Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

'Fiddler's neck' is a condition affecting violin and viola players. Although well known to musicians it is not well recognized by dermatologists. Clinically the lesions usually consist of a localized area of lichenification of the left side of the neck--just below the angle of the jaw. Pigmentation, erythema and inflammatory papules or pustules are frequently present, while severe inflammatory induration, cyst formation and scarring occur in more severely affected subjects. The aetiology of the skin changes is probably due to a combination of factors; friction giving rise to lichenification, while local pressure, shearing stress and occlusion may play a part in producing the acne-like changes and cyst formation. In addition, poor hygiene may predispose to local sepsis.
Br J Dermatol 1978 Jun
PMID:'Fiddler's neck'. 15 Feb 81

An elderly man with Hodgkin's disease who was receiving multiple drug chemotherapy became septic and a wide spread bullous eruption developed. Intraepidermal cleavage on skin biopsy supported a diagnosis of the staphylococcal scalded skin syndrome (SSSS) type of toxic epidermal necrolysis. Blood cultures confirmed a staphylococcal septicemia. Occurrence of this syndrome in an adult is unusual. A review of the literature on SSSS indicates an increased mortality when adults are compared with children with this syndrome.
Arch Dermatol 1979 May
PMID:Staphylococcal scalded skin syndrome in an adult with Hodgkin's disease. 44 34

In order to elucidate the pathogenesis of the skin lesions in 'benign gonococcal sepsis' direct immunofluorescence of an early macular lesion and routine histopathology of a mature papulopustular lesion in a patient with septic gonococcal dermatitis have been performed. Histopathology of the mature skin lesion revelaed a pattenr of 'allergic vasculitis'. Direct immunofluorescence showed exclusively deposits of C3 around and within the capillaries and in the basement membrane zone. No specific IgG, IgM, IgA or C4 deposits could be demonstrated. This, together with serological findings and reports from the literature, suggests an important pathogenetic function for complement, activated through the alternative pathway by means of gonococcal endotoxic lipopolysaccharide, in the pathogenesis of the skin lesions in benign gonococcal sepsis.
Br J Dermatol 1976 Sep
PMID:Alternative pathway complement activation:a possible mechanism inducing skin lesions in benign gonococcal spesis. 78 66

A case of right-sided Pseudomonas cepacia endocarditis in a heroin addict is presented in which septic cutaneous vasculitis (ecthyma gangrenosum) is a prominent feature. Ecthyma gangrenosum, most commonly associated with sepsis due to P aeruginosa, has not been previously described with P cepacia septicemia.
Arch Dermatol 1977 Feb
PMID:Pseudomonas cepacia endocarditis and ecthyma gangrenosum. 83 96

More than 2 million persons sustain thermal injuries in the United States annually (Monafo and Crabtree, 1985) and more than 10,000 burn victims die (Collini and Kealey, 1989). The principal factors affecting mortality are the total area burned and the area of third degree (full thickness) burns (Tompkins et al., 1985) with wound sepsis being the leading cause of mortality. Early aggressive excision and immediate covering of the wounds improve survival (Herndon and Parks, 1986). Various biological and synthetic substrates have been employed to replace the injured skin. Most of these provide a permeability barrier which substitutes for the epidermal function of the lost skin. An ideal skin replacement should also provide a substitute for dermis, which provides both support and stability for the epidermal replacement and prevents wound contraction. The dermal and epidermal replacement should be firmly integrated by a complete basement membrane zone (BMZ).
J Dermatol Sci 1992 Nov
PMID:Treatment of burns with skin substitutes. 128 67

The Wiskott-Aldrich syndrome is an uncommon X-linked recessive disease characterized by eczema, thrombocytopenia, and immunodeficiency. The clinical features begin early in life and include recurrent infections, bleeding, and severe eczema. Unless the condition is treated by bone marrow transplantation, the prognosis of Wiskott-Aldrich syndrome is grave, and premature death caused by sepsis, hemorrhage, or lymphoreticular malignancy is common. Although the biochemical defect responsible for the syndrome is not known, recent investigations with restriction fragment length polymorphisms have mapped the Wiskott-Aldrich syndrome locus to the proximal portion of the short arm of the human X chromosome (Xp11). The isolation of these DNA markers makes feasible both carrier detection and prenatal diagnosis of Wiskott-Aldrich syndrome and provides an important adjunct to the management of Wiskott-Aldrich syndrome for patients and their families. These genetic data, in conjunction with the recent identification of a specific O-glycosylation defect in lymphocytes from patients with Wiskott-Aldrich syndrome, present an opportunity for the eventual isolation of the Wiskott-Aldrich syndrome gene and identification of the underlying cellular defect. We review the clinical and laboratory features of this syndrome and summarize the new molecular and biochemical approaches that can be used in diagnosis, genetic counseling, and treatment.
J Am Acad Dermatol 1992 Oct
PMID:Wiskott-Aldrich syndrome: new molecular and biochemical insights. 140 1

Toxic epidermal necrolysis (TEN) is a life-threatening bullous dermatosis characterized by the sudden onset of full-thickness epidermal necrosis. TEN is a disease of both children and adults, but TEN in early infancy is a rare event; only two well-documented cases in infants less than 6 months of age have been reported. We report a third case of a 6-week-old infant with Escherichia coli sepsis who received ampicillin and other antibiotics and subsequently developed TEN. Despite the withdrawal of ampicillin and aggressive systemic and wound care, the infant died. The infants in the other two reported cases also died, which suggests that TEN in early infancy has an extremely poor prognosis.
J Am Acad Dermatol 1992 Aug
PMID:Toxic epidermal necrolysis in early infancy. 151 1

The clinicopathological features of 22 cases of the Dowling-Meara form of epidermolysis bullosa simplex (DM-EBS) (11 males, 11 females; aged 5 days-46 years) were reviewed using data collected over a 10-year period. All cases presented clinically within the first 5 days of life. Early blisters were often large (up to 5 cm in diameter), and were mostly acral and particularly periungual. Some cases presented with more widespread erosive skin changes, and two neonates with extensive skin involvement died as a result of overwhelming sepsis. After the neonatal period a different pattern of blistering occurred with more proximal haemorrhagic, herpetiform clusters of blisters. Central healing with recurrent blistering at the margins of these areas was frequently noted. Other physical signs included varying degrees of intra-oral blistering, nail shedding, nail dystrophy, minor scarring, palmo-plantar keratoderma, a lack of seasonal variation and improvement during later childhood. The underlying pathological mechanism in DM-EBS is basal cell cytolysis, or rarely acantholysis, in association with tonofilament (TF) clumping. TF clumping was found in lesional, perilesional and some non-lesional skin, suggesting that the tonofilament abnormality may be of primary aetiological significance in DM-EBS. TF clumping may be due to specific keratin abnormalities because the altered TF were found in a distribution similar to the known distribution of the basal cell keratins, K5 and K14. The level of blistering was invariably very low within the epidermal basal layer and often less than 0.5 microns above the basement membrane. We conclude that DM-EBS is a distinct, and probably under-recognized genodermatosis which tends to have a good prognosis. However, the disease can occasionally be severe, especially during the neonatal period, when it may be confused with junctional or severe recessive dystrophic EB. Electron microscopy is the best means for demonstrating the characteristics cytoskeletal disorder and confirming the diagnosis.
Br J Dermatol 1992 May
PMID:Epidermolysis bullosa simplex (Dowling-Meara). A clinicopathological review. 161 Jun 81

The cases of three HIV-positive men with generalized psoriasis and staphylococcal sepsis are reported. In each case the skin appeared to be the source of infection. While the patients received antibiotic therapy, the psoriatic plaques resolved despite minimal or no topical treatment.
J Am Acad Dermatol 1991 Jun
PMID:Staphylococcal sepsis in HIV antibody seropositive psoriasis patients. 186 86

Purpura fulminans is a rare disease characterized by purpura ecchymosis, hypotension, and fever associated with disseminated intravascular coagulation. It often begins as a benign infectious process and subsequently progresses to a severe, catastrophic outcome. It is recognized to originate from congenital or acquired protein C deficiency. We present an unusual case of an adult with Xanthomonas maltophilia sepsis that subsequently developed into purpura fulminans with involvement of the four extremities. We discuss the importance of the protein C system in coagulation homeostasis and its relationship to purpura fulminans.
J Dermatol 1991 Apr
PMID:Purpura fulminans secondary to Xanthomonas maltophilia sepsis in an adult with aplastic anemia. 191 97


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