Immunohistochemical investigation of the coma blister and its pathogenesis

Abstract

: The erythematous patches and vesicles that are observed in coma patients, usually from an overdose of medication, are known as coma blisters. However, it is unknown whether the degenerated sweat gland is a necrosis or apoptosis. We immunohistochemically examined such skin lesions to investigate the characteristics and pathogenesis of the coma blister. Skin lesions were obtained from a forensic autopsy case, a woman in her thirties, of caffeine intoxication. Those lesions were observed in the left femoral, the lower left thigh, and the right knee. Histologically, the skin lesions showed that the keratinocytes had necrosed and the epidermis was thin in some areas. Eccrine sweat gland degeneration was observed. Obvious inflammatory cell infiltrations were not detected. Immunohistochemically, we stained each skin lesion against CD3, CD8, CD45RO, cytokeratin, 70 kD heat shock protein, ubiquitin, 150 kD oxygen regulated protein, and caspase-cleaved keratin 18 neo-epitope M30. They were also stained with an in situ apoptosis detection kit. Degenerated sweat glands featured CD45RO and M30 immunoreactivity. Immunohistochemical staining for CD45RO, CK-L, and M30 might be useful to observe sweat gland degeneration in the coma blister. Therefore, the apoptosis might be related to coma blisters and sweat gland degenerations. J. Med. Invest. 60 : 256-261, August, 2013

Peripheral Neuropathy Presenting as Myopathy That was Confused With Inflammatory Myositis

“…If the skin cells are damaged by various causes and their structural function is affected, the cells separate from each other and fluids build up between the separated cells, causing bullae. 6,7 In our case, a similar mechanism was suggested that the rapid progression of myopathy accompanied by neuropathy caused cutaneous edema and dermoepidermal disruption, resulting in bullae.…”

Bispectral index in predicting the prognosis of patients with coma in intensive care unit

“…The coma patients in ICU always have complex and critical primary diseases, such as cerebrovascular disease, traumatic brain injury, and diseases that need cardiopulmonary resuscitation, and also have a high morbidity and mortality. [11][12][13] In this study, the prognosis of patients with a vegetative state and brain death was the observation target, and the rest of mental state was considered as concious coma. Moreover, we explored the specifi city, sensitivity and accuracy of BIS in predicting the prognosis of patients with coma.…”

Drug Overdose-Induced Coma Blisters: Pathophysiology and Clinical and Forensic Diagnosis

“…Indeed, during epithelial cell apoptosis, intermediate filaments are reorganized and keratin 18 is cleaved by caspases to release M30, which is one of the most specific and earliest detected biomarkers of apoptosis [40]. This study also offered a tool for differential diagnosis for postmortem putrefaction artifacts typically observed in forensic autopsy cases [39]. Moreover, since sweat gland degenerations were only registered in coma blister areas, authors suggested that sweat gland degeneration was considered as specific finding for coma blister.…”

“…An interesting work [39] performed analysis of the skin lesions in order to understand the pathogenesis of the coma blisters in a forensic autopsy after caffeine overdose. Skin lesions exhibited necrotic keratinocytes, thin epidermis in some areas, degeneration of eccrine sweat glands and a nonclear inflammatory cells infiltration.…”

“…Authors suggested that these biomarkers may be useful in observing the sweat gland degeneration in coma blisters. They also concluded that apoptosis might be implicated in coma blisters pathophysiology and sweat gland degenerations due to M30 immunoreactivity [39]. Indeed, during epithelial cell apoptosis, intermediate filaments are reorganized and keratin 18 is cleaved by caspases to release M30, which is one of the most specific and earliest detected biomarkers of apoptosis [40].…”