Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034186 (pyelonephritis)
 6,144 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The results from the treatment of 1086 patients, treated at the Therapeutic Clinic, HMI- Sofia were followed up for the period 1961-1970 incld. Acute bacterial and vuris-bacterial pneumonias were found in 318 patients, 475 of the patients were with exacerbated chronic bronchitis and bronchiectasis, with exacerbated chronic pyelo-nephritis -216 patients and with exacerbated chronic cholecystitis and cholangiohepatitis --92 patients. The effect of the treatment was determined according to a three-stage scale "good" with complete clinical healing (in acute pneumonia), with "improvement"--with complete clinical remission (in chronic infections) and "without effect". Clinical and paraclinical indices were used as criteria in the determination of the effectiveness. The data are statistically processed according to the method of variation analysis. In patients with acute pneumonia the- best effectiveness was manifested by tetraolean (88,7 per cent), tetracylins (77,8 per cent), chloramphenicol (76,8 per cent), penicillin (72,5 per cent), the combination penicillin-streptomycin (71,9 per cent); in patients with exacerbated chronic bronchitis--tetraolean (88,0 per cent), chloramphenicol (73,2 per cent), tetracylins (65,3 per cent); in patients with exacerbated chronic pyelonephritis - chloramphenicol (65,5 per cent); in patients with exacerbated chronic cholecystitis and cholecysto-cholangiohepatitis-tetraolean (70,7 per cent), tetracyclins (66,7 per cent), chloramphenicol (66,1 per cent).
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PMID:[Comparative clinical studies of the effectiveness of the most frequently used antibiotics in the period of 1961-1970]. 77 78

Twenty-four children, ten of whom had an infection due to ticarcillin-resistant, Timentin-sensitive bacteria, were treated with Timentin. A full clinical success was obtained in sixteen cases (13 pyelonephritis, nine of them due to ticarcillin-resistant, Timentin-sensitive Escherichia coli, two neonatal infections and one pneumonia). Four children were improved (1 bronchiectasis, 3 leukaemias), three were unassessable and one failure occurred with a staphylococcal urinary tract infection. A pharmacokinetic study was performed in three newborns (under three months) and ten children (mean age 3 years). Timentin was administered as four daily 30-min iv infusions. The mean dosage used in patients under three months was 225 mg/kg/d ticarcillin and 9 mg/kg/d clavulanic acid. In infants older than three months of age the mean dosage was 250 mg/kg/d ticarcillin and 16 mg/kg/d clavulanic acid. The pharmacokinetic results demonstrated similar serum concentrations of ticarcillin to those in earlier studies, and serum concentrations of clavulanic acid of 3.1 +/- 0.63 mg/l and 2.18 +/- 0.17 mg/l at 1 h and 2 h respectively after infusion in newborns. For children, at the same times, the serum levels were respectively 2.3 +/- 0.9 mg/l and 1.4 +/- 0.9 mg/l. The peak serum concentrations of clavulanic acid were the same in the two groups of dosages (4.7 mg/l), but the half-lives of clavulanic acid were 1.1 h in children older than three months and 1.8 h in infants younger than 3 months. The tolerance was good. Timentin may be useful as a first line antibiotic in infections in hospitalized children in the dosage described, as three or four injections daily, according to the age and the severity of the disease.
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PMID:Efficacy and pharmacokinetics of Timentin in paediatric infections. 363 39

Amyloid lymphadenopathy has only been reported in case report form, or in small groups of patient groups within large series. We believe that amyloid lymphadenopathy is common in uremic patients, and thus designed this study to determine the frequency of this condition in hemodialysis patients, and to assess its types and patterns. We reevaluated 46 uremic patients' lymph node biopsies for amyloid deposits. We also immunohistochemically identified the protein origin of these deposits using Amyloid A, kappa, lambda, beta2 microglobulin, and transthyretin antibodies. Histopathologically, we observed for vascular involvement, follicular deposition, and diffuse deposition. We detected amyloid deposits in 10 of the 46 (22%) patients' lymph nodes. The patterns of deposition were vascular involvement alone in six specimens, vascular involvement plus follicular deposition in three, and vascular involvement plus diffuse deposition in one specimen. Amyloid AA type protein was present in seven nodes, beta2 microglobulin-related amyloid in two nodes, and immunoglobulin-derived protein (AL) in one node. We assessed these 10 patients for causes of end-stage renal disease (ESRD) and other conditions that might relate to amyloidosis. The cause of ESRD in the seven patients with AA amyloid were renal amyloidosis secondary to Familial Mediterranean Fever in four, glomerulonephritis in one patient who had bronchiectasis and Castleman's disease, unknown in one patient who had bronchial asthma, and pyelonephritis in one patient who had no characteristics that could be linked with AA type amyloidosis. The causes of ESRD in the two individuals with beta2 microglobulin-related amyloidosis who had been on long-term hemodialysis were pyelonephritis and glomerulonephritis. The cause of ESRD in the patient with AL type protein was glomerulonephritis, and this patient had no systemic disease. We conclude that amyloid lymphadenopathy is, indeed, common in uremic patients. Amyloid type AA is the most prevalent form of amyloid protein in uremic patients, but amyloid type does not always correspond with underlying cause of renal failure, or with the presence of systemic disease.
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PMID:High frequency of amyloid lymphadenopathy in uremic patients. 1104 Dec 93

Secondary amyloidosis is a relatively common pathology in which chronic infectious diseases are common causes, especially infected bronchiectasis, osteomyelitis or chronic ulcers. The association of xanthogranulomatous pyelonephritis and systemic amyloidosis is extremely rare. To our knowledge, despite innumerable cases of xanthogranulomatous pyelonephritis reported in the literature, this association has been reported in only 8 previous cases. Patients usually complain of fever, back or flank pain and urinary tract symptoms. A long lasting evolution of the process is frequent. We report a 70 year old patient who developed amyloidosis secondary to xanthogranulomatous pyelonephritis. As well as the rarity of this association, this case is exceptional in its clinical presentation, without any urinary tract symptoms that could suggest the diagnosis.
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PMID:[Systemic amyloidosis secondary to xanthogranulomatous pyelonephritis]. 1179 22

The symptomatic phases of many inflammatory diseases are characterized by migration of large numbers of neutrophils (PMN) across a polarized epithelium and accumulation within a lumen. For example, acute PMN influx is common in diseases of the gastrointestinal system (ulcerative colitis, Crohn's disease, bacterial enterocolitis, gastritis), hepatobiliary system (cholangitis, acute cholecystitis), respiratory tract (bronchial pneumonia, bronchitis, cystic fibrosis, bronchiectasis), and urinary tract (pyelonephritis, cystitis). Despite these observations, the molecular basis of leukocyte interactions with epithelial cells is incompletely understood. In vitro models of PMN transepithelial migration typically use N-formylated bacterial peptides such as fMLP in isolation to drive human PMNs across epithelial monolayers. However, other microbial products such as lipopolysaccharide (LPS) are major constituents of the intestinal lumen and have potent effects on the immune system. In the absence of LPS, we have shown that transepithelial migration requires sequential adhesive interactions between the PMN beta2 integrin CD11b/CD18 and JAM protein family members. Other epithelial ligands appear to be abundantly represented as fucosylated proteoglycans. Further studies indicate that the rate of PMN migration across mucosal surfaces can be regulated by the ubiquitously expressed transmembrane protein CD47 and microbial-derived factors, although many of the details remain unclear. Current data suggests that Toll-like receptors (TLR), which recognize specific pathogen-associated molecular patterns (PAMPs), are differentially expressed on both leukocytes and mucosal epithelial cells while serving to modulate leukocyte-epithelial interactions. Exposure of epithelial TLRs to microbial ligands has been shown to result in transcriptional upregulation of inflammatory mediators whereas ligation of leukocyte TLRs modulate specific antimicrobial responses. A better understanding of these events will hopefully provide new insights into the mechanisms of epithelial responses to microorganisms and ideas for therapies aimed at inhibiting the deleterious consequences of mucosal inflammation.
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PMID:Neutrophil transepithelial migration: role of toll-like receptors in mucosal inflammation. 1596 22