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Article Synopsis
  • The study analyzed the enzymatic activity of several dehydrogenases in lymphocytes from 183 women with pelvic varicose veins (PVV) and a control group of 30 women.
  • Results showed that women with stage II PVV had increased activity in certain enzymes like NAD-GDH and lactate dehydrogenase, while showing decreased activity in NAD-ICDH.
  • In stage III PVV, lower levels of succinate dehydrogenase and NAD-MDH were observed, alongside increased levels of other enzymes, highlighting changes in enzyme activity as the disease progresses and suggesting potential for targeted treatment options.
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: To evaluate the clinical findings of glucose 6-phosphate dehydrogenase (G6PD) and pyruvate kinase (PK) deficiency in prolonged jaundice and to determine whether the systemic immune inflammation index (SII), neutrophil-to-lymphocyte ratio (NLR), and platelet-to-lymphocyte ratio (PLR) can be used in the diagnosis of neonatal prolonged jaundice. : Among full-term neonates with hyperbilirubinemia who were admitted to Medicine Hospital between January 2019 and January 2024 with the complaint of jaundice, 167 infants with a serum bilirubin level above 10 mg/dL, whose jaundice persisted after the 10th day, were included in this study. : G6PD activity was negatively correlated with NLR, SII, age, and hematocrit (Hct).

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The global role of G6PD in infection and immunity.

Front Immunol

June 2024

Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, NC, United States.

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common enzymopathy in humans. G6PD is an essential enzyme in the pentose phosphate pathway (PPP), generating NADPH needed for cellular biosynthesis and reactive oxygen species (ROS) homeostasis, the latter especially key in red blood cells (RBCs). Beyond the RBC, there is emerging evidence that G6PD exerts an immunologic role by virtue of its functions in leukocyte oxidative metabolism and anabolic synthesis necessary for immune effector function.

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Determinants, profile and outcomes of hepatitis A virus-associated severe acute liver injury in adults.

Indian J Gastroenterol

April 2024

Department of Gastroenterology, Institute of Gastrosciences and Liver Transplantation, Apollo Multispeciality Hospitals, Kolkata, 700 054, India.

Background And Objectives: Hepatitis A virus (HAV)-related hepatitis is witnessing an epidemiological transition with increasing trends in adults. While uncomplicated hepatitis remains common, evidence suggests it to be a growing cause for acute liver failure (ALF). In between the two extremes exists severe acute liver injury (s-ALI) which has a propensity to transition to ALF.

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The X-linked A variant (rs1050828, Val68Met) in accounts for glucose-6-phosphate (G6PD) deficiency in approximately 11% of African American males. This common, hypomorphic variant may impact pulmonary host defense and phagocyte function during pneumonia by altering levels of reactive oxygen species produced by host leukocytes. We used CRISPR-Cas9 technology to generate novel mouse strain with "humanized" G6PD A- variant containing non-synonymous Val68Met single nucleotide polymorphism.

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