Given an abstract of a paper, generate a title for this paper such that conveys the key focus of the paper.

Input: Consider Input: Abstract: Heparin-induced thrombocytopenia with thromboembolism calls for an immediate substitution of the heparin with other potent anticoagulants, such as coumarin derivatives. The occurrence of this adverse effect in pregnancy poses an additional dilemma because the use of coumarin derivatives is not acceptable during pregnancy, while other medications may not be as effective. In a pregnant patient treated with mucous sodium heparin for deep vein thrombosis, recurrent heparin-induced thrombosis and disseminated intravascular coagulation (DIC) occurred. Replacing the heparin with a different brand of the same drug resulted in reversal of the DIC and in clinical improvement. If severe heparin-induced thrombosis occurs in a patient in whom anticoagulation with other drugs is contraindicated, substituting one brand of heparin for another could be of value.

Output: Heparin-induced thrombocytopenia and recurrent thrombosis in pregnancy. A case report.

Input: Consider Input: Abstract: Because scald burns are reported to be the leading cause of burn injuries to children, little is written about other etiologies of burn injury in the pediatric literature. To test the hypothesis that burns from other etiologies are more serious and require longer hospitalizations than scald burns, a retrospective chart review was undertaken. The charts of all patients less than 16 years of age who were admitted to Harborview Medical Center Burn Unit in the years 1979 to 1984 were reviewed. Four hundred sixty-four children were admitted to the regional burn center during that time. We found that children under four years of age are at greatest risk for being hospitalized for thermal injury, that the burn most commonly occurs inside the home between 6 PM and midnight, and that scalds are the most common etiology for thermal injuries in children (54%). However, 46% of the burns resulting in admission to our burn center were from etiologies other than scald injury. There was no significant correlation between etiology of the burns and length of hospital stay, rate of infection, or need for excision and grafting. Thermal injuries to children from any etiology are serious; pediatric health care providers should be aware that children may be burned in a variety of ways and should direct some of their well-child visit time to the topic of burn prevention in the home.

Output: Pediatric patients in a regional burn center.

Input: Consider Input: Abstract: The role in the pathogenesis of immune complex-mediated glomerulonephritis of C5 or some terminal complement component dependent upon C5 for activation was explored in a congenic strain of C5 sufficient (NSN) and C5 deficient (OSN) mice. When these mice were given daily injections of heterologous protein, horse apoferritin (HAF), there were profound differences between the strains in the development of glomerulonephritis and renal dysfunction. When NSN and OSN mice produced low levels of anti-HAF, NSN mice developed extensive glomerular deposits of HAF and immune reactants and a mild proliferative glomerulonephritis. In contrast, comparable OSN mice developed only trace mesangial localization of HAF and no glomerular lesions by light microscopy. When NSN and OSN mice produced high levels of anti-HAF, both strains had equivalent glomerular immune deposits; however, NSN mice developed a severe necrotizing and crescentic glomerulonephritis, while OSN mice had much less glomerular injury. Compared to OSN mice, these NSN mice also had much more severe tubulointerstitial injury, and significantly higher serum creatinine levels. Thus, in this experimental model, the absence of C5 resulted in reduced glomerular immune complex localization when there were small amounts of circulating immune reactants; and in markedly reduced glomerular leukocyte influx, necrosis and crescent formation, when large amounts of immune reactants have localized in glomeruli. These effects could be mediated by C5 (such as C5a) or by some terminal complement component(s) dependent upon C5 for activation.
Output: Immune complex induced glomerular lesions in C5 sufficient and deficient mice.