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)

Proteinase-3 (PR3) is an abundant serine proteinase stored in the azurophilic granules of neutrophils and released to the cell surface upon activation where it contributes to local tissue destruction and inflammation. The sub-population of membrane PR3 (mPR3) high expression (PR3-high) varies among individuals. There are many reports about PR3 in Wegener's granulomatosis, but few about PR3 expression in patients with common inflammatory disorders, such as sepsis. The mPR3 expression on neutrophils from 56 patients with inflammatory disorders and from 64 healthy volunteers was examined by flow cytometry. High variability in the percentage of PR3-high (%PR3-high) neutrophils was observed in healthy volunteers and patients with inflammatory disease, and the %PR3-high was significantly greater in the patients (72 +/- 19% vs 55 +/- 20%, P < 0.0001). Overall neutrophil PR3 expression in patients with infectious diseases, especially systemic inflammatory response syndrome (SIRS) was significantly high (P < 0.01) and showed a positive correlation with C-reactive protein (CRP). Even under inflammatory conditions not involving autoimmune vasculitis, there are significant increases in both the absolute surface expression of PR3 and the numbers of neutrophils expressing high levels of PR3 and these correlate with CRP levels. The data are consistent with a model in which neutrophil membrane expression of PR3 is greatly influenced by an in vivo inflammatory environment.
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PMID:Proteinase 3 expression on neutrophil membranes from patients with infectious disease. 1687 19

In summer 1996, a 31-year-old woman developed arthralgia, subfebrility, and papular efflorescences on the skin, clinically and histologically suspect of vasculitis, to be followed by severe lung edema and anuria, with serum creatinine up to 1182 mol/L in the autumn 1996. The administration of high dose corticosteroids, plasmapheresis and hemodialysis resulted in regression of the clinical symptoms and considerable improvement of the kidney function. Kidney biopsy revealed sclerosing extracapsular glomerulonephritis with extensive fibrocellular crescents. Thereafter, the patient felt well, however, renal insufficiency showed gradual progression, so the patient was continuously treated with hemodialysis from January 1998. Two more episodes of severe lung edema occurred at the beginning of 1998 and in the autumn 1998, with rapid symptom regression upon the administration of high dose corticosteroids. In April 1998, during the episode of staphylococcal sepsis, multiple nodose shadows of the lungs were detected, to persist asymptomatically for the next six months. Toward the end of November, nodal enlargement and disruption, with the formation of cavitations occurred. The patient's general condition deteriorated gradually, and she died from respiratory arrest in February 1999. The patient received corticosteroids during most of the disease course, and cyclophosphamide only once, during the first episode of lung edema. On autopsy, a number of cavitations were observed in the lungs, with necrotic areas of a varying size and numerous cicatrices in the rest of pulmonary parenchyma. Besides fibrosis and areas of necrosis, histology showed palisading granulomas, with erythrocytes, macrophages and siderophages within the alveoles. Apart from candidal colonization of the airways, which developed in the terminal stage of the disease, all tests for fungi, Staphylococcus aureus and Mycobacterium tuberculosis were repeatedly negative. ANCA and other immunoassays were also negative on several occasions. Differential diagnosis of multiple nodose lesions of the lungs is discussed. The authors believe the patient suffered from Wegener's granulomatosis.
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PMID:[Multiple nodose shadows of the lungs as a differential diagnosis problem]. 1693 41

Each factor infection or non-infection (surgery, burn) can be the cause of inflammatory reaction development and in turn releasing of pro- and antiinflammatory mediators. Excessive or/and uncontrol releasing of these mediators leads to endothelium damage and organ dysfunction. Standard analysis of common infection markers, i.e. peripheral blood leukocytes, C-reactive protein, reaction of Biernacki measurements, do not allow to distinguish infection and noninfection reason of systemic inflammatory response. Procalcitonin is the specific marker for bacterial and fungal infection. Its level is low during local bacterial and virus infection, autoimmunological diseases, but it is increased at the patients with sepsis, severe sepsis. In described case (patient with Wegener's granulomatosis) applying procalcitonin measurement and sensitive and specific microbiological diagnostic by using bronchio-alveolal lavage leads to successful treatment.
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PMID:[Severe sepsis or clinical view of autoaggressive disease. Wegener's granulomatosis--case report]. 1720 75

The bacillus Listeria monocytogenes is widely distributed in the environment. Listeria monocytogenes most often causes infection in the neonates, pregnant women, elderly and immunosuppressed persons. We report on a case of fatal sepsis and meningitis in a 59-year-old woman receiving cyclophosphamide and glucocorticoid therapy for Wegener's granulomatosis over a 10-year period. Listeriosis should be suspected in case of sepsis and/or meningitis in patients who receive immunosuppressive agents. Since meningitis due to Listeria monocytogenes is not distinguishable clinically from other types of bacterial meningitis, antibiotics against Listeria monocytogenes should be included in the initial empirical therapy of bacterial meningitis in immunosuppressed patients, antibiotics against Listeria monocytogenes should be included.
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PMID:[A fatal case of Listeria monocytogenes sepsis and meningitis in a patient with Wegener's granulomatosis]. 1721 9

A young female patient presented as an acute medical emergency with hypoglycaemia. Investigations revealed panhypopituitarism and an inflammatory pituitary mass. An antibody screen was negative for anti-neutrophil cytoplasmic antibodies with cytoplasmic distribution (cANCA). Pituitary histology showed lymphocytic infiltration and a few Langerhan's cells. The pituitary mass rapidly expanded to involve the optic nerves and led to bilateral blindness. Later, the patient developed diarrhoea, a vasculitis rash, scleritis, and proteinuria. In subsequent investigations cANCA became positive. The patient responded to steroids and cyclophosphamide treatment and remained in partial remission for six months before dying of severe sepsis. This is the first description of Wegener's granulomatosis presenting with acute anterior pituitary failure in the absence of other organ involvement and negative serology.
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PMID:Fatal inflammatory hypophysitis. 1731 40

Wegener's Granulomatosis (WG) in its limited form can be a challenging diagnosis. ANCA, radiological investigations and histology should be interpreted in light of clinical findings. A delay in diagnosis can have profound visual consequences. Immunosuppressive therapy and co-morbidities can mask signs of orbital sepsis. A low threshold for further exploration and biopsy should be maintained if an orbital abscess is suspected. This report describes a complex case of WG that illustrates the diagnostic and therapeutic challenges inherent in this form of orbital inflammatory disease.
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PMID:A complex orbit. 1871 68

Fifteen patients with vasculitis and renal manifestations have been analyzed. All patients had renal manifestation of vasculitis. Renal biopsy was performed in 13 patients: 6 patients had microscopic polyangiitis, 4 Wegener's granulomatosis, 2 microscopic polyangiitis limited to the kidneys and 3 polyarteritis nodosa. Renal biopsy was not performed in 2 patients. One patient had renal insufficiency and small kidneys and one patient had polyarteritis nodosa. The diagnosis of the polyarteritis nodosa in this last patient was made because of other clinical and laboratory data. Pauci-immune type of glomerulonephritis was found in 11 patients. The crescents, usually cellular, fibrocellular and rarely fibrotic, were present in 20-100% glomeruli. Renal insufficiency at baseline was present in 14 patients (creatinine 215-1224 micromol/L). Only one patient had borderline renal function when the diagnosis of vasculitis was made (creatinine 115 micromol/L). All patients with glomerulonephritis were treated with glucocorticosteroids and cyclophosphamide. Five patients with pulmonary manifestations of disease or advanced renal failure also were treated with plasmapheresis. Eight patients were treated by hemodyalisis. The complete or partial remission in the first year of the follow-up was reached in 9 patients, and 5 patients were treated by chronic dialysis due to chronic renal failure. One patient with Wegener's granulomatosis died after he developed toxic megacolon and postoperative sepsis.
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PMID:[Renal changes in vasculitis: case report]. 1934 48

Acute rehabilitation refers to the multidisciplinary rehabilitative treatment of patients in continuing need of integrated acute and rehabilitative longterm care. As a result of the advances in acute rheumatology and improved emergency services, an increasing number of patients survive episodes of severe disease and complications of immunosuppressive therapy. These patients require not only treatment of their acute medical problems but also specialized multidisciplinary acute rehabilitation starting as early as possible during their hospital stay. We describe 4 typical cases from the major fields of rheumatology. (1) Acute rehabilitation of a 63-year-old woman with rheumatoid arthritis after replacement of both preexisting knee endoprostheses in one session and removal of the left hip endoprosthesis due to infection and sepsis. (2) Rehabilitation of a 29-year-old man with a 7-year history of ankylosing spondylitis who lived in an adjustable easy chair for 2 years due to severe pain prior to admission. (3) A 61-year-old woman with active refractory Wegener's granulomatosis who developed respiratory insufficiency due to aspergillus and pseudomonas pneumonia. (4) The acute rehabilitation of a 21-year-old woman with systemic lupus erythematosus and a history of 14 laparotomies due to severe acute pancreatitis and multiple gut perforations. Acute rehabilitation was complicated by a large defect of the abdominal wall and significant critical illness polyneuropathy. Our report points out differences between acute, postacute, and longterm rehabilitation, describes the mobilization of patients in acute rheumatology units, and defines specific problems encountered in acute hospital-based rehabilitation of rheumatological patients.
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PMID:Severe disease activity and complications of immunosuppressive therapy: a challenge for acute hospital-based rehabilitation in rheumatology. 1953 61

Calcific uremic arteriolopathy (CUA) is a rare, life-threatening disease, typically affecting patients with end-stage renal disease. It is characterized by widespread vascular calcification, endothelial fibrosis and end-organ ischemia. The mortality rate is high with infection and sepsis being the most common causes of death. Common therapies include restoration of calcium and phosphorous homeostasis, wound care and pain control. Although soft tissue calcification is a known complication in children with advanced renal disease, the incidence of CUA in pediatrics remains unknown. Additionally, current literature regarding its management in pediatric patients is lacking. We report the case of a 17-year-old African-American male patient with end-stage renal disease secondary to Wegener's granulomatosis who developed CUA after 3 years on peritoneal dialysis. Treatment with sodium thiosulfate (STS) and hyperbaric oxygen (HBO) therapy alone was ineffective, forcing the patient to undergo bilateral below the-knee-amputation (BKA) 5 months after presentation. It was not until peritoneal dialysis had been changed to daily hemodialysis, while continuing STS and HBO therapy, that the patient demonstrated complete resolution of CUA on repeat bone scan. Based on these findings, and the extremely high mortality rate associated with this disease, CUA management requires early and aggressive intervention with multi-faceted therapy, including prompt conversion from peritoneal dialysis to hemodialysis, STS infusions and hyperbaric oxygen therapy.
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PMID:Successful treatment of calcific uremic arteriolopathy in a pediatric dialysis patient. 1988 86

Hypercalcaemia occurs in many granulomatous diseases. Among them, sarcoidosis and tuberculosis are the most common causes. Other causes include berylliosis, coccidioidomycosis, histoplasmosis, Crohn's disease, silicone-induced granulomas, cat-scratch disease, Wegener's granulomatosis and Pneumocystis carinii pneumonia. Hypercalcaemia in granulomatous disease occurs as a consequence of dysregulated production of 1,25-(OH)2 D3 (calcitriol) by activated macrophages in granulomas. Hypercalcaemia in patients with Mycobacterium tuberculosis infection has been reported in 0%-28% of cases. Uncultured bronchoalveolar lavage cells from patients with M. tuberculosis produce greater amounts of calcitriol compared with controls. Although Nayar et al described hypercalcaemia in a case of sepsis associated with intravesical Bacille Calmette Guerin therapy, there are no published reports describing hypercalcaemia in patients with pulmonary M. bovis infection. We describe a patient with M. bovis cavitary pulmonary infection with sustained hypercalcaemia that fluctuated and recurred repeatedly over the course of therapy, ultimately culminating in normalisation of serum calcium when therapy had led to cure. Treatment consisted of antituberculous therapy, oral corticosteroids and intravenous bisphosphonates with a favourable outcome.
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PMID:Fluctuating hypercalcaemia caused by cavitary Mycobacterium bovis pulmonary infection. 2937 38


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