Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bone necrosis of the jaws is often related to head and neck radiotherapy, to surgical procedures at maxillary or mandibular level but also to various local and systemic factors such as haematological diseases, haemoglobinopathies and systemic lupus eritematosus; its pathogenesis maybe associated with defects of vascularization. Bisphosphonate are synthetic analogues of pyrophosphate used for the treatment of hypercalcemia in patients with malignancies and bone metastasis and for the treatment of many other disorders such as metabolic bone diseases, Paget's disease, and osteoporosis; their pharmacological activity is related to the inhibition of the osteoclastic function which leads to resorption and reduction of bone vascularization. Since the end of 2003 Bisphosphonate-associated Osteonecrosis (BON) has become an increasing problem and the test of that is the increase of the relative published case report and case series. Here we report 29 cases of bone necrosis of the jaws in patients treated with pamidronate (Aredia), zoledronate (Zometa) and alendronate: 15 underwent surgical procedures and 14 occurred spontaneously. Among these patients (21 females, 8 males; mean age between 45 and 83 years); 14 were treated for bone metastasis, 12 for multiple myeloma and 3 for osteoporosis. Bone necrosis involved only maxilla in 7 patients, only mandible in 20 patients and both in 2 patients. Six patients had multiple osteonecrotic lesions, 3 contemporary lesions and 3 non contemporary. In these patients we performed 3 kinds of therapy, associated or not: medical therapy (with antibiotic drugs, antimycotics and antiseptic mouthwashes), surgical therapy with curettage or sequestrectomy and Nd:YAG laser biostimulation.
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PMID:Bone necrosis of the jaws associated with bisphosphonate treatment: a report of twenty-nine cases. 1717 92

Most common bacterial species causing peritonitis in the course of peritoneal dialysis (PDP) are coagulase-negative staphylococci, Staphylococcus aureus and streptococci. Haemophilus influenzae is rarely associated with PDP. Hereby we present the first known case of APD-associated peritonitis caused by non-type able H. influenzae (NTHi) presenting the beta-lactamase negative, ampicillin-resistant (BLNAR) phenotype. An 18 year old boy who had been treated with the APD for 12 months due to SLE was admitted in good general condition with diagnosis of PDP. Standard diagnostic and therapeutical procedures were initiated. Dialysis fluid was turbid with cytosis of 435 WBC/ml. From dialysis fluid pure culture of Gram-negative coccobacillus was isolated. The isolate was identified as a BLNAR phenotype. The same bacterium was isolated from nasal swab. Blood cultures were negative. After evaluation of antimicrobial susceptibility the treatment was changed for the oral ciprofloxacin. The treatment was successful. Control tests 2 days later revealed cytosis of 15 WBC/mm3 and control cultures of peritoneal fluid were negative. After two weeks of treatment the patient was discharged in a good condition. Haemophilus influenzae is a bacterium frequently colonizing the nasopharyngeal cavity. A PCR-based method allowed to classify isolates as NTHi. Infection was probably of the respiratory origin as the isolates (from peritoneal fluid and nasal swab) were undistinguishable. There are only few reports describing this species as an ethiologic agent of peritonitis. This case prove that Haemophilus species should be taken into account as a possible aethiologic agent of PDP, especially in patients on immunosupression with carrier state of H. influenzae in the upper respiratory tract. This kind of microorganism requires specific conditions during its growing in vitro. Identification of its sensitivity to antibiotics is essential in order to detect strains of BLNAR phenotype, as it is a crucial part of an effective antibiotic therapy.
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PMID:[Peritonitis in the course of peritoneal dialisis caused by Haemophilus influenzae with BLNAR phenotype]. 1958 Feb