This research paper will be an in-depth description of Toxic Epidermal Necrolysis (TENS) Syndrome, focusing on its pathophysiology, epidemiology, the various diagnostic measures, diagnosis, and its evaluation and management.

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Toxic Epidermal Necrolysis (TENS) Syndrome is a severe dermatologic disorder resulting from adverse drug reactions in the body. According to Barvaliya et al. (2011), the elderly aged above 70 are at more risk of developing Toxic Epidermal Necrolysis complications. However, other risk factors such as a compromised immune system, malignancies, viral pneumonia, and autoimmune conditions may make even the younger individuals susceptible to TENS Syndrome. Toxic Epidermal Necrolysis Syndrome is an advanced case of Stevens-Johnson Syndrome caused by a reaction to drugs such as antibiotics and anticonvulsants. As a result, there is a 20% increment in skin involvement from Stevens-Johnson Syndrome (10%) to TENS syndrome (30%). As a result, the condition causes widespread erythema, skin necrosis, and detachment of the epidermal layer from the mucous membranes, compromising skin integrity. All these symptoms are life-threatening and may result in death. Therefore, early diagnosis and aggressive treatment are essential in the management of the condition. This research paper will be an in-depth description of Toxic Epidermal Necrolysis (TENS) Syndrome, focusing on its pathophysiology, epidemiology, the various diagnostic measures, diagnosis, and its evaluation and management. Finally, the paper will highlight the important role of the nurse practitioner in the management of patients affected by the condition, employing the Shuler Framework.


The exact mechanism of the genesis of Toxic Epidermal Necrolysis Syndrome has not been fully explained. However, various theories have been proposed to explain the pathogenesis of the condition, many having gained worldwide acceptance. Initially, Fas or Granulysin-mediated apoptotic processes were identified as the pathomechanism behind the etiology of TEN syndrome. Recently, there have been developments in the studies of the condition's pathophysiology, resulting in the proposition of another pathway system, the reactive oxygen species (Ros), to explain the mechanism of TEN Syndrome. They all attempt to explain how apoptosis is induced in the epidermal cells, an accepted TEN Syndrome mechanism.

  1. Fas-mediated Apoptosis

Fas is a membrane-bound protein expressed in almost all cells. Its activation results in the activation of caspases, which in turn induce apoptosis. The natural ligand to the Fas protein is the Fas ligand produced by the natural killer cells and the cytotoxic T lymphocytes. The successful binding of the Fas ligand (FasL) to its receptor has been determined to induce keratinocyte apoptosis. The high concentration of the Fas ligand in the keratinocytes was revealed by immunostained sections of the skin tissue acquired from patients. Therefore, it was proposed that the Fas ligand has a role in the mass destruction of keratinocytes in patients with TEN Syndrome.

  1. Granulysin Cell-Mediated Apoptosis

Granulysisn serves as a pro-apoptotic protein that can affect apoptosis without direct cell-cell contact. Chung et al. identified the activity of these proteins in 2008 following an initial disregard of all the proposed mechanisms involving cell-mediated immunity due to poor infiltration of the cells in the epidermal tissue of the patients. However, Chung's findings and conclusions concerning the role of granulysin protein gained popularity and acceptance after a series of pieces of evidence was presented. Therefore, granulysin has been identified as one of the initiators of apoptosis of the keratinocytes by their cytotoxic activity. Actually, it is a direct determinant of the severity of the condition in patients with TEN Syndrome.

  1.  Reactive Oxygen Species

Oxidative stress is a possible cause of intracellular keratinocyte damage, and therefore a possible mechanism for the development of TEN. Impaired detoxification pathways result in the production of the reactive oxygen species. This is toxic to cells and results in the destruction of the cell membrane and major cell activities to the extent that the cells are eliminated by apoptosis via the natural mechanism of FasL and tumor necrosis factor. The GST-π is often used as an indicator to confirm the evidence of oxidative stress in the epidermal cells in TEN. Tissue necrosis factor α (TNF α) is thought to be responsible for producing the reactive oxygen species. It impairs the electron transport chain by a progressive increase in nitric oxide production in the mitochondria. The impaired transport chain subsequently lessens the detoxifying ability of the mitochondria and thus the accumulation of the reactive oxygen species that is lethal to the cells.

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Additional to the mentioned proposed mechanisms, other theories include alternative cell-mediated apoptotic pathways that do not involve the protein granulysin and cytokine-induced enhancement of the apoptotic pathways. As aforementioned, the generally accepted pathomechanism of TEN Syndrome is by the apoptotic killing of the epidermal cells and the keratinocytes. Therefore, all these theories try to explain the exact processes that result in induced apoptosis.


TEN is a rare condition with an incidence of 0.4-1.2 per million persons annually. More women are affected than men, in the ratio of 1.5: 1 (French, 2006). The incidence of occurrence of TEN progressively ...

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