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Mikiya Fujieda - One of the best experts on this subject based on the ideXlab platform.
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Acidosis with hyperuricemia and renal tubular damage in Viral Gastroenteritis.
Pediatric nephrology (Berlin Germany), 2011Co-Authors: Taku Morita, Mikiya FujiedaAbstract:Sir, We read with interest the article entitled “Cause of uric acid stones in rotavirus-associated Gastroenteritis” by Kaneko et al., which was recently published in Pediatric Nephrology [1]. We encountered four cases of postrenal renal failure induced by ammonium acid urate (AAU) stones associated with rotavirus Gastroenteritis in patients without metabolic disorder, drug administration, abnormality of the urinary tract, urinary tract infection, or mutation of the human urate transporter 1 (hURAT1) associated with SLC22A12. Ashida et al. described a case with postrenal renal failure caused by an AAU stone associated with norovirus Gastroenteritis [2], but most case reports of this condition have been associated with rotavirus infection. To examine these issues, we compared clinical and laboratory data in patients with rotavirus and norovirus Gastroenteritis. Participants in our study were patients with rotavirus or norovirus Gastroenteritis who were admitted for treatment of diarrhea and vomiting with dehydration between January 2006 and March 2009. These patients included 42 with rotavirus infection (Group R; mean age, 1.7 years; range, 0.3–2.0 years; 32 boys, 10 girls) and 23 with norovirus infection (Group N; mean age, 1.7 years; range, 0.5–2.5 years; 14 boys, 9 girls). None of the patients had any bacterial infection or underlying disease such as metabolic disorder, and none developed postrenal renal failure. RT-PCR was used to detect rotavirus or norovirus genome in stools. Age, sex, and results from blood chemistry tests, blood gas tests (venous), and urinalysis were compared between groups. The two-sample t test, Mann–Whitney test, and Fisher’s exact test were used for comparisons between groups. Values of p 595 μmol/l (Group R: 31.0%, Group N 0%) were significantly higher in Group R (p = 0.04, p = 0.01 respectively). Urinary pH was lower and urinary excretion of UA (UA/Crn), β2-microglobulin (β2MG) and N-acetyl-β-glucosaminidase (NAG) were higher in Group R. Urinary UA/Crn >1.2 was found in 13 out of 20 patients in Group R, compared with 3 out of 11 patients in Group N (p = 0.04). Excretion of β2MG >500 μg/l occurred in 12 out of 20 patients (mean, 2,004 μg/l; range, 638–3,383 μg/l) in Group R and only 1 out of 9 patients (906 μg/l) in Group N (p = 0.02). Urinary excretion of NAG >10 U/l occurred in 8 out of 25 patients (mean, 29.0 U/l; range, 13.3–75.0 U/l) in Group R and only 1 out of 9 patients (16.3 U/l) in Group N. Blood levels of β2MG were similar in the two groups (data not shown). Viral Gastroenteritis induces frequent diarrhea and loss of bicarbonate by small intestinal epithelial cells. This damage results in metabolic acidosis and a subsequent increase in urinary ammonium excretion in response to the acidosis. The combination of aciduria, hyperuricemia, and hyperammonuria can induce formation of AAU stones and crystals. Severe and persistent acidosis induced by rotavirus or norovirus infection may thus cause postrenal renal failure due to AAU stones. Our data showed that patients with rotavirus Gastroenteritis experience high fever, high levels of hyperuricemia and acidosis, and a tendency toward high levels of urinary excretion of UA, β2MG, and NAG, compared with patients with norovirus Gastroenteritis. These findings suggest that tissue damage caused by rotavirus is more severe than that caused by norovirus, and that rotavirus might be toxic to both tubular epithelial cells and small intestinal epithelial cells. Urinary pH and blood bicarbonate levels did not differ significantly between groups, possibly because most patients received intravenous fluids before admission. We recently detected rotavirus in urinary sediment cells of patients with rotavirus Gastroenteritis [3], suggesting that rotavirus may attack tubular epithelial cells directly. Acidosis, hyperuricemia, and urine output after hydration should be considered in patients with Viral Gastroenteritis for prevention of postrenal renal failure due to AAU stones or crystals. However, many children with rotavirus or norovirus infection are treated annually, and only a small proportion of patients develop stones. A large-scale study and worldwide survey are required to clarify risk factors for the formation of AAU stones, and to determine whether Viral Gastroenteritis caused by rotavirus or norovirus plays any significant role in the formation of AAU stones that result in postrenal renal failure.
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acidosis with hyperuricemia and renal tubular damage in Viral Gastroenteritis
Pediatric Nephrology, 2011Co-Authors: Taku Morita, Mikiya FujiedaAbstract:Sir, We read with interest the article entitled “Cause of uric acid stones in rotavirus-associated Gastroenteritis” by Kaneko et al., which was recently published in Pediatric Nephrology [1]. We encountered four cases of postrenal renal failure induced by ammonium acid urate (AAU) stones associated with rotavirus Gastroenteritis in patients without metabolic disorder, drug administration, abnormality of the urinary tract, urinary tract infection, or mutation of the human urate transporter 1 (hURAT1) associated with SLC22A12. Ashida et al. described a case with postrenal renal failure caused by an AAU stone associated with norovirus Gastroenteritis [2], but most case reports of this condition have been associated with rotavirus infection. To examine these issues, we compared clinical and laboratory data in patients with rotavirus and norovirus Gastroenteritis. Participants in our study were patients with rotavirus or norovirus Gastroenteritis who were admitted for treatment of diarrhea and vomiting with dehydration between January 2006 and March 2009. These patients included 42 with rotavirus infection (Group R; mean age, 1.7 years; range, 0.3–2.0 years; 32 boys, 10 girls) and 23 with norovirus infection (Group N; mean age, 1.7 years; range, 0.5–2.5 years; 14 boys, 9 girls). None of the patients had any bacterial infection or underlying disease such as metabolic disorder, and none developed postrenal renal failure. RT-PCR was used to detect rotavirus or norovirus genome in stools. Age, sex, and results from blood chemistry tests, blood gas tests (venous), and urinalysis were compared between groups. The two-sample t test, Mann–Whitney test, and Fisher’s exact test were used for comparisons between groups. Values of p < 0.05 were considered statistically significant. Age, male-to-female ratio, and days from onset to admission did not differ between the groups. Degree of dehydration and duration of fever and hospitalization were similar in the two groups (data not shown), but temperature on admission was significantly higher (p = 0.04) in Group R. No differences in creatinine (Crn) or blood urea nitrogen (BUN) levels were seen between groups. HCO3− level in blood tended to be lower, venous gas pH (Group R: mean, 7.360; range, 7.268–7.442, Group N: mean, 7.410; range, 7.283–7.432) was significantly lower (p = 0.03), and concentrations of uric acid (UA) in blood (Group R: mean, 440 μmol/l; range,184–708 μmol/l, Group N: mean, 363 μmol/l; range, 184–630 μmol/l), and frequency of UA >595 μmol/l (Group R: 31.0%, Group N 0%) were significantly higher in Group R (p = 0.04, p = 0.01 respectively). Urinary pH was lower and urinary excretion of UA (UA/Crn), β2-microglobulin (β2MG) and N-acetyl-β-glucosaminidase (NAG) were higher in Group R. Urinary UA/Crn >1.2 was found in 13 out of 20 patients in Group R, compared with 3 out of 11 patients in Group N (p = 0.04). Excretion of β2MG >500 μg/l occurred in 12 out of 20 patients (mean, 2,004 μg/l; range, 638–3,383 μg/l) in Group R and only 1 out of 9 patients (906 μg/l) in Group N (p = 0.02). Urinary excretion of NAG >10 U/l occurred in 8 out of 25 patients (mean, 29.0 U/l; range, 13.3–75.0 U/l) in Group R and only 1 out of 9 patients (16.3 U/l) in Group N. Blood levels of β2MG were similar in the two groups (data not shown). Viral Gastroenteritis induces frequent diarrhea and loss of bicarbonate by small intestinal epithelial cells. This damage results in metabolic acidosis and a subsequent increase in urinary ammonium excretion in response to the acidosis. The combination of aciduria, hyperuricemia, and hyperammonuria can induce formation of AAU stones and crystals. Severe and persistent acidosis induced by rotavirus or norovirus infection may thus cause postrenal renal failure due to AAU stones. Our data showed that patients with rotavirus Gastroenteritis experience high fever, high levels of hyperuricemia and acidosis, and a tendency toward high levels of urinary excretion of UA, β2MG, and NAG, compared with patients with norovirus Gastroenteritis. These findings suggest that tissue damage caused by rotavirus is more severe than that caused by norovirus, and that rotavirus might be toxic to both tubular epithelial cells and small intestinal epithelial cells. Urinary pH and blood bicarbonate levels did not differ significantly between groups, possibly because most patients received intravenous fluids before admission. We recently detected rotavirus in urinary sediment cells of patients with rotavirus Gastroenteritis [3], suggesting that rotavirus may attack tubular epithelial cells directly. Acidosis, hyperuricemia, and urine output after hydration should be considered in patients with Viral Gastroenteritis for prevention of postrenal renal failure due to AAU stones or crystals. However, many children with rotavirus or norovirus infection are treated annually, and only a small proportion of patients develop stones. A large-scale study and worldwide survey are required to clarify risk factors for the formation of AAU stones, and to determine whether Viral Gastroenteritis caused by rotavirus or norovirus plays any significant role in the formation of AAU stones that result in postrenal renal failure.
Ahmed N. El-taweel - One of the best experts on this subject based on the ideXlab platform.
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Prediction of gut wall integrity loss in Viral Gastroenteritis by non-invasive marker.
Open access Macedonian journal of medical sciences, 2015Co-Authors: Hala G. Elnady, Lobna S. Sherif, Maysa T. Saleh, Inas R. El-alameey, Mai M. Youssef, Amal I. El Shafie, Iman Helwa, Haiam Abdel Raouf, Ahmed N. El-taweelAbstract:BACKGROUND: Intestinal fatty acid binding proteins (I-FABPs) are mainly expressed in the intestinal villi, which are the initial site of destruction in Viral Gastroenteritis. AIM: This study was designed to assess serum I-FABPs as a predictor of gut wall integrity loss in Viral Gastroenteritis. PATIENTS AND METHODS: This case-control cross-sectional study was conducted on 93 cases of acute Viral Gastroenteritis. Twenty-eight healthy children matching in age were recruited as control group. Serum I-FABPs were measured using ELISA technique. Viral detection and typing were done by PCR for adenovirus, and by Reverse transcriptase PCR for rotavirus, astrovirus and norovirus. RESULTS: Serum I-FABPs level was significantly higher in the cases compared to the controls and was also higher in the 46 rotavirus Gastroenteritis cases compared to other Viral Gastroenteritis cases. Serum I- FABPs level was significantly higher in severely dehydrated cases as compared to mildly dehydrated ones (P=0.037). CONCLUSION: Serum I-FABPs could be used as an early and sensitive predictor marker of gut wall integrity loss in children with Viral Gastroenteritis and its level can indicate case severity.
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PO-0993a Fatty Acid Binding Proteins As An Uprising Non Invasive Predictor Of Gut Wall Integrity Loss In Viral Gastroenteritis
Archives of Disease in Childhood, 2014Co-Authors: Maysa T. Saleh, Hala G. Elnady, Lobna S. Sherif, Inas R. El-alameey, Mai M. Youssef, Iman Helwa, Ai El Shafie, Naglaa Kholoussi, H Abdel Raouf, Ahmed N. El-taweelAbstract:Background and aim Serum intestinal fatty acid binding proteins (I-FABPs) are cytosolic proteins mainly expressed in the intestinal villi which are affected early in Viral Gastroenteritis (GE) pathphysiology. So it can be used as an early and sensitive marker for the evaluation of gut wall integrity loss in GE particularly rotavirus Gastroenteritis (RV-GE) in Egypt. Patients and methods This case-control cross-sectional study was conducted on 93 Egyptian cases who suffered from acute Viral Gastroenteritis. 28 healthy children matching in age were recruited as the control group. We collect all clinical data concerning disease manifestations and severity criteria. Serum I-FABPs were measured using the Enzyme linked Immune Sorbent Assay (ELISA) technique. Viral detection and typing was done by Polymerase Chain Reaction (PCR) for adenovirus, and by Reverse transcriptase PCR (RT-PCR) for rotavirus, astrovirus and norovirus. Results Results of this work revealed that serum I-FABPs levels were generally higher in the study group cases compared to the control group (1026.4 ± 494.4 pg/ml versus 267.9 ± 200.4 pg/ml, P Conclusion Serum I-FABPs can be successfully used not only as early and sensitive predictor marker of gut wall integrity loss in Viral GE (especially RV-GE) but also their levels can indicate case severity.
Marion Koopmans - One of the best experts on this subject based on the ideXlab platform.
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is not associated with outbreaks of Viral Gastroenteritis in the elderly in the Netherlands
European Journal of Clinical Microbiology and Infectious Diseases, 2010Co-Authors: S. Svraka, E. Kuijper, E. Duizer, D. Bakker, Marion KoopmansAbstract:The coincidental increase in norovirus outbreaks and infection (CDI) raised the question of whether these events could be related, e.g. by enhancing spread by diarrhoeal disease outbreaks. Therefore, we studied the prevalence of in outbreaks of Viral Gastroenteritis in nursing homes for the elderly and characterised enzyme immunoassay (EIA)-positive stool samples. Stool samples from nursing home residents ( = 752) in 137 outbreaks of Viral aetiology were investigated by EIA for the presence of toxins. Positive samples were further tested by a cell neutralisation cytotoxicity test, a second EIA and culture. Cultured isolates were tested for the presence of toxin genes, the production of toxins and characterised by 16S rRNA polymerase chain reaction (PCR) and sequencing. Twenty-four samples (3.2%) tested positive in the EIA. Of these 24 positive samples, only two were positive by cytotoxicity and three by a second EIA. Bacterial culture of 21 available stool samples yielded a toxinogenic PCR ribotype 001 in one patient sample only. In conclusion, we found no evidence in this retrospective study for an association between Viral Gastroenteritis outbreaks and . The high rate of false-positive EIA samples emphasises the need for second confirmation tests to diagnose CDI.
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Clostridium difficile is not associated with outbreaks of Viral Gastroenteritis in the elderly in the Netherlands.
European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology, 2010Co-Authors: S. Svraka, E. Duizer, D. Bakker, Ed J. Kuijper, Marion KoopmansAbstract:The coincidental increase in norovirus outbreaks and Clostridium difficile infection (CDI) raised the question of whether these events could be related, e.g. by enhancing spread by diarrhoeal disease outbreaks. Therefore, we studied the prevalence of C. difficile in outbreaks of Viral Gastroenteritis in nursing homes for the elderly and characterised enzyme immunoassay (EIA)-positive stool samples. Stool samples from nursing home residents (n = 752) in 137 outbreaks of Viral aetiology were investigated by EIA for the presence of C. difficile toxins. Positive samples were further tested by a cell neutralisation cytotoxicity test, a second EIA and culture. Cultured isolates were tested for the presence of toxin genes, the production of toxins and characterised by 16S rRNA polymerase chain reaction (PCR) and sequencing. Twenty-four samples (3.2%) tested positive in the EIA. Of these 24 positive samples, only two were positive by cytotoxicity and three by a second EIA. Bacterial culture of 21 available stool samples yielded a toxinogenic C. difficile PCR ribotype 001 in one patient sample only. In conclusion, we found no evidence in this retrospective study for an association between Viral Gastroenteritis outbreaks and C. difficile. The high rate of false-positive EIA samples emphasises the need for second confirmation tests to diagnose CDI.
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outbreaks of Viral Gastroenteritis what s new in 2004
Current Opinion in Infectious Diseases, 2005Co-Authors: Marion KoopmansAbstract:Purpose of reviewDescriptions of outbreaks of Viral Gastroenteritis have become a prominent feature in scientific journals and other media such as the electronic reporting service ‘promed’. A review of outbreak reports was done to further our understanding of the burden of disease, common and rare m
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Outbreaks of Viral Gastroenteritis: what's new in 2004?
Current opinion in infectious diseases, 2005Co-Authors: Marion KoopmansAbstract:Purpose of reviewDescriptions of outbreaks of Viral Gastroenteritis have become a prominent feature in scientific journals and other media such as the electronic reporting service ‘promed’. A review of outbreak reports was done to further our understanding of the burden of disease, common and rare m
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Viral Gastroenteritis outbreaks in europe 1995 2000
Emerging Infectious Diseases, 2003Co-Authors: Ben Lopman, Mark Reacher, Yvonne Van Duijnhoven, Francoisxavier Hanon, David M Brown, Marion KoopmansAbstract:To gain understanding of surveillance and epidemiology of Viral Gastroenteritis outbreaks in Europe, we compiled data from 10 surveillance systems in the Foodborne Viruses in Europe network. Established surveillance systems found Norovirus to be responsible for >85% (N=3,714) of all nonbacterial outbreaks of Gastroenteritis reported from 1995 to 2000. However, the absolute number and population-based rates of Viral Gastroenteritis outbreaks differed markedly among European surveillance systems. A wide range of estimates of the importance of foodborne transmission were also found. We review these differences within the context of the sources of outbreak surveillance information, clinical definitions, and structures of the outbreak surveillance systems.
Taku Morita - One of the best experts on this subject based on the ideXlab platform.
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Acidosis with hyperuricemia and renal tubular damage in Viral Gastroenteritis.
Pediatric nephrology (Berlin Germany), 2011Co-Authors: Taku Morita, Mikiya FujiedaAbstract:Sir, We read with interest the article entitled “Cause of uric acid stones in rotavirus-associated Gastroenteritis” by Kaneko et al., which was recently published in Pediatric Nephrology [1]. We encountered four cases of postrenal renal failure induced by ammonium acid urate (AAU) stones associated with rotavirus Gastroenteritis in patients without metabolic disorder, drug administration, abnormality of the urinary tract, urinary tract infection, or mutation of the human urate transporter 1 (hURAT1) associated with SLC22A12. Ashida et al. described a case with postrenal renal failure caused by an AAU stone associated with norovirus Gastroenteritis [2], but most case reports of this condition have been associated with rotavirus infection. To examine these issues, we compared clinical and laboratory data in patients with rotavirus and norovirus Gastroenteritis. Participants in our study were patients with rotavirus or norovirus Gastroenteritis who were admitted for treatment of diarrhea and vomiting with dehydration between January 2006 and March 2009. These patients included 42 with rotavirus infection (Group R; mean age, 1.7 years; range, 0.3–2.0 years; 32 boys, 10 girls) and 23 with norovirus infection (Group N; mean age, 1.7 years; range, 0.5–2.5 years; 14 boys, 9 girls). None of the patients had any bacterial infection or underlying disease such as metabolic disorder, and none developed postrenal renal failure. RT-PCR was used to detect rotavirus or norovirus genome in stools. Age, sex, and results from blood chemistry tests, blood gas tests (venous), and urinalysis were compared between groups. The two-sample t test, Mann–Whitney test, and Fisher’s exact test were used for comparisons between groups. Values of p 595 μmol/l (Group R: 31.0%, Group N 0%) were significantly higher in Group R (p = 0.04, p = 0.01 respectively). Urinary pH was lower and urinary excretion of UA (UA/Crn), β2-microglobulin (β2MG) and N-acetyl-β-glucosaminidase (NAG) were higher in Group R. Urinary UA/Crn >1.2 was found in 13 out of 20 patients in Group R, compared with 3 out of 11 patients in Group N (p = 0.04). Excretion of β2MG >500 μg/l occurred in 12 out of 20 patients (mean, 2,004 μg/l; range, 638–3,383 μg/l) in Group R and only 1 out of 9 patients (906 μg/l) in Group N (p = 0.02). Urinary excretion of NAG >10 U/l occurred in 8 out of 25 patients (mean, 29.0 U/l; range, 13.3–75.0 U/l) in Group R and only 1 out of 9 patients (16.3 U/l) in Group N. Blood levels of β2MG were similar in the two groups (data not shown). Viral Gastroenteritis induces frequent diarrhea and loss of bicarbonate by small intestinal epithelial cells. This damage results in metabolic acidosis and a subsequent increase in urinary ammonium excretion in response to the acidosis. The combination of aciduria, hyperuricemia, and hyperammonuria can induce formation of AAU stones and crystals. Severe and persistent acidosis induced by rotavirus or norovirus infection may thus cause postrenal renal failure due to AAU stones. Our data showed that patients with rotavirus Gastroenteritis experience high fever, high levels of hyperuricemia and acidosis, and a tendency toward high levels of urinary excretion of UA, β2MG, and NAG, compared with patients with norovirus Gastroenteritis. These findings suggest that tissue damage caused by rotavirus is more severe than that caused by norovirus, and that rotavirus might be toxic to both tubular epithelial cells and small intestinal epithelial cells. Urinary pH and blood bicarbonate levels did not differ significantly between groups, possibly because most patients received intravenous fluids before admission. We recently detected rotavirus in urinary sediment cells of patients with rotavirus Gastroenteritis [3], suggesting that rotavirus may attack tubular epithelial cells directly. Acidosis, hyperuricemia, and urine output after hydration should be considered in patients with Viral Gastroenteritis for prevention of postrenal renal failure due to AAU stones or crystals. However, many children with rotavirus or norovirus infection are treated annually, and only a small proportion of patients develop stones. A large-scale study and worldwide survey are required to clarify risk factors for the formation of AAU stones, and to determine whether Viral Gastroenteritis caused by rotavirus or norovirus plays any significant role in the formation of AAU stones that result in postrenal renal failure.
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acidosis with hyperuricemia and renal tubular damage in Viral Gastroenteritis
Pediatric Nephrology, 2011Co-Authors: Taku Morita, Mikiya FujiedaAbstract:Sir, We read with interest the article entitled “Cause of uric acid stones in rotavirus-associated Gastroenteritis” by Kaneko et al., which was recently published in Pediatric Nephrology [1]. We encountered four cases of postrenal renal failure induced by ammonium acid urate (AAU) stones associated with rotavirus Gastroenteritis in patients without metabolic disorder, drug administration, abnormality of the urinary tract, urinary tract infection, or mutation of the human urate transporter 1 (hURAT1) associated with SLC22A12. Ashida et al. described a case with postrenal renal failure caused by an AAU stone associated with norovirus Gastroenteritis [2], but most case reports of this condition have been associated with rotavirus infection. To examine these issues, we compared clinical and laboratory data in patients with rotavirus and norovirus Gastroenteritis. Participants in our study were patients with rotavirus or norovirus Gastroenteritis who were admitted for treatment of diarrhea and vomiting with dehydration between January 2006 and March 2009. These patients included 42 with rotavirus infection (Group R; mean age, 1.7 years; range, 0.3–2.0 years; 32 boys, 10 girls) and 23 with norovirus infection (Group N; mean age, 1.7 years; range, 0.5–2.5 years; 14 boys, 9 girls). None of the patients had any bacterial infection or underlying disease such as metabolic disorder, and none developed postrenal renal failure. RT-PCR was used to detect rotavirus or norovirus genome in stools. Age, sex, and results from blood chemistry tests, blood gas tests (venous), and urinalysis were compared between groups. The two-sample t test, Mann–Whitney test, and Fisher’s exact test were used for comparisons between groups. Values of p < 0.05 were considered statistically significant. Age, male-to-female ratio, and days from onset to admission did not differ between the groups. Degree of dehydration and duration of fever and hospitalization were similar in the two groups (data not shown), but temperature on admission was significantly higher (p = 0.04) in Group R. No differences in creatinine (Crn) or blood urea nitrogen (BUN) levels were seen between groups. HCO3− level in blood tended to be lower, venous gas pH (Group R: mean, 7.360; range, 7.268–7.442, Group N: mean, 7.410; range, 7.283–7.432) was significantly lower (p = 0.03), and concentrations of uric acid (UA) in blood (Group R: mean, 440 μmol/l; range,184–708 μmol/l, Group N: mean, 363 μmol/l; range, 184–630 μmol/l), and frequency of UA >595 μmol/l (Group R: 31.0%, Group N 0%) were significantly higher in Group R (p = 0.04, p = 0.01 respectively). Urinary pH was lower and urinary excretion of UA (UA/Crn), β2-microglobulin (β2MG) and N-acetyl-β-glucosaminidase (NAG) were higher in Group R. Urinary UA/Crn >1.2 was found in 13 out of 20 patients in Group R, compared with 3 out of 11 patients in Group N (p = 0.04). Excretion of β2MG >500 μg/l occurred in 12 out of 20 patients (mean, 2,004 μg/l; range, 638–3,383 μg/l) in Group R and only 1 out of 9 patients (906 μg/l) in Group N (p = 0.02). Urinary excretion of NAG >10 U/l occurred in 8 out of 25 patients (mean, 29.0 U/l; range, 13.3–75.0 U/l) in Group R and only 1 out of 9 patients (16.3 U/l) in Group N. Blood levels of β2MG were similar in the two groups (data not shown). Viral Gastroenteritis induces frequent diarrhea and loss of bicarbonate by small intestinal epithelial cells. This damage results in metabolic acidosis and a subsequent increase in urinary ammonium excretion in response to the acidosis. The combination of aciduria, hyperuricemia, and hyperammonuria can induce formation of AAU stones and crystals. Severe and persistent acidosis induced by rotavirus or norovirus infection may thus cause postrenal renal failure due to AAU stones. Our data showed that patients with rotavirus Gastroenteritis experience high fever, high levels of hyperuricemia and acidosis, and a tendency toward high levels of urinary excretion of UA, β2MG, and NAG, compared with patients with norovirus Gastroenteritis. These findings suggest that tissue damage caused by rotavirus is more severe than that caused by norovirus, and that rotavirus might be toxic to both tubular epithelial cells and small intestinal epithelial cells. Urinary pH and blood bicarbonate levels did not differ significantly between groups, possibly because most patients received intravenous fluids before admission. We recently detected rotavirus in urinary sediment cells of patients with rotavirus Gastroenteritis [3], suggesting that rotavirus may attack tubular epithelial cells directly. Acidosis, hyperuricemia, and urine output after hydration should be considered in patients with Viral Gastroenteritis for prevention of postrenal renal failure due to AAU stones or crystals. However, many children with rotavirus or norovirus infection are treated annually, and only a small proportion of patients develop stones. A large-scale study and worldwide survey are required to clarify risk factors for the formation of AAU stones, and to determine whether Viral Gastroenteritis caused by rotavirus or norovirus plays any significant role in the formation of AAU stones that result in postrenal renal failure.
S. Arista - One of the best experts on this subject based on the ideXlab platform.
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Viral Gastroenteritis in children hospitalised in Sicily, Italy
European Journal of Clinical Microbiology and Infectious Diseases, 2006Co-Authors: C. Colomba, S. Grazia, G. M. Giammanco, L. Saporito, F. Scarlata, L. Titone, S. AristaAbstract:The aim of the present study was to describe the epidemiologic and clinical characteristics of acute Viral Gastroenteritis in hospitalised Italian children. A total of 215 stool specimens were collected from January to December 2003 from patients hospitalised in Palermo for acute diarrhoea. Samples were tested for group A rotavirus, astrovirus, adenovirus, norovirus, enteropathogenic bacteria, and parasites. Rotaviruses, mostly belonging to types G1–G4, were detected in 25.1% of samples, astrovirus in 7%, adenovirus in 6%, norovirus in 18.6%, and bacterial agents in 17.2%. No parasitic infections were diagnosed. Mixed infections represented 9.8% of all cases. The mean and median ages of children with rotavirus Gastroenteritis were lower than those of children with other viruses ( p =0.029), with the highest median ages being found in astrovirus-infected patients. Vomiting and dehydration were more frequent among patients with Viral infection ( p
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Viral Gastroenteritis in children hospitalised in sicily italy
European Journal of Clinical Microbiology & Infectious Diseases, 2006Co-Authors: C. Colomba, S. Grazia, G. M. Giammanco, L. Saporito, F. Scarlata, L. Titone, S. AristaAbstract:The aim of the present study was to describe the epidemiologic and clinical characteristics of acute Viral Gastroenteritis in hospitalised Italian children. A total of 215 stool specimens were collected from January to December 2003 from patients hospitalised in Palermo for acute diarrhoea. Samples were tested for group A rotavirus, astrovirus, adenovirus, norovirus, enteropathogenic bacteria, and parasites. Rotaviruses, mostly belonging to types G1–G4, were detected in 25.1% of samples, astrovirus in 7%, adenovirus in 6%, norovirus in 18.6%, and bacterial agents in 17.2%. No parasitic infections were diagnosed. Mixed infections represented 9.8% of all cases. The mean and median ages of children with rotavirus Gastroenteritis were lower than those of children with other viruses (p=0.029), with the highest median ages being found in astrovirus-infected patients. Vomiting and dehydration were more frequent among patients with Viral infection (p<0.01), and the severity score was significantly higher for children infected with astrovirus or group A rotavirus (p=0.008). Rotavirus was the leading cause of prolonged hospitalisation (p=0.005). In conclusion, viruses were confirmed in Italy as the most common cause of severe enteric illness in childhood, with rotavirus types G1–G4, which correspond to those included in the rotavirus vaccines being developed, playing the main role. Routine testing should be introduced for noroviruses, since they seem to represent an important cause of sporadic paediatric Gastroenteritis.
