Splanchnic Vein Thrombosis in the Mediterranean Area in Children

Abdominal venous thrombosis may present as splanchnic venous thrombosis (SVT) (occlusion of portal, splenic, superior or inferior mesenteric veins) or Budd- Chiari Syndrome (BCS) (thrombosis of inferior vena cava and/or hepatic veins). The aim of this review is to report the scanty data available for SVT in the South Mediterranean area. In one Egyptian study, the possible circumstantial risk factors for portal vein thrombosis (PVT) were found in 30% of cases: 19% neonatal sepsis, 8.7% umbilical catheterization, 6% severe gastroenteritis and dehydration. Another Egyptian study concluded that hereditary thrombophilia was common in children with PVT (62.5%), the commonest being factor V Leiden mutation (FVL) (30%). Concurrence of more than one hereditary thrombophilia was not uncommon (12.5%). The first international publication on hepatic veno-occlusive disease (VOD) in Egypt was in 1965 in children who rapidly develop abdominal distention with ascites and hepatomegaly. This disease was more frequent in malnourished children coming from rural areas; infusions given at home may contain noxious substances that were hepatotoxic and infections might play a role. VOD of childhood is rarely seen nowadays. Data from South Mediterranean area are deficient and this may be attributable to reporting in local medical journals that are difficult to access. Medical societies concerned with this topic could help distribute this information

Acute lower respiratory tract infection due to respiratory syncytial virus in a group of Egyptian children under 5 years of age

<p>Abstract</p> <p>Background and aim</p> <p>Respiratory syncytial virus (RSV) is one of the most important causes of acute lower respiratory tract infections (ALRTI) in infants and young children. This study was conducted to describe the epidemiology of ALRTI associated with RSV among children ≤ 5 years old in Egypt.</p> <p>Patients and Methods</p> <p>We enrolled 427 children ≤ 5 years old diagnosed with ALRTI attending the outpatient clinic or Emergency Department (ED) of Children Hospital, Cairo University during a one- year period. Nasopharyngeal aspirates were obtained from the patients, kept on ice and processed within 2 hours of collection. Immunoflourescent assay (IFA) for RSV was performed.</p> <p>Results</p> <p>91 cases (21.3%) had viral etiology with RSV antigens detected in 70 cases (16.4%). The RSV positive cases were significantly younger than other non-RSV cases (mean age 8.2 months versus 14.2 months, p <0.001). RSV cases had significantly higher respiratory rate in the age group between 2-11 months (mean 58.4 versus 52.7/minute, p < 0.001) and no significant difference in the mean respiratory rate in the age group between 12-59 months. More RSV cases required supplemental oxygen (46% versus 23.5%, p < 0.001) with higher rate of hospitalization (37.1% versus 11.2%, p < 0.001) than the non-RSV cases. 97% of RSV cases occurred in winter season (p < 0.001).</p> <p>Conclusion</p> <p>RSV is the most common viral etiology of ALRTI in children below 5 years of age, especially in young infants below 6 months of age. It is more prevalent in winter and tends to cause severe infection.</p

Growth and Final Height in Children with Autoimmune Hepatitis; A long term observation

Background: Abnormal growth in children with autoimmune hepatitis (AIH) is anticipated, either due to hepatic affection or the growth inhibitory effects of corticosteroids. We aimed to describe children's anthropometry with AIH, and study the factors affecting height.Methods: The present observational study investigates the anthropometric measures of 28 children with AIH followed at a university hospital for 9.5±3 years. We calculated the initial AIH score, the Child-Pugh score, and the pediatric end-stage liver disease score (PELD), follow-up anthropometry, and corticosteroid history. We defined abnormal growth as under nutrition (underweight, wasting, stunting), short stature, overweight, and obesity.Results: At AIH diagnosis, children had a mean age of 7.4±3.1 years, ranging from 2 to 13.8; among whom ~20% had ascites, ~79% had jaundice, and ~82% had type 1 AIH, ~70% had a definite diagnosis of AIH, ~64% were Child-Pugh Score B, ~64% showed severe fibrosis/cirrhosis, and the median PELD score was 8.1 (0.1-12.1). At follow-up, their mean age was 15.9±1.6 years, with mean corticosteroid duration of 7.1±3.1 years, and remission occurred in 50%. We observed a significant improvement in the initial rates of underweight (46.4% vs. 17.8%), mainly stunted, and increased rates of overweight/obesity (14.3% vs. 32.2%). The final rates of height affection without weight affection were comparable to the initials (28.6% vs. 32.1%). Cases with abnormally low final height had significantly more frequent Child-Pugh Score B, higher PELD score, and severe hepatic fibrosis at presentation, with no difference regarding the continuation/ total duration of steroids.Conclusion: the final height in children with AIH is significantly affected by the disease severity at presentation and not the continuation or the duration of corticosteroids use.Background: Abnormal growth in children with autoimmune hepatitis (AIH) is anticipated, either due to hepatic affection or the growth inhibitory effects of corticosteroids. We aimed to describe children's anthropometry with AIH, and study the factors affecting height.Methods: The present observational study investigates the anthropometric measures of 28 children with AIH followed at a university hospital for 9.5±3 years. We calculated the initial AIH score, the Child-Pugh score, and the pediatric end-stage liver disease score (PELD), follow-up anthropometry, and corticosteroid history. We defined abnormal growth as under nutrition (underweight, wasting, stunting), short stature, overweight, and obesity.Results: At AIH diagnosis, children had a mean age of 7.4±3.1 years, ranging from 2 to 13.8; among whom ~20% had ascites, ~79% had jaundice, and ~82% had type 1 AIH, ~70% had a definite diagnosis of AIH, ~64% were Child-Pugh Score B, ~64% showed severe fibrosis/cirrhosis, and the median PELD score was 8.1 (0.1-12.1). At follow-up, their mean age was 15.9±1.6 years, with mean corticosteroid duration of 7.1±3.1 years, and remission occurred in 50%. We observed a significant improvement in the initial rates of underweight (46.4% vs. 17.8%), mainly stunted, and increased rates of overweight/obesity (14.3% vs. 32.2%). The final rates of height affection without weight affection were comparable to the initials (28.6% vs. 32.1%). Cases with abnormally low final height had significantly more frequent Child-Pugh Score B, higher PELD score, and severe hepatic fibrosis at presentation, with no difference regarding the continuation/ total duration of steroids.Conclusion: the final height in children with AIH is significantly affected by the disease severity at presentation and not the continuation or the duration of corticosteroids use

Incidental hypertransaminasemia in children: Potential delay in diagnosis of muscle disease

Many physicians believe that muscle disease leads either to sole elevation of aspartate aminotransferase (AST) or a disproportionate increase in AST versus alanine aminotreansferase (ALT). We herein report 25 patients with muscle disease who presented erroneously to the hepatologist with an incidental finding of elevated ALT/AST. Data of 25 patients with elevated ALT/AST who proved to have muscle disease and underwent extensive liver workup were analyzed. The time lapse until diagnosis of muscle disease and costs of unnecessary liver workup were calculated. The time interval from the incidental finding of elevated transaminases to diagnosis of skeletal muscle disease ranged between 2 months to 10 years with a median (IQR) of 2 (3.6) years. The mean ALT:AST ratio was 1.24. Creatine phosphokinase (CPK) level correlated positively and significantly with both ALT (p = 0.002) and AST (p = 0.0007). The costs of unnecessary liver workup, before muscle disease was diagnosed, ranged between 5000 and 10,000 Egyptian pounds. Unawareness of physicians with muscle origin of ALT/AST may cause delay in diagnosis of muscle disease. Early determination of CPK could save a lot of stress and money. Keywords: Alanine aminotransferase, Aspartate aminotransferase, Creatine phosphokinase, Skeletal muscle diseas

Routine analysis of ascitic fluid for evidence of infection in children with chronic liver disease: Is it mandatory?

Ascitic fluid infection is a major cause of morbidity and mortality in cirrhotic patients, requiring early diagnosis and therapy. We aimed to determine predictors of ascitic fluid infection in children with chronic liver disease. The study included 45 children with chronic liver disease and ascites who underwent 66 paracentesis procedures. Full history taking and clinical examination of all patients were obtained including fever, abdominal pain and tenderness and respiratory distress. Investigations included: complete blood count, C-reactive protein, full liver function tests, ascitic fluid biochemical analysis, cell count and culture. Our results showed that patients' ages ranged between 3 months to 12 years. Prevalence of ascitic fluid infection was 33.3%. Gram-positive bacteria were identified in six cases, and Gram-negative bacteria in five. Fever and abdominal pain were significantly more associated with infected ascites (p value = 0.004, 0.006). Patients with ascitic fluid infection had statistically significant elevated absolute neutrophilic count and C-reactive protein. Logistic regression analysis showed that fever, abdominal pain, elevated absolute neutrophilic count and positive C-reactive protein are independent predictors of ascitic fluid infection. Fever, elevated absolute neutrophilic count and positive C-reactive protein raise the probability of ascitic fluid infection by 3.88, 9.15 and 4.48 times respectively. The cut-off value for C-reactive protein for ascitic fluid infection was 7.2 with sensitivity 73% and specificity of 71%. In conclusion, prevalence of ascitic fluid infection in pediatric patients with chronic liver disease and ascites was 33.3%. Fever, abdominal pain, positive C-reactive protein and elevated absolute neutrophilic count are strong predictors of ascitic fluid infection. Therefore an empirical course of first-line antibiotics should be immediately started with presence of any of these predictors after performing ascitic fluid tapping for culture and sensitivity. In absence of these infection parameters, routine ascitic fluid analysis could be spared

Ocular manifestations in Egyptian children with chronic hepatitis C treated with pegylated interferon and ribavirin

Objectives The aim of this study was to report the prevalence of interferon (IFN)-associated retinopathy and other serious ocular complications in a prospectively studied group of children with chronic hepatitis C virus (HCV) receiving pegylated IFN α2b and ribavirin. Patients and methods Prospective comprehensive ophthalmologic examinations were performed by the first author (D.H.A.R.K.) for all included children bilaterally at 0, 12, 24, and 48 weeks after the start of treatment, and at 6 months after the end of treatment. Data recorded included visual complaints, visual acuity, pupillary reactions, and retinal findings. Results All patients aged 3–17 years who were healthy enough to participate in an ophthalmological examination were included. The number of children who remained on treatment and underwent ophthalmologic examinations was 136 after 48 weeks of treatment (90 boys and 46 girls). No patient had ischemic retinopathy at the screening eye examination before initiation of treatment. After 24 weeks of treatment, two (1.5%) patients developed anterior uveitis and another two (1.5%) patients developed retinal ischemia with cotton-wool spots. Conclusion Ophthalmologic complications are infrequent in children who are treated with pegylated IFN α2b for HCV (3%). Because of the potential severity of ischemic retinopathy and uveitis, prospective ocular assessment should remain a part of the monitoring strategy for children who are treated with IFN for HCV