PedAM
Pediatric Disease Annotations & Medicines
| Disease | thrombocytopenia |
| Phenotype | C0035078|renal failure |
| Sentences | 5 |
| PubMedID- 22368449 | The incidence of lzd-induced thrombocytopenia was higher in patients with renal failure than in patients with normal renal function, although the underlying mechanisms of this toxicity are still unknown.23 a meta-analysis including nine relevant randomized, controlled trials studied 2489 clinically assessed patients and found that lzd showed higher clinical effect for skin and soft tissue infection (odds ratio [or], 1.40; 95% ci: 1.01–1.95), while it showed equivalent therapeutic effect with vancomycin for bacteremia (or, 0.88; 95% ci: 0.49–1.58), pneumonia (or, 1.16; 95% ci: 0.85–1.57) patients.24 in contrast, there was no difference in total adverse effects (or, 1.14; 95% ci: 0.82–1.59). |
| PubMedID- 21694933 | Hemolytic uremic syndrome (hus) is a thrombotic microangiopathy characterized by hemolytic anemia and thrombocytopenia often complicated by acute renal failure in children.1 both typical or diarrhea-associated hus form is associated with infection by escherichia coli and has a good prognosis.2 a second less common from, termed atypical, nondiarrhea-associated hus (ahus) is a heterogeneous recurrent disorder which displays high mortality and morbidity.3 this form can occur at any age with familial and sporadic cases. |
| PubMedID- 26266247 | In the literature, the dug is confirmed to cause prolonged thrombocytopenia especially in patients with end-stage renal failure [19]. |
| PubMedID- 20392606 | Recent studies have reported that the incidence of linezolid-induced thrombocytopenia was higher in patients with renal failure than in patients with normal renal function, although the underlying mechanisms of this toxicity are still unknown. |
| PubMedID- 26091445 | Hus was first described by gasser et al in 1955.2 the primary clinical features are thrombocytopenia, hemolysis with fragmentocytes, and renal failure.3 the primary pathophysiologic mechanism in hus is endothelial damage caused by shiga toxin followed by activation of the complement cascade,3–6 leading to thrombotic microangiopathy mainly in the kidney. |
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