Ferda Ozbay Hosnut

Bio: Ferda Ozbay Hosnut is an academic researcher from Başkent University. The author has contributed to research in topics: Malabsorption & Medicine. The author has an hindex of 4, co-authored 7 publications receiving 49 citations.

Adenovirus infection as possible cause of acute liver failure in a healthy child: a case report.

Abstract: Adenoviruses are common viral pathogens in childhood; however, they can cause serious disease in an immunocompromised host. Fulminant hepatitis is a rare complication of adenoviral infection. We report herein a case of fatal fulminant hepatitis possibly caused by adenovirus infection. Although rare, adenovirus infection should be considered in the differential diagnosis of acute liver failure in immunocompetent children.

Etiology of hemolysis in two patients with hepatitis A infection: glucose-6-phosphate dehydrogenase deficiency or autoimmune hemolytic anemia.

Abstract: We report two children with hemolytic anemia during the course of hepatitis A infection. On admission, the patients had high blood urea nitrogen, creatinine, and uric acid levels, as well as anemia, leucocytosis, and direct and indirect hyperbilirubinemia. Both patients had a glucose-6-phosphate dehydrogenase deficiency (G6PD) and autoimmune antibodies. They were given vitamin K on admission. Inadvertent administration of vitamin K could have been related to an acute reduction in hemoglobin concentration. To prevent renal damage, plasmapheresis with fresh frozen plasma was done to clear bilirubin and plasma hemoglobin. The hyperbilirubinemia responded to plasmapheresis. However, acute tubular necrosis complicated the clinical course in one patient, and several sessions of hemodialysis were required. In conclusion, intravascular hemolysis should be considered in patients with hepatitis A infection, marked hyperbilirubinemia, and anemia. Although hepatitis A vaccination is not yet recommended for routine administration, high-risk patients, including those with a G6PD deficiency, should be vaccinated against hepatitis A.

Severe adenovirus infection associated with hemophagocytic lymphohistiocytosis.

Abstract: Ferda Özbay Hoşnut1, Figen Özçay1, Barış Malbora2, Şamil Hızlı3, namık Özbek4 1Başkent University Faculty of Medicine, Department of Pediatric Gastroenterology, Hepatology, and Nutrition, Ankara, Turkey 2Dr. Sami Ulus Research and Training Hospital of Women’s and Children’s Health and Diseases, Ankara, Turkey 3Dr. Sami Ulus Research and Training Hospital of Women’s and Children’s Health and Diseases, Department of Pediatric Gastroenterology, Hepatology, and Nutrition, Ankara, Turkey 4Başkent University Faculty of Medicine, Department of Pediatric Hematology, Ankara, Turkey

A Turkish case of congenital chloride diarrhea with SLC26A3 gene (c.2025_2026insATC) mutation: diagnostic pitfalls.

Abstract: Congenital chloride diarrhea is a rare autosomal recessively inherited disorder characterized by impairment of Cl-/HCO3- exchange in an otherwise normal distal ileum and colon. Infrequency of congenital chloride diarrhea makes diagnostics difficult. The typical presentation is watery Cl- rich diarrhea, hypochloremia, hypokalemia, metabolic alkalosis and failure to thrive. This is a report of a Turkish female infant who was falsely diagnosed with Bartter syndrome when she was two months old. Ibuprofen was commenced at that time. However, severe watery diarrhea, dehydration, failure to thrive, abdominal distention, and electrolyte abnormalities persisted. She was diagnosed with congenital chloride diarrhea based on high fecal Cl- level and SLC26A3 gene c.2025_2026insATC mutation at the age of eight months. Oral NaCl and KCl supplementation was started. Our patient is now 26 months old. Her growth and development are normal. Early diagnosis and treatment are essential for normal growth and development and prevention of other severe complications of congenital chloride diarrhea.

Is it necessary to re-evaluate diagnostic criteria for Wilson disease in children?

Abstract: Background/Aims: The differential diagnosis of Wilson Disease (WD) is challenging, especially in children, because liver copper levels may also increase in other chronic liver diseases with bile stasis. The aim of this study is to determine urine and liver copper cut-off values to differentiate WD from other chronic liver diseases (non-WD, NWD) in children. Materials and Methods: Seventy-six patients participated in the study, 35 with WD and 41 with NWD. The two groups were divided into two subgroups according to the presence of cholestasis. At the time of diagnosis, age, sex, biochemical test results, serum ceruloplasmin, baseline 24-h urinary copper levels, liver biopsy histological findings, liver copper levels, and Child-Pugh scores were obtained from medical records. Copper content in liver tissue and copper levels in urine were measured by atomic absorption spectrometry. Cut-off values for differentiation of WD from NWD were determined by receiver operating characteristic (ROC) analysis. Results: A liver copper cut-off value of 98 µg/g indicated WD with 91% sensitivity and 65.4% specificity (area under the curve =0.838, 95% CI: 0.749-0.927). A 24-h urinary copper cut-off value of 67.5 µg/24h indicated WD with 85% sensitivity and 71% specificity (area under the curve =0.843, 95% CI: 0.752-0.934). Conclusion: In this study of pediatric chronic liver disease patients, copper cut-off values for distinguishing WD differed substantially from those used for diagnosis. A larger scale study is warranted to re-evaluate liver copper and 24-h urinary copper cut-offs for children with suspected WD.

The Redox Role of G6PD in Cell Growth, Cell Death, and Cancer.

Abstract: The generation of reducing equivalent NADPH via glucose-6-phosphate dehydrogenase (G6PD) is critical for the maintenance of redox homeostasis and reductive biosynthesis in cells. NADPH also plays key roles in cellular processes mediated by redox signaling. Insufficient G6PD activity predisposes cells to growth retardation and demise. Severely lacking G6PD impairs embryonic development and delays organismal growth. Altered G6PD activity is associated with pathophysiology, such as autophagy, insulin resistance, infection, inflammation, as well as diabetes and hypertension. Aberrant activation of G6PD leads to enhanced cell proliferation and adaptation in many types of cancers. The present review aims to update the existing knowledge concerning G6PD and emphasizes how G6PD modulates redox signaling and affects cell survival and demise, particularly in diseases such as cancer. Exploiting G6PD as a potential drug target against cancer is also discussed.

The Repertoire of Adenovirus in Human Disease: The Innocuous to the Deadly.

Abstract: Adenoviridae is a family of double-stranded DNA viruses that are a significant cause of upper respiratory tract infections in children and adults Less commonly, the adenovirus family can cause a variety of gastrointestinal, ophthalmologic, genitourinary, and neurologic diseases Most adenovirus infections are self-limited in the immunocompetent host and are treated with supportive measures Fatal infections can occur in immunocompromised patients and less frequently in the healthy Adenoviral vectors are being studied for novel biomedical applications including gene therapy and immunization In this review we will focus on the spectrum of adenoviral infections in humans

A Case Series of Children with Acute Hepatitis and Human Adenovirus Infection

Abstract: Human adenoviruses typically cause self-limited respiratory, gastrointestinal, and conjunctival infections in healthy children. In late 2021 and early 2022, several previously healthy children were identified with acute hepatitis and human adenovirus viremia.We used International Classification of Diseases, 10th Revision, codes to identify all children (<18 years of age) with hepatitis who were admitted to Children's of Alabama hospital between October 1, 2021, and February 28, 2022; those with acute hepatitis who also tested positive for human adenovirus by whole-blood quantitative polymerase chain reaction (PCR) were included in our case series. Demographic, clinical, laboratory, and treatment data were obtained from medical records. Residual blood specimens were sent for diagnostic confirmation and human adenovirus typing.A total of 15 children were identified with acute hepatitis - 6 (40%) who had hepatitis with an identified cause and 9 (60%) who had hepatitis without a known cause. Eight (89%) of the patients with hepatitis of unknown cause tested positive for human adenovirus. These 8 patients plus 1 additional patient referred to this facility for follow-up were included in this case series (median age, 2 years 11 months; age range, 1 year 1 month to 6 years 5 months). Liver biopsies indicated mild-to-moderate active hepatitis in 6 children, some with and some without cholestasis, but did not show evidence of human adenovirus on immunohistochemical examination or electron microscopy. PCR testing of liver tissue for human adenovirus was positive in 3 children (50%). Sequencing of specimens from 5 children showed three distinct human adenovirus type 41 hexon variants. Two children underwent liver transplantation; all the others recovered with supportive care.Human adenovirus viremia was present in the majority of children with acute hepatitis of unknown cause admitted to Children's of Alabama from October 1, 2021, to February 28, 2022, but whether human adenovirus was causative remains unclear. Sequencing results suggest that if human adenovirus was causative, this was not an outbreak driven by a single strain. (Funded in part by the Centers for Disease Control and Prevention.).

Fatal pneumonia cases caused by human adenovirus 55 in immunocompetent adults.

Abstract: Background: Adenovirus is a frequent cause of mild self-limiting upper respiratory tract infection, gastroenteritis, and conjunctivitis Severe or fatal infection mostly occurs in newborn, elderly or immunocompromised persons Methods: Fatal adenovirus pneumonia in three immunocompetent adults was identified The clinical data and virological findings were reported from patients Additional review of recently recorded fatal patients with adenovirus infection was carried out Results: The patients presented with sudden onset respiratory distress that progressed rapidly to respiratory failure and death Human adenovirus (HAdV)-55 was detected in both nasopharyngeal aspirates and serum samples in all three cases, and moreover detected in lung, liver, and kidney in one case In another case, remarkably elevated aspartate aminotransferase, alanine transaminase, and lactate dehydrogenase were identified Three HAdV-55 strains were isolated and genome sequencing revealed a high similarity with other strains from