fluids and electrolytic correction till the time restoration is not achieved. There is no specific treatment for this disease which is a cause of worry and because these are due to consumption of medicines, many pharmaceuticals are facing legal ca

INDONESIA VERSION

Sindrom Stevens-Johnson


Sindrom Stevens-Johnson
Klasifikasi dan sumber daya eksternal

Manusia dengan sindrom Stevens-Johnson
ICD-10 L51.1
ICD-9 695,13
OMIM 608579
DiseasesDB 4450
MedlinePlus 000851
eMedicine emerg/555 derm/405
MESH D013262

Sindrom Stevens-Johnson (SJS) dan toksik epidermal nekrolisis (SEPULUH) [1] adalah dua bentuk kondisi kulit mengancam jiwa, di mana kematian sel menyebabkan epidermis untuk terpisah dari dermis. Sindrom ini dianggap kompleks hipersensitivitas yang mempengaruhi kulit dan selaput lendir. Meskipun mayoritas kasus idiopatik (tanpa diketahui penyebabnya), kelas utama dari penyebab yang diketahui adalah obat, diikuti oleh infeksi dan, jarang, kanker.

Isi
1 Klasifikasi
2 Tanda dan gejala
2.1 Patologi
3 Penyebab
3.1 Infeksi
3.2 Obat / obat
3.3 Genetika
4 Pengobatan
5 Prognosis
6 Epidemiologi
7 Sejarah
8 Terkemuka kasus
9 Referensi
10 Pranala luar
 

 Klasifikasi
Ada kesepakatan dalam literatur medis yang sindrom Stevens-Johnson (SJS) dapat dianggap sebagai bentuk ringan dari nekrolisis epidermal toksik (TEN). Kondisi ini pertama kali diakui pada tahun 1922. [2]

Kedua penyakit dapat keliru untuk eritema multiforme. Eritema multiforme kadang-kadang disebabkan oleh reaksi terhadap obat, tetapi lebih sering tipe III reaksi hipersensitivitas terhadap infeksi (yang disebabkan paling sering oleh Herpes simpleks) dan relatif jinak. Meskipun kedua SJS dan TEN juga bisa disebabkan oleh infeksi, mereka yang paling sering efek samping dari obat. Konsekuensi mereka berpotensi lebih berbahaya daripada orang-orang dari eritema multiforme.

 Tanda dan gejala

Deskuamasi mukosa pada orang dengan sindrom Stevens-Johnson

Konjungtivitis (radang mata dan kelopak mata) di SJS
SJS biasanya dimulai dengan demam, sakit tenggorokan, dan kelelahan, yang salah didiagnosis dan biasanya diobati dengan antibiotik. Ulkus dan lesi lainnya mulai muncul di selaput lendir, hampir selalu di mulut dan bibir tapi juga di daerah genital dan anal. Mereka di mulut biasanya sangat menyakitkan dan mengurangi kemampuan pasien untuk makan atau minum. Konjungtivitis mata terjadi pada sekitar 30% anak-anak yang mengembangkan SJS. Ruam lesi putaran sekitar satu inci di seluruh timbul pada, wajah batang, lengan dan kaki, dan telapak kaki, tetapi biasanya tidak kulit kepala [3].

 Patologi

Mikrograf menunjukkan nekrosis epidermal ketebalan penuh dengan keranjang menenun seperti stratum korneum dan pemisahan dermis dan epidermis. Biopsi kulit. H & E noda.
SJS, seperti nekrolisis epidermal toksik dan eritema multiforme, yang ditandai dengan nekrosis epidermis konfluen dengan peradangan yang terkait minimal. Ketajaman ini terlihat dari keranjang (normal) menenun seperti pola stratum korneum.

 Penyebab
SJS diduga timbul dari gangguan sistem kekebalan tubuh. [3] Reaksi kekebalan dapat dipicu oleh infeksi, obat-obatan, atau obat. Pada beberapa kelompok, reaksi obat dapat diperburuk oleh faktor genetik.

Infeksi
SJS dapat disebabkan oleh infeksi. Ini biasanya mengikuti infeksi biasa seperti virus herpes simpleks, influenza, gondok, kucing-awal demam, histoplasmosis, virus Epstein-Barr, Mycoplasma pneumoniae, atau mirip.

Obat / obat
Lihat juga: Daftar zat merangsang SJS
Meskipun Stevens-Johnson Syndrome dapat disebabkan oleh infeksi virus, keganasan, atau reaksi alergi yang parah terhadap pengobatan, penyebab utama tampaknya penggunaan antibiotik dan obat sulfa.

SJS dapat disebabkan oleh efek samping obat allopurinol (alias Aloprim), Zyloprim, Dilantin, Depakote, Levaquin, diklofenak, etravirine, isotretinoin (Accutane alias), flukonazol, [4] valdecoxib, sitagliptin, oseltamivir, penisilin, barbiturat, sulfonamida, fenitoin, azitromisin, oxcarbazepine, zonisamide, modafinil, [5] lamotrigin, nevirapine, pirimetamin, ibuprofen, [6] ethosuximide, carbamazepine, nistatin, dan obat asam urat [7]. [8]

Obat-obat yang secara tradisional telah dikenal untuk menyebabkan SJS, eritema multiforme dan nekrolisis epidermal toksik termasuk sulfonamide (antibiotik), penisilin (antibiotik), barbiturat (obat penenang), lamotrigin, dan fenitoin (Dilantin misalnya) (antikonvulsan). Menggabungkan lamotrigin dengan valproate natrium meningkatkan risiko SJS.

Non-steroid anti-inflamasi obat adalah penyebab langka SJS pada orang dewasa;. Risiko lebih tinggi untuk pasien yang lebih tua, perempuan dan orang-orang memulai pengobatan [2] Biasanya, gejala obat-induced SJS muncul dalam waktu seminggu dari mulai obat . Orang dengan lupus eritematosus sistemik atau infeksi HIV lebih rentan terhadap obat-induced SJS. [3]

SJS juga bisa disebabkan oleh penggunaan kokain. [9]

Genetika
Dalam beberapa populasi Asia Timur dipelajari (Han China dan Thailand), karbamazepin dan fenitoin-diinduksi SJS sangat terkait dengan HLA-B * 1502 (HLA-B75), sebuah serotipe HLA-B dari serotipe HLA-B15 yang lebih luas [10. ] [11] [12] Sebuah penelitian di Eropa menunjukkan bahwa penanda gen hanya relevan untuk Asia Timur. [13] [14]

Berdasarkan temuan di Asia, penelitian serupa di Eropa menunjukkan 61% dari allopurinol-induced SJS / TEN pasien membawa HLA-B58 (fenotip frekuensi alel B * 5801 di Eropa biasanya 3%). Satu studi menyimpulkan: “Bahkan ketika alel HLA-B berperilaku sebagai faktor resiko yang kuat, seperti untuk allopurinol, mereka tidak cukup dan tidak perlu untuk menjelaskan penyakit.” [15]

Pengobatan
SJS merupakan darurat dermatologis. Semua obat harus dihentikan, terutama yang diketahui menyebabkan reaksi SJS. Pasien dengan infeksi Mycoplasma didokumentasikan dapat diobati dengan doksisiklin oral atau makrolida lisan. [3]

Awalnya, pengobatan mirip dengan yang untuk pasien dengan luka bakar termal, dan perawatan lanjutan hanya dapat mendukung (misalnya cairan intravena dan pemberian makan nasogastrik atau parenteral) dan gejala (misalnya, analgesik mulut berkumur selama sariawan). Dermatologists dan ahli bedah cenderung tidak setuju tentang apakah kulit harus debridement. [3]

Selain jenis perawatan suportif, tidak ada pengobatan diterima untuk SJS. Pengobatan dengan kortikosteroid masih kontroversial. Studi retrospektif awal menyarankan bahwa kortikosteroid peningkatan rawat inap dan tingkat komplikasi. Tidak ada uji coba acak dari kortikosteroid untuk SJS, dan dapat dikelola berhasil tanpa mereka. [3]

Agen lainnya telah digunakan, termasuk cyclophosphamide dan cyclosporine, tetapi tidak ada yang menunjukkan banyak keberhasilan terapi. Imunoglobulin pengobatan (IVIG) intravena telah menunjukkan beberapa janji dalam mengurangi panjang dari reaksi dan meningkatkan gejala. Lain langkah-langkah dukungan umum termasuk penggunaan anestesi nyeri topikal dan antiseptik, menjaga lingkungan yang hangat, dan analgesik intravena. Dokter mata harus berkonsultasi langsung, karena SJS sering menyebabkan pembentukan jaringan parut di dalam kelopak mata, menyebabkan vaskularisasi kornea, gangguan penglihatan dan sejumlah masalah mata lainnya.

 Prognosa
SJS yang tepat (dengan kurang dari 10% dari luas permukaan tubuh terlibat) memiliki angka kematian sekitar 5%. Risiko kematian dapat diperkirakan dengan menggunakan skala SCORTEN, yang membutuhkan sejumlah indikator prognostik ke account [9]. Hasil lainnya termasuk kerusakan organ / kegagalan, kornea menggaruk, dan kebutaan.

 Epidemiologi
Sindrom Stevens-Johnson adalah suatu kondisi yang jarang, dengan insiden dilaporkan sekitar 2,6 [3] untuk 6,1 [2] kasus per juta orang per tahun. Di Amerika Serikat, ada sekitar 300 diagnosa baru per tahun. Kondisi ini lebih umum pada orang dewasa dibandingkan pada anak-anak. Wanita lebih sering terkena daripada pria, dengan kasus yang terjadi pada rasio 0:58 (2:1). [2]

 Sejarah
Sindrom Stevens-Johnson adalah nama untuk Albert Mason Stevens dan Frank Chambliss Johnson, dokter anak Amerika yang pada tahun 1922 bersama-sama menerbitkan deskripsi gangguan dalam American Journal of Penyakit Anak [16] [17] [18] [19].

 kasus Terkemuka
Padma Lakshmi, aktris, model, kepribadian televisi, dan penulis buku resep; [20]
Tessa Keller dari MTV menunjukkan Laguna Beach; [21]
Sabrina Brierton Johnson, yang keluarganya tidak berhasil menggugat produsen, Motrin Anak Johnson & Johnson, setelah kasus SJS membutakannya [22].
Manute Bol, mantan pemain basket profesional dan anggota NBA Washington Bullets, Golden State Warriors, Philadelphia 76ers, dan Miami Heat, yang meninggal dari komplikasi.

 
 
 

 

 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

the end @ copyright dr Iwan suwandy 2011

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