Acute non-inflammatory encephalopathy with fatty hepatic failure is the definition of Reye syndrome, a rare and potentially fatal juvenile condition. This syndrome was first outlined by Australian pathologist R.D.K. Reye in 1963. Early in the 1970s, Reye syndrome became the focus of national surveillance in the United States, which resulted in strong recommendations against giving children aspirin.
In youngsters, Reye syndrome often starts with nausea and bewilderment before quickly progressing to life-threatening coma and death. This syndrome frequently manifests in the days following healing from a viral illness treated with aspirin.
Toxins, drug interactions, and inborn metabolic errors—particularly those involving the metabolism of fatty acids—may also contribute to or contribute to the progression of Reye’s disease. In addition to laboratory tests, clinical symptoms are used to make this diagnosis. However, Reye syndrome-specific tests are lacking.
Epidemiology
Since 1994, less than two cases of Reye disease have been officially reported, making it a rare diagnosis. However, since reporting instances to the CDC that’s no longer needed, the exact incidence might not be known. Although cases have been documented in infants as young as one year old, the peak age of onset is between the ages of 5 & 14. There is no information on gender as a contributing factor. The majority of instances recorded between December and April show seasonal fluctuation.
In 1973, Reye syndrome surveillance was implemented nationally. 555 instances were reported to the CDC between 1979 & 1980. Reye sickness was recorded in 1207 infections in the U.S. between December 1980 and November 1997, according to the CDC. During 1991, there were between 0.2 and 1.1 incidents per million recorded in the US between 1991 & 1994. In the U.S., aspirin use in children was warned against widely in 1980.
Following this publication, there was a dramatic drop in the quantity of Reye fever cases that were recorded. Incidence patterns that were comparable were seen in the UK. The UK issued a warning against giving aspirin to children under 12 in 1986. The incidence decreased as a result of the warning, going from 0.63 instances per 100,000 people in 1983 to 1984 to 0.11 instances per 100,000 people in 1990 to 1991 instead.
Comparable decreases were seen in France as well. It should be underlined that aspirin continues to be a cornerstone of care for kids with Kawasaki illness. Clinicians and parents should keep a close eye out for Reye’s disease symptoms and signs in children who need chronic-term salicylate treatment.
Anatomy
Pathophysiology
Reye syndrome’s precise etiology is unknown; however, it tends to include mitochondrial damage in the context of a viral infection. Aspirin may inflict or maintain damage to the cell’s mitochondria, which inhibits the metabolism of fatty acids.
Reye syndrome’s neurologic symptoms are most likely caused by liver mitochondrial failure, which raises ammonia concentration.
Hyperammonemia may cause widespread cerebral edema and subsequently increased intracranial tension by inducing astrocytic edema. Pathology research has discovered astrocytic edema, neuronal loss, fatty kidney degeneration, and enlarged and fewer mitochondria.
Etiology
The most frequent causes of Reye sickness are viral diseases like varicella and influenza A & B. According to surveillance information collected by the CDC (Centers for Disease Control and Prevention) between 1980 & 1997, influenza infestation occurred in 73 percent, varicella infestation in 21 percent and infections of gastrointestinal in 14 percent of instances of Reye sickness. In 82 percent of instances, plasma salicylic concentrations could be found.
Coxsackie, adenovirus, EBV (Epstein-Barr), parainfluenza, hepatitis, and CMV (cytomegalovirus) are less frequently related to viral connections. Reye disease has also been linked to bacterial diseases such as Bordetella pertussis, Shigella, Mycoplasma, and Chlamydia. Studies on the epidemiology of the disease have linked salicylate consumption to the emergence of Reye disease.
More than 80 percent of kids who were diagnosed with Reye disease had taken aspirin in the past three weeks, even though Reye’s disorder only occurred in less than 0.1 percent of children who received aspirin. As a result of these findings, aspirin usage in children was discouraged in 1980. Following the widespread recommendations against giving aspirin to young children, the number of Reye disease cases that have been reported has substantially decreased.
Genetics
Prognostic Factors
Clinical History
Physical Examination
Age group
Associated comorbidity
Associated activity
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References
https://www.ncbi.nlm.nih.gov/books/NBK526101/
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Acute non-inflammatory encephalopathy with fatty hepatic failure is the definition of Reye syndrome, a rare and potentially fatal juvenile condition. This syndrome was first outlined by Australian pathologist R.D.K. Reye in 1963. Early in the 1970s, Reye syndrome became the focus of national surveillance in the United States, which resulted in strong recommendations against giving children aspirin.
In youngsters, Reye syndrome often starts with nausea and bewilderment before quickly progressing to life-threatening coma and death. This syndrome frequently manifests in the days following healing from a viral illness treated with aspirin.
Toxins, drug interactions, and inborn metabolic errors—particularly those involving the metabolism of fatty acids—may also contribute to or contribute to the progression of Reye’s disease. In addition to laboratory tests, clinical symptoms are used to make this diagnosis. However, Reye syndrome-specific tests are lacking.
Since 1994, less than two cases of Reye disease have been officially reported, making it a rare diagnosis. However, since reporting instances to the CDC that’s no longer needed, the exact incidence might not be known. Although cases have been documented in infants as young as one year old, the peak age of onset is between the ages of 5 & 14. There is no information on gender as a contributing factor. The majority of instances recorded between December and April show seasonal fluctuation.
In 1973, Reye syndrome surveillance was implemented nationally. 555 instances were reported to the CDC between 1979 & 1980. Reye sickness was recorded in 1207 infections in the U.S. between December 1980 and November 1997, according to the CDC. During 1991, there were between 0.2 and 1.1 incidents per million recorded in the US between 1991 & 1994. In the U.S., aspirin use in children was warned against widely in 1980.
Following this publication, there was a dramatic drop in the quantity of Reye fever cases that were recorded. Incidence patterns that were comparable were seen in the UK. The UK issued a warning against giving aspirin to children under 12 in 1986. The incidence decreased as a result of the warning, going from 0.63 instances per 100,000 people in 1983 to 1984 to 0.11 instances per 100,000 people in 1990 to 1991 instead.
Comparable decreases were seen in France as well. It should be underlined that aspirin continues to be a cornerstone of care for kids with Kawasaki illness. Clinicians and parents should keep a close eye out for Reye’s disease symptoms and signs in children who need chronic-term salicylate treatment.
Reye syndrome’s precise etiology is unknown; however, it tends to include mitochondrial damage in the context of a viral infection. Aspirin may inflict or maintain damage to the cell’s mitochondria, which inhibits the metabolism of fatty acids.
Reye syndrome’s neurologic symptoms are most likely caused by liver mitochondrial failure, which raises ammonia concentration.
Hyperammonemia may cause widespread cerebral edema and subsequently increased intracranial tension by inducing astrocytic edema. Pathology research has discovered astrocytic edema, neuronal loss, fatty kidney degeneration, and enlarged and fewer mitochondria.
The most frequent causes of Reye sickness are viral diseases like varicella and influenza A & B. According to surveillance information collected by the CDC (Centers for Disease Control and Prevention) between 1980 & 1997, influenza infestation occurred in 73 percent, varicella infestation in 21 percent and infections of gastrointestinal in 14 percent of instances of Reye sickness. In 82 percent of instances, plasma salicylic concentrations could be found.
Coxsackie, adenovirus, EBV (Epstein-Barr), parainfluenza, hepatitis, and CMV (cytomegalovirus) are less frequently related to viral connections. Reye disease has also been linked to bacterial diseases such as Bordetella pertussis, Shigella, Mycoplasma, and Chlamydia. Studies on the epidemiology of the disease have linked salicylate consumption to the emergence of Reye disease.
More than 80 percent of kids who were diagnosed with Reye disease had taken aspirin in the past three weeks, even though Reye’s disorder only occurred in less than 0.1 percent of children who received aspirin. As a result of these findings, aspirin usage in children was discouraged in 1980. Following the widespread recommendations against giving aspirin to young children, the number of Reye disease cases that have been reported has substantially decreased.
https://www.ncbi.nlm.nih.gov/books/NBK526101/
medtigo
Reye syndrome
Updated :
September 5, 2023
Acute non-inflammatory encephalopathy with fatty hepatic failure is the definition of Reye syndrome, a rare and potentially fatal juvenile condition. This syndrome was first outlined by Australian pathologist R.D.K. Reye in 1963. Early in the 1970s, Reye syndrome became the focus of national surveillance in the United States, which resulted in strong recommendations against giving children aspirin.
In youngsters, Reye syndrome often starts with nausea and bewilderment before quickly progressing to life-threatening coma and death. This syndrome frequently manifests in the days following healing from a viral illness treated with aspirin.
Toxins, drug interactions, and inborn metabolic errors—particularly those involving the metabolism of fatty acids—may also contribute to or contribute to the progression of Reye’s disease. In addition to laboratory tests, clinical symptoms are used to make this diagnosis. However, Reye syndrome-specific tests are lacking.
Since 1994, less than two cases of Reye disease have been officially reported, making it a rare diagnosis. However, since reporting instances to the CDC that’s no longer needed, the exact incidence might not be known. Although cases have been documented in infants as young as one year old, the peak age of onset is between the ages of 5 & 14. There is no information on gender as a contributing factor. The majority of instances recorded between December and April show seasonal fluctuation.
In 1973, Reye syndrome surveillance was implemented nationally. 555 instances were reported to the CDC between 1979 & 1980. Reye sickness was recorded in 1207 infections in the U.S. between December 1980 and November 1997, according to the CDC. During 1991, there were between 0.2 and 1.1 incidents per million recorded in the US between 1991 & 1994. In the U.S., aspirin use in children was warned against widely in 1980.
Following this publication, there was a dramatic drop in the quantity of Reye fever cases that were recorded. Incidence patterns that were comparable were seen in the UK. The UK issued a warning against giving aspirin to children under 12 in 1986. The incidence decreased as a result of the warning, going from 0.63 instances per 100,000 people in 1983 to 1984 to 0.11 instances per 100,000 people in 1990 to 1991 instead.
Comparable decreases were seen in France as well. It should be underlined that aspirin continues to be a cornerstone of care for kids with Kawasaki illness. Clinicians and parents should keep a close eye out for Reye’s disease symptoms and signs in children who need chronic-term salicylate treatment.
Reye syndrome’s precise etiology is unknown; however, it tends to include mitochondrial damage in the context of a viral infection. Aspirin may inflict or maintain damage to the cell’s mitochondria, which inhibits the metabolism of fatty acids.
Reye syndrome’s neurologic symptoms are most likely caused by liver mitochondrial failure, which raises ammonia concentration.
Hyperammonemia may cause widespread cerebral edema and subsequently increased intracranial tension by inducing astrocytic edema. Pathology research has discovered astrocytic edema, neuronal loss, fatty kidney degeneration, and enlarged and fewer mitochondria.
The most frequent causes of Reye sickness are viral diseases like varicella and influenza A & B. According to surveillance information collected by the CDC (Centers for Disease Control and Prevention) between 1980 & 1997, influenza infestation occurred in 73 percent, varicella infestation in 21 percent and infections of gastrointestinal in 14 percent of instances of Reye sickness. In 82 percent of instances, plasma salicylic concentrations could be found.
Coxsackie, adenovirus, EBV (Epstein-Barr), parainfluenza, hepatitis, and CMV (cytomegalovirus) are less frequently related to viral connections. Reye disease has also been linked to bacterial diseases such as Bordetella pertussis, Shigella, Mycoplasma, and Chlamydia. Studies on the epidemiology of the disease have linked salicylate consumption to the emergence of Reye disease.
More than 80 percent of kids who were diagnosed with Reye disease had taken aspirin in the past three weeks, even though Reye’s disorder only occurred in less than 0.1 percent of children who received aspirin. As a result of these findings, aspirin usage in children was discouraged in 1980. Following the widespread recommendations against giving aspirin to young children, the number of Reye disease cases that have been reported has substantially decreased.
https://www.ncbi.nlm.nih.gov/books/NBK526101/
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