Development Of Thrombotic Thrombocytopenic Purpura Research Articles

Is severe deficiency of ADAMTS-13 specific for thrombotic thrombocytopenic purpura? Yes

Is severe deficiency of ADAMTS-13 specific for thrombotic thrombocytopenic purpura? Yes

Thrombotic thrombocytopenic purpura associated with ticlopidine. A review of 60 cases.

Thrombotic thrombocytopenic purpura, a life-threatening multisystem disease, has been infrequently associated with use of ticlopidine, a platelet anti-aggregating agent. To review 60 cases of ticlopidine-associated thrombotic thrombocytopenic purpura. Medical records, published case reports, and case reports submitted to the U.S. Food and Drug Administration. Instances of ticlopidine-associated thrombotic thrombocytopenic purpura were identified. Ticlopidine had been prescribed for less than 1 month in 80% of the patients, and normal platelet counts had been found within 2 weeks of the onset of thrombotic thrombocytopenic purpura in most patients. Mortality rates were higher among patients who were not treated with plasmapheresis than among those who underwent plasmapheresis (50% compared with 24%; P < 0.05). Ticlopidine use may be associated with the development of thrombotic thrombocytopenic purpura, usually within 1 month of initiation of therapy. The onset of ticlopidine-associated thrombotic thrombocytopenic purpura is difficult to predict, despite close monitoring of platelet counts.

4. Fatal influenza in otago during 1976

An extensive outbreak of influenza caused by an H3N2 A75 Victoria like strain of influenza occurred in Otago from May to August 1976. Despite the generally mild nature of the illness several confirmed fatalities occurred. Postmortem findings together with aspects of the clinical course are discussed in 7 fatal cases presumptively diagnosed as demonstrating the consequences of influenza. Virus was isolated in 5 instances. Four fatalities occurred in children aged 8 mth or younger. Two developed features of congestive cardiac failure weeks after an influenzal episode, one of which was confirmed virologically. Evidence of extensive healed myocarditis was found in each case. A third child aged 8 mth developed progressive respiratory failure over 48 h and demonstrated an extensive viral pneumonitis with alveolar exudate and hyaline membranes. Histological evidence of a viral pneumonitis with isolation of the virus was demonstrated in a 10-wk-old infant in whom there was no history of illness prior to death. Of two middle-aged adults both yielding virus on culture one developed progressive influenzal pneumonitis complicated by early straphylococcal bronchopneumonia, while the other developed an extensive necrotizing pneumonia and cerebral abscesses caused by an aspergillus species. A third, previously fit young woman, developed klebsiella pneumonia complicating an influenzal-like illness with development of thrombotic thrombocytopenic purpura and renal cortical necrosis.