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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Erysipelothrix infections have been a well-known clinical entity for over a century. Only a few cases have been studied histologically, and the agent has rarely been cultured from infected patients. We present here a case of erysipeloid of Rosenbach, in which histologic study and electron microscopy document the presence of microorganisms. We also present a complete review of the clinical and pathologic features of Erysipelothrix infections and their treatment. Our observations suggest that Erysipelothrix rhusiopathiae is capable of producing L forms that may revert to a bacterial form and produce sepsis at a later time.
J Am Acad Dermatol 1983 Jul
PMID:Erysipeloid. 688 93

Vibrio vulnificus infections is being reported with increasing frequency in coastal regions of the United States. Raw seafood consumption, particularly raw oysters, and wounds acquired in a marine environment predispose to infection. Patients with advanced liver disease are at increased risk of developing septicemia. V. vulnificus is a virulent pathogen producing significant morbidity and mortality; its virulence relates in part to the production of exotoxin. Skin lesions occur early in the clinical course of infection and provide means of specific diagnosis. The patient and the consulting physician are well served by the dermatologist capable of recognizing this infectious disease.
J Am Acad Dermatol 1983 Aug
PMID:Vibrio vulnificus infection. Case report and update since 1970. 688 15

Trichosporon beigelii fungemia and multiple, purpuric, papular skin lesions developed on the chest wall and extremities of a 22-year-old man with acute granulocytic leukemia. Histologically, the skin lesions demonstrated dermal budding yeasts, which were identified as T beigelii in culture. Unexplained biventricular, congestive heart failure and sepsis wit Streptococcus intermedius developed, and the patient died 28 days after his admission to the hospital.
Arch Dermatol 1982 May
PMID:Trichosporon beigelii fungemia and cutaneous dissemination. 695 20

Human graft versus host disease is composed of 2 distinct clinical entities, acute graft versus host disease and chronic graft versus host disease, which have different pathogenesis. Acute graft versus host disease is produced by the attack of donor immunocompetent T or null lymphocytes against recipient histocompatibility antigens. The null lymphocytes may attack antigens shared by the donor and recipient and are autocytotoxic lymphocytes which can produce acute graft versus host disease in recipients of identical twin transplants. The cessation of acute graft versus host disease occurs when suppressor lymphocytes appear in the recipient's peripheral circulation. Chronic graft versus host disease is produced by immunocompetent lymphocytes that differentiate in the recipient. Its control is unknown. Some patients with chronic graft versus host disease have in vivo activated suppressor lymphocytes which produce a secondary immunoincompetence and an increased susceptibility to bacterial sepsis and death.
J Invest Dermatol 1980 May
PMID:Human graft versus host disease. 699 70

A 50-year-old man with recurrent life-threatening sepsis and a cutaneous condition resembling pyoderma gangrenosum, was found to have a defect of neutrophil phagocytic function. Phagocytosis could be enhanced by corticosteroids, both in vitro in a dose-dependent manner, and in vivo, when it was accompanied by rapid clinical improvement. Studies with steroid hormones and immuno-stimulatory drugs are described.
Br J Dermatol 1982 Jun
PMID:Pharmacological modulation of neutrophil phagocytic function in a patient with recurrent sepsis, pyoderma gangrenosum and impaired phagocytosis. 708 73

Pemphigus is frequently a fatal skin disease. The cause of death and the events leading to it were investigated by examining patient records and autopsy data of thirteen patients who died as a result of this disease at the UCLA Hospital between 1965 and 1980. The diagnosis was confirmed histologically and/or by immunofluorescent studies of the skin and serum. Infection was the most frequent cause of death, and septicemia was found in nine of thirteen cases. The most commonly found organism was Staphylococcus aureus. The skin was usually the source of infection. Nine patients had pneumonia on chest x-ray and autopsy examination. Most patients had low levels of serum proteins and serum albumin. Since the patients were on long-term high doses of corticosteroids, the signs and symptoms of inflammation were often masked. This study demonstrated that for this reason, long-term corticosteroid therapy is one of the significant factors contributing to the death of these patients. A cautious and judicious use of steroids is suggested.
J Am Acad Dermatol 1982 Aug
PMID:Death in pemphigus. 713 Apr 83

Hyperbilirubinemia in the newborn results not only in visible yellow discoloration of the skin but, in high concentration, may cause bilirubin encephalopathy. Such damage to the central nervous system may be subtle and not apparent for several years, as with visual-motor perceptive defects; or it may cause severe neurologic damage (Kernicterus)--even death. Sick and immature infants are the most vulnerable to bilirubin toxicity. Although this condition affects nearly half of all newborns to some degree, only about 10% require treatment. Two methods of treatment are really effective in correcting hyperbilirubinemia, exchange blood transfusions, and/or phototherapy with light radiation in the blue part of the visible spectrum. If the rate of production of bilirubin is excessive or an infant's capacity to conjugate and excrete the pigment is deficient, bilirubin will accumulate in plasma, and will be taken up by other lipid-containing tissues, collagen, and (unless firmly bound to albumin) brain tissue. Many factors combine to raise plasma levels of bilirubin to toxic levels; for example, acidosis, sepsis, hypoxia, hemolysis, hypoalbuminemia, and certain competitive albumin binders. Bilirubin is photolabile in vivo, and if the whole body is irradiated with visible light in the absorption band (450-490 nm) of bilirubin, the pigment will undergo photocatabolism. Under phototherapy bilirubin undergoes photoisomerization at the meso double-bond to conformations less lipophyllic. It is now known that the major photo products of bilirubin IX-alpha are an unresolved mixture of its E, Z and Z, E isomers, easily excreted by the liver. Thus, phototherapy will reduce the accumulation of bilirubin in skin and other tissues and in circulating plasma.
J Invest Dermatol 1981 Jul
PMID:Molecular basis of hyperbilirubinemia and phototherapy. 725 51

A characteristic intermittent neutrophilic dermatosis, associated with polyarthritis, tenosynovitis, malaise, fever, and cryoglobulinemia, occurs in 20% of patients who undergo ileojejunal bypass surgery for the treatment of morbid obesity. The clinical syndrome may mimic gonococcal sepsis. The histologic changes in the skin are those of Sweet's syndrome. The syndrome remits spontaneously in most cases, but it may recur intermittently over a period of years. Treatment with low-dose steroids, tetracycline, or metronidazole suppresses symptoms in most cases, and restoration of normal bowel anatomy is curative. Skin testing with Streptococcus pyogenes antigen causes an excerbation of symptoms, or may provoke the entire syndrome de novo. Bacterial peptidoglycans, especially those of group A streptococci, produce similar arthritis and skin lesions in animal models. Peptidoglycans from numerous intestinal bacteria share common structural and antigenic features with S. pyrogenes peptidoglycan and are suggested as causative of the toxic and immunologic features of this syndrome.
J Am Acad Dermatol 1980 Jun
PMID:The bowel bypass syndrome: a response to bacterial peptidoglycans. 740 Apr 4

Indurated, erythematous plaques of the left arm and left flank developed in a 69-year-old white man with multiorgan failure from Escherichia coli sepsis. Cutaneous malacoplakia was diagnosed. Intravenous antibiotic therapy resulted in resolution of the malacoplakia and the E. coli sepsis.
J Am Acad Dermatol 1994 May
PMID:Cutaneous malacoplakia. 751 27

We report a severe case of Wells' syndrome, or eosinophilic cellulitis, after a bee sting in a 4-year-old girl. The patient had a widespread, painful, blistering eruption that was subsequently complicated by Pseudomonas aeruginosa superinfection and septicemia, hypoalbuminemia, anemia, and neutropenia. The skin lesions responded to systemic steroid therapy. There was residual scarring alopecia of the scalp. There have been 17 previous reports of childhood Wells' syndrome. We believe that this disorder is a distinct entity that should be considered in the differential diagnosis of blistering diseases in children.
J Am Acad Dermatol 1995 Nov
PMID:Wells' syndrome in childhood: case report and review of the literature. 759 97


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