Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal TB is difficult to diagnose, because many patients present themselves with lower urinary symptoms which are typical of bacterial cystitis. We report a case of a young woman with renal TB and ESRD. She was admitted with complaints of adynamia, anorexia, fever, weight loss, dysuria and generalized edema for 10 months. At physical examination she was febrile (39 degrees C), and her abdomen had increased volume and was painful at palpation. Laboratorial tests showed serum urea = 220 mg/dL, creatinine = 6.6 mg/dL, hemoglobin = 7.9 g/dL, hematocrit = 24.3%, leukocytes = 33,600/mm(3) and platelets = 664,000/mm(3). Urinalysis showed an acid urine (pH = 5.0), leukocyturia (2+/4+) and mild proteinuria (1+/4+). She was also oliguric (urinary volume < 400 mL/day). Abdominal echography showed thick and contracted bladder walls and heterogeneous liquid collection in the left pelvic region. Two laparotomies were performed, in which abscess in pelvic region was found. Anti-peritoneal tuberculosis treatment with rifampin, isoniazid and pyrazinamide was started. During the follow-up, the urine culture was found to be positive for M. tuberculosis. Six months later the patient had complaints of abdominal pain and dysuria. New laboratorial tests showed serum urea = 187 mg/dL, creatinine = 8.0 mg/dL, potassium = 6.5 mEq/L. Hemodialysis was then started. The CT scan showed signs of chronic nephropathy, dilated calyces and thinning of renal cortex in both kidneys and severe dilation of ureter. The patient developed neurologic symptoms, suggesting tuberculous meningoencephalitis, and died despite of support measures adopted. The patient had ESRD due to secondary uropathy to prolonged tuberculosis of urinary tract that was caused by delayed clinical and laboratorial diagnosis, and probably also due to inadequate antituberculous drugs administration.
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PMID:End-stage renal disease due to delayed diagnosis of renal tuberculosis: a fatal case report. 1762 50

Chlamydial-induced cystitis in the koala (Phascolarctos cinereus) is currently treated by antibiotics. However, while reducing the chlamydial load, this treatment can also lead to gastrointestinal complications and death. Development of alternative treatments, such as a therapeutic chlamydial vaccine, are hindered by the lack of detailed understanding of the innate immune response to chlamydial clearance and disease regression during antibiotic treatment. Through clinical, microbiological and transcriptomic approaches, disease regression, bacterial clearance and innate immune responses were mapped in koalas with signs of chlamydial-induced cystitis while receiving anti-chlamydial antibiotics. Significant reduction in the signs of cystitis were observed during and post antibiotic treatment. This was observed as a thinning of the bladder wall and complete reversal of urinary incontinence. Transcriptomic analysis before treatment, at the end of treatment and prior to release identified significant down-regulation of specific genes involved in 21 biological pathways. Of these, the chemokine receptor signalling and NOD-like receptor signalling pathways where identified as important markers of inflammation. Specific genes within these pathways (NCF1 and NOX2) were significantly down-regulated, suggesting a decrease in reactive oxygen species production. Through the monitoring of specific clinical and transcriptomic markers, these findings allow detailed profiling of the clinical response to therapeutic vaccination in koalas with current signs of disease. This also adds to our understanding of innate immune responses to chlamydial infections and indicates that chlamydial-induced cystitis in the koala is linked to the regulation of reactive oxygen pathways.
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PMID:Antibiotic treatment of Chlamydia-induced cystitis in the koala is linked to expression of key inflammatory genes in reactive oxygen pathways. 3141 33