Reye syndrome: Treatment by exchange transfusion with special reference to the 1974 epidemic in Cincinnati, Ohio

Bobo, Robert C.; Schubert, William K.; Partin, John C.

doi:10.1016/s0022-3476(75)80898-5

Cited by 31 publications

(4 citation statements)

References 14 publications

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“…14 The latter two methods have been used particularly in patients in Lovejoy stage 3 and 4. In the past four years the use of exchange transfusion'4 16 and peritoneal dialysis'7 has been abandoned. In each of the 23 patients, however, neomycin and lactulose were given by nasogastric tube to reduce the production of various toxic nitrogenous metabolites, such as ammonia, in the colon.…”

Section: Discussionmentioning

confidence: 99%

Clinical features and prognosis of Reye's syndrome.

Glasgow¹

1984

Archives of Disease in Childhood

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Section: Discussionmentioning

confidence: 99%

Clinical features and prognosis of Reye's syndrome.

Glasgow¹

1984

Archives of Disease in Childhood

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“…The encephalopathy is a progressive one with four or five stages "each correlating with progressive rostral-caudal central nervous system involvement" as first recognized by Lovejoy et al. (3) and subsequently corroborated by others (4)(5)(6).…”

mentioning

confidence: 88%

Development of encephalopathic features similar to Reye syndrome in rabbits.

Kang¹,

Olson²,

Jabbour³

et al. 1984

Proc. Natl. Acad. Sci. U.S.A.

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The progression of neurological abnormalities through four or five clinically distinguishable levels of deepening coma and the development of a fatty liver are the hallmarks of Reye syndrome. A number of animal models have been described that result in fatty liver formation with minimal, static, or catastrophic neurological changes. In this study, we attempted to produce neurological features in rabbits that reflected a rostral-caudal progression of abnormalities that could be categorized into clinically distinguishable levels reminiscent of Reye syndrome. This was accomplished by the intracisternal administration of 0.5-25 mg of 11,14-icosadienoic acid (20:2wo6) suspended in a mixture of rabbit serum and isotonic saline solution. A reproducible, dose-titratable spectrum of at least four levels of deepening coma could be produced at will. Increases in serum glutamate-oxaloacetate transaminase and creatine kinase and changes in serum glucose resulted 1-2 hr after the neurological abnormalities were evoked. Other unsaturated fatty acids produced similar responses. Those tested included 18:1w9, 18:2w6, 18:3a3, 20:3w6, 20:4o6, and 22:4w6 fatty acids. Saturated fatty acids, including 6:0, 8:0, 16:0, 18:0, and 20:0, failed to elicit these effects. The abnormalities were sustained for 30-120 min after a single dose. Full recovery was observed in some animals that had not reached the fourth level of our grading system for coma. Pretreatment of the rabbits with aspirin modulated the neurological abnormalities. Twenty micrograms of bee venom melittin, which activates endogenous phospholipase A2, administered intracisternally into rabbits also produced signs of level 3 (our grading system) coma for several hours. These findings suggest a possible role for polyunsaturated fatty acids in the development of Reye syndrome and offer a means of producing the neurological components of that syndrome in a laboratory animal.Reye syndrome is a rare but clinically important childhood encephalopathy of unknown origin associated with fatty visceral changes and complex metabolic abnormalities (1, 2). The encephalopathy is a progressive one with four or five stages "each correlating with progressive rostral-caudal central nervous system involvement" as first recognized by Several animal models have been proposed, including the use of a specific inhibitor of fatty acid oxidation (7), the infusion of those metabolites that are found in increased concentrations in the blood of affected patients (8, 9), and the inoculation of animals with viruses, either alone or in conjunction with special diets or prior exposure of the animals to chemicals (10-13). Fatty liver formation and biochemical evidence of liver dysfunction have been observed in each of these models. However, from the neurological point of view, only minimal, nonprogressive changes or, alternatively, collapse and death have been reported. In some instances, the infusion of glucose reversed or prevented these neurological abnormalities (7). Such features are in contrast to t...

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“…During my “GI Fellowship” at CCHMC a major focus of our clinical attention was Reye's syndrome—acute encephalopathy and fatty degeneration of the viscera . In the early 1970s there was a marked increase in the incidence of this enigmatic disease and the ability to recognize all stages of the illness.…”

Section: The Rise (And Fall) Of Reye'smentioning

confidence: 99%

Growth and development of a new subspecialty: Pediatric hepatology

Balistreri

2013

Hepatology

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Several major forces converged to catalyze the formal emergence of a body of knowledge and an organized focus on disorders of the liver in early life. Attendant to the development of a focused clinical subspecialty the pace of patient-and laboratory-based research in the field quickened in parallel to decipher the consequences of genetic or metabolic aberrations on immature liver structure and function. The key research observations that catalyzed the emergence and subsequent rapid growth of Pediatric Hepatology include: (1) an understanding of the dynamic events occurring during hepatobiliary development and the importance of these physiologic variables that occur during liver maturation; (2) the recognition of the unique nature of inherited and acquired liver diseases that affect infants and children-such as biliary atresia and Reye's syndrome; and (3) redefinition of the once obscure inherited intrahepatic cholestatic diseases of the liver, which, in turn, provided insight into normal and abnormal hepatobiliary physiology. The clinical advances were highlighted by the development of specific approaches to the diagnosis and management of liver disease in infants and children, including both liver transplantation and nontransplant treatment options. These seminal events led to the expansion of the workforce, creating a critical mass consisting of individuals with focused, specialized skills and techniques. In-depth expertise allowed more accurate diagnosis and highly effective treatment strategies for advanced hepatobiliary disease in children. The demand for pediatric clinicians with experience in advanced hepatology allowed sub-sub-specialization to flourish. Continued maturation of the field led to definition of hepatology-focused curricular elements and educational content for Pediatric Gastroenterology training programs, and subsequently the development of program requirements for those who wished to acquire additional training in Pediatric Hepatology. A significant rite of passage was marked by the election of pediatric hepatologists to leadership positions in the American Association for the Study of Liver Diseases (AASLD). Further validation of the field occurred with approval of the petition for establishing a Certificate of Added Qualification in Transplant Hepatology by the American Board of Pediatrics. Here I relate my perspective on the history of the advances in our field and the contributions of many of the clinicians and scientists whose efforts led to the development of focused clinical, research, and training programs that improved the care of children with diseases of the liver. (HEPATOLOGY 2013;58:458-476) The ChallengeSince there was not a single linear pathway it appeared at first to be a daunting task to reconstruct the history and sequence of events leading to the emergence and maturation of a field of subspecialization. Therefore, it was a bit overwhelming to be asked by the editors of HEPATOLOGY to "look back on my career" and not only "tell us about your life story" but also "illus...

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Reye syndrome: Treatment by exchange transfusion with special reference to the 1974 epidemic in Cincinnati, Ohio

Cited by 31 publications

References 14 publications

Clinical features and prognosis of Reye's syndrome.

Clinical features and prognosis of Reye's syndrome.

Development of encephalopathic features similar to Reye syndrome in rabbits.

Growth and development of a new subspecialty: Pediatric hepatology

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