Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Toxic epidermal necrolysis is perhaps the most formidable disease encountered by dermatologists. Uncommon but not rare, toxic epidermal necrolysis occurs in 60 to 70 persons per year in France. It remains as puzzling a disorder as it was 34 years ago, when described by Lyell. Whether or not toxic epidermal necrolysis is the most severe form of erythema multiforme is still the subject of discussion. The physiopathologic events that lead to this rapidly extensive necrosis of the epidermis are not understood. Indirect evidence suggests a hypersensitivity reaction, but the search for potential immunologic mechanisms has resulted in little data to support this hypothesis. Accumulated clinical evidence points to drugs as the most important, if not the only, cause of toxic epidermal necrolysis. Sulfonamides, especially long-acting forms, anticonvulsants, nonsteroidal anti-inflammatory agents, and certain antibiotics are associated with most cases of toxic epidermal necrolysis. Many other drugs have been implicated in isolated case reports. All organs may be involved either by the same process of destruction of the epithelium as observed in the epidermis or by the same systemic consequences of "acute skin failure" as seen in patients with widespread burns. Sepsis is the most important complication and cause of death. Approximately 20% to 30% of all patients with toxic epidermal necrolysis die. Elderly patients and patients with extensive lesions have a higher mortality rate. Surviving patients completely heal in 3 to 4 weeks, but up to 50% will have residual, potentially disabling ocular lesions. The prognosis is improved by adequate therapy, as provided in burn units, that is, aggressive fluid replacement, nutritional support, and a coherent antibacterial policy. Corticosteroids, advocated by some in high doses to halt the "hypersensitivity" process, have been shown in several studies to be detrimental and should be avoided.
J Am Acad Dermatol 1990 Dec
PMID:Toxic epidermal necrolysis (Lyell syndrome). 227 3

A 31-year-old Hispanic man presented in the pancytopenic phase of acute myelocytic leukemia and was treated with the chemotherapeutic agents mitoxantrone and cytarabine. After 5 days, an erythematous, blanching, papular, crusted eruption developed on his forehead, chest, and legs. Some lesions showed confluence and all were at the same developmental stage. Clinical diagnoses included necrotizing vasculitis and sepsis. A biopsy specimen revealed widespread noninflammatory syringometaplasia of eccrine ducts. Well-developed intercellular bridges and eosinophilic cytoplasm were seen within the metaplastic cells; apoptoses and occasional mitoses were present. This process is distinct and probably occurred secondary to direct toxic injury from the chemotherapeutic drugs. Because similar changes have occurred in patients with neutrophilic eccrine hidradenitis, we believe our patient represents an example of the noninflammatory end of the spectrum of chemotherapeutic eccrine gland reactions.
Arch Dermatol 1990 Jan
PMID:Eccrine squamous syringometaplasia. A cutaneous sweat gland reaction in the histologic spectrum of 'chemotherapy-associated eccrine hidradenitis' and 'neutrophilic eccrine hidradenitis'. 240 65

The myeloperoxidase-hydrogen peroxide-chloride (MPO-H2O2-Cl) system is an antimicrobial system of polymorphonuclear leukocytes. We demonstrated that the MPO-H2O2-Cl system is fungicidal for Trichophyton rubrum. Fungal growth of a synchronous cell culture of T. rubrum germlings was assayed by measuring the uptake of tritiated N-acetyl-D-glucosamine, and the viability of the fungi was assayed by counting colony-forming units. Cytotoxins produced by the interaction of myeloperoxidase with hydrogen peroxide and chloride ion were fungicidal for T. rubrum. Growth inhibition was abolished in the presence of catalase or L-methionine. Polymorphonuclear leukocytes through the MPO-H2O2-Cl system may prevent invasion and sepsis by dermatophytes even in the absence of specific immunity.
J Invest Dermatol 1989 Apr
PMID:Inhibition of growth of Trichophyton rubrum by the myeloperoxidase-hydrogen peroxide-chloride system. 253 15

A 68-year-old Japanese woman with sepsis developed a gangrene on her left cheek from a small wound in contact with a gastric tube. Klebsiella pneumoniae was cultured from the sputum, wound, and the blood and was assumed to be responsible for this condition, possibly through thrombosis of an artery.
J Dermatol 1989 Jun
PMID:Bacterial gangrene on the cheek of a comatose patient--necrotizing fasciitis or noma. 279 26

To determine the potential steroid sparing effect of plasma exchange in pemphigus we enrolled 40 patients in a multicenter randomized study. Eighteen patients were treated by prednisolone alone, 22 by prednisolone plus ten large-volume plasma exchanges over four weeks. All patients received oral prednisolone in the same initial dosage (0.5 mg/kg/d), which was increased weekly if needed. The number of cases controlled at each therapeutic step did not differ between the two groups. In eight cases, four in each group, the disease was not controlled by the highest therapeutic step of the protocol, with four deaths from sepsis in the plasma exchange group. The controlled cases needed similar cumulative prednisolone doses (5237 +/- 5512 mg in the plasma exchange group vs 4246 +/- 1601 mg in the control group). The evolution of serum pemphigus antibody was not different in the two groups. These findings suggest that plasma exchange in association with low steroid doses alone are not effective in the treatment of pemphigus and may even promote sepsis.
Arch Dermatol 1988 Nov
PMID:Controlled study of plasma exchange in pemphigus. 317 48

We examined a patient with systemic lupus erythematosus and sepsis due to Pseudomonas aeruginosa. Early in the infection, she developed skin lesions that consisted of indurated tender nodules and hemorrhagic and nonhemorrhagic bullae. Blister fluid contained gram-negative rods, which were identified as P. aeruginosa on culture. Bullae and nodules, as well as ecthyma gangrenosum, can be early cutaneous signs of pseudomonal sepsis.
Pediatr Dermatol 1987 May
PMID:Pseudomonas septicemia with nodules and bullae. 329 25

A 14-year-old boy developed group JK corynebacteria sepsis and a generalized erythematous macular and papular skin eruption following chemotherapy for relapse of acute lymphocytic leukemia. Lesional skin biopsy demonstrated effacement of eccrine glands by numerous pleomorphic gram-positive bacilli, morphologically consistent with Corynebacterium and confirmed by culture. This is the first known report documenting the generalized skin manifestations and histopathologic features associated with Corynebacterium sepsis.
J Am Acad Dermatol 1987 Feb
PMID:Cutaneous manifestations of Corynebacterium group JK sepsis. 346 29

Accelerated muscle proteolysis is a characteristic of systemic reaction following trauma, sepsis, or extensive thermal injury. The factors involved in this accelerated muscle breakdown have not been fully described. However, recently leukocytic pyrogen or interleukin 1 (IL-1) have been implicated in the induction of muscle protein degradation in septicemia or trauma. The epidermal cytokine epidermal cell-derived thymocyte activating factor (ETAF) is biochemically and functionally similar to IL-1. Injury to skin can augment ETAF activity. Using a murine model, we found that thermal injury can significantly enhance ETAF/IL-1 activity in a dose-dependent fashion. In addition, ETAF can cause net muscle protein breakdown in vitro. Thus, increased amounts of ETAF produced by thermally injured skin may contribute to the accelerated muscle breakdown in extensive thermal injury.
J Invest Dermatol 1986 Dec
PMID:Stimulation of muscle protein degradation by murine and human epidermal cytokines: relationship to thermal injury. 353 47

A patient with acquired immunodeficiency syndrome presented with multiple pruritic papules and nodules over the trunk and extremities. Biopsy specimens from two of these lesions contained granules within abscesses of the papillary dermis. There were numerous gram-positive cocci within the granules. Culture of one lesion failed to produce growth. A mouse inoculated with tissue from a lesion revealed no evidence of sepsis or organ involvement. The skin lesions showed no obvious response to systemic antimicrobial therapy but gradually resolved after treatment had been discontinued. Such lesions should be clinically distinguished from other cutaneous manifestations of acquired immunodeficiency syndrome, such as Kaposi's sarcoma.
J Am Acad Dermatol 1987 Jan
PMID:Cutaneous botryomycosis in a patient with acquired immunodeficiency syndrome. 381 60

Toxic epidermal necrolysis was documented in a 6-week-old infant with Klebsiella pneumoniae sepsis who received many medications. We inoculated infant mice with the K. pneumoniae isolate but were unable to produce histologic changes resembling those seen in our patient. This condition should be included in the differential diagnosis of severe drug reactions in very young infants with clinical scalded-skin syndromes.
Pediatr Dermatol 1985 Mar
PMID:Toxic epidermal necrolysis in a 6-week-old infant. 388 41


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