4^th Annual World Congress on Pediatric Nutrition, Gastroenterology and Child Development March 18-19, 2019 Chicago, USA

Biography:

Abstract:

Statement of the Problem: Delayed investigations may result in skewed patient assessment especially with varied clinical presentations.

A 2 year old male presented with fever, abdominal pains and generalized seizure activity two days after receiving Penadur for an exudative tonsillitis. Symptoms persisted resulting in depressed Glasgow Coma scale (GCS 10/15), associated with nystagmus, absent gag reflex, hypotonic upper limbs and hypertonic lower limbs, hyperreflexia and clonus. Currently, the patient is alive, but minimal neurological improvement is seen up to 3 months after presentation.  Initial investigations revealed a hemoglobin of 7.8, thrombocytopenia of 61 and elevated transaminases. No electrolyte imbalance was noted. Dengue viral studies done 6 days after symptom onset showed negative NS1 antigen and positive IgM and IgG antibodies. CSF analysis showed no cells, and no increase in CSF globulins. CSF dengue antigen and IgM antibodies and serum and CSF PCR was unavailable. TORCH, HIV, syphilis, hepatitis, or Zika virus investigations were negative. Cranial CT revealed possible pontine infarct with hypodensity in bilateral frontal lobe white matter, possibly ischemic or inflammatory in origin. Magnetic resonance diffusion weighted imaging of the brain, done 20 days after presentation, showed subtle T2 hyperintense signal changes in the posterior periventricular white matter, which may be related to ongoing myelination. Imaging suggests underlying metabolic disturbance, central-pontine myelinolysis or sequelae of infection. Although dengue is not considered a neurotropic virus, in recent years, there has been documentation of neurological complications associated with dengue fever.¹ These complications in general are unusual. MRI findings are usually normal, but may vary. In a cohort of patients, findings include cerebral oedema, encephalitis-like changes and one patient had intracranial hemorrhage.² Diagnosis in this case is limited by the absence of CSF dengue antigen and IgM as well as CSF PCR. Also, MRI findings are time-sensitive and delayed imaging results in inability to assess acute intracranial changes.

Biography:

Abstract:

Statement of the Problem: Delayed investigations may result in skewed patient assessment especially with varied clinical presentations.

A 2 year old male presented with fever, abdominal pains and generalized seizure activity two days after receiving Penadur for an exudative tonsillitis. Symptoms persisted resulting in depressed Glasgow Coma scale (GCS 10/15), associated with nystagmus, absent gag reflex, hypotonic upper limbs and hypertonic lower limbs, hyperreflexia and clonus. Currently, the patient is alive, but minimal neurological improvement is seen up to 3 months after presentation.  Initial investigations revealed a hemoglobin of 7.8, thrombocytopenia of 61 and elevated transaminases. No electrolyte imbalance was noted. Dengue viral studies done 6 days after symptom onset showed negative NS1 antigen and positive IgM and IgG antibodies. CSF analysis showed no cells, and no increase in CSF globulins. CSF dengue antigen and IgM antibodies and serum and CSF PCR was unavailable. TORCH, HIV, syphilis, hepatitis, or Zika virus investigations were negative. Cranial CT revealed possible pontine infarct with hypodensity in bilateral frontal lobe white matter, possibly ischemic or inflammatory in origin. Magnetic resonance diffusion weighted imaging of the brain, done 20 days after presentation, showed subtle T2 hyperintense signal changes in the posterior periventricular white matter, which may be related to ongoing myelination. Imaging suggests underlying metabolic disturbance, central-pontine myelinolysis or sequelae of infection. Although dengue is not considered a neurotropic virus, in recent years, there has been documentation of neurological complications associated with dengue fever.¹ These complications in general are unusual. MRI findings are usually normal, but may vary. In a cohort of patients, findings include cerebral oedema, encephalitis-like changes and one patient had intracranial hemorrhage.² Diagnosis in this case is limited by the absence of CSF dengue antigen and IgM as well as CSF PCR. Also, MRI findings are time-sensitive and delayed imaging results in inability to assess acute intracranial changes.

Biography:

Young Youn Choi has completed his PhD at the age of 29 years from Chonnam National University Medical School, Korea. She had been studied at Tokushima University, Kurume University in Japan, and Joint Program in Neonatology at Harvard Medical School in USA. She was the director of NICU of Chonnam National University Children’s Hospital and vice dean of Chonnam National University Medical School. She is a member of Korean Society of Pediatrics and of Korean Neonatology Society. She has published more than 80 papers in reputed journals and had been serving as an editorial board member of repute.

Abstract:

Introduction: International marriages have been steadily increasing since the 1990s and began to increase rapidly after 2003 in Korea. The recent data by Statistics Korea 2016, the rate of multi-cultural family (MCF) marriage accounted for 7.7% of the total number of marriages. The health status and socioeconomic and cultural differences of immigrant pregnant women can affect the fetal and neonatal health. The aim of this study is to investigate the periodical changes of the rate of newborns of MCF with their perinatal risk factors and neonatal outcome who admitted to Chonnam National University Hospital for the past 15 years and to emphasize the role of women doctors in this field.

Methods: Medical records of newborns admitted to NICU between January 2001 and December 2015 were collected retrospectively. Study period was categorized into three periods: data from 2001 to 2005 was defined as period I, from 2006 to 2010 as period II and from 2011 to 2015 as period III. The clinical data of the rate of newborns of MCF with their perinatal risk factors and outcome were reviewed.

Biography:

Mohammed Beshir is a pediatrician in Jimma University, Ethiopia. He graduated from Jimma Medical School, Ethiopia.

Abstract:

In Ethiopia, malaria is endemic and commonly caused by Plasmodium vivax and Plasmodium falciparum species. Among the hematological alterations occurring in malaria: anemia, leucopenia, and thrombocytopenia are known. While severe thrombocytopenia is a feature of Plasmodium falciparum species. It is rare in Plasmodium vivax malaria. Similarly, acute renal failure due to Plasmodium vivax malaria is rare in Plasmodium vivax malaria. In view of the rarity of this unusual combination of the case, here we report a 14 years-old boy presented with a 5 days history of intermittent fever with chills & rigors, 3 days history of abdominal pain, distension of abdomen, unable to pass feces and decreased urine output. He was diagnosed to have Plasmodium vivax malaria. Acute pancreatitis, ascites, severe thrombocytopenia, severe anemia, and acute renal failure was diagnosed. These constellations of complications in P. vivax infection has never been reported in the past. The patient responded to antimalarial and supportive treatment. Its presentation, diagnosis, management & natural course will be discussed.

Biography:

Basma Elhaddad is a faculty member (demonstrator) at the Pathology Department, Faculty of Medicine, Alexandria University, Egypt. Basma graduated from the faculty of medicine, Alexandria University in 2010 (MBBch)". Basma is a master’s degree student with a thesis in the Pathology of Gastrointestinal tract and liver  “Master of Basic Medical Sciences in Pathology (MSc.); GPA: Excellent with Honour”.

Abstract:

Liver cell regeneration takes place through mature hepatocytes. However, in cases of chronic or severe injury, an alternative pathway takes place through the proliferation of hepatic progenitor cells (HPCs). The aim of the study was to investigate the distribution and number of Foxl1 positive HPCs in the livers of infants with different cholestatic diseases. Therefore, immunohistochemistry using Foxl1 antibody (ab190226) was conducted on fifty-three formalin fixed paraffin embedded blocks of liver biopsies from infants with neonatal cholestasis with the following diagnoses: Thirty cases of extrahepatic biliary atresia (EHBA), eleven cases of paucity of intrahepatic bile ducts (PIBD), eight cases of idiopathic neonatal giant cell hepatitis (NGCH) and four cases of galactosemia. Trichrome staining was done to asses the stage of fibrosis according to a previously published modified scoring system. Foxl1 Positive cells were seen in the periportal area and their numbers were much higher in liver biopsies obtained from infants with EHBA compared to the other diagnoses. Significant positive correlations were found between the number of HPCs and stage of fibrosis, the degree of ductular proliferation, the presence of portal tract neutrophils as well as higher levels of serum gamma-glutamyltransferase. In conclusion, HPCs are markedly activated in EHBA and their activation might be the reason for the associated ductular proliferation and fibrosis. However,  the type of inflammatory infiltrate might play a role in HPC activation as well. This may help to guide further research on animal models to design HPC-based antifibrotic therapies for cholestatic liver diseases.