Isoniazid and hypoglycaemia in a premature infant

F Ovali1, N Samanci, E Sevinç

  • 1Neonatal Unit, Department of Obstetrics and Gynecology, Istanbul Medical Faculty, Istanbul University, Turkey. fovali@yahoo.com

Insights

Severe hypoglycemia in a premature infant was linked to the mother's isoniazid treatment for tuberculosis. Stopping the medication led to the infant's recovery, suggesting a potential drug-induced effect requiring further study.

Area of Science:

  • Neonatal Medicine
  • Pharmacology
  • Infectious Disease

Background:

  • A premature infant presented with severe hypoglycemia, necessitating aggressive glucose infusion.
  • The infant's mother had active tuberculosis and was receiving prophylactic isoniazid therapy during pregnancy.

Observation:

  • The infant exhibited persistent and severe hypoglycemia unresponsive to standard treatments.
  • A notable correlation was observed between the mother's isoniazid use and the infant's hypoglycemic episodes.

Findings:

  • Discontinuation of maternal isoniazid therapy resulted in a rapid and complete resolution of the infant's hypoglycemia.
  • This clinical observation strongly suggests a potential causal link between maternal isoniazid and neonatal hypoglycemia.

Implications:

  • This case highlights a potential adverse drug effect of isoniazid in neonates via maternal transfer.
  • Further pharmacological investigations are warranted to elucidate the mechanism and confirm the cause-and-effect relationship.
  • Clinicians should consider maternal isoniazid exposure in the differential diagnosis of severe neonatal hypoglycemia.

Related Concept Videos

Hypoglycemia and Glucagon01:15

Hypoglycemia and Glucagon

Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...
Inborn Errors of Metabolism01:20

Inborn Errors of Metabolism

Phenylketonuria (PKU) is a protein metabolism disorder characterized by high blood levels of the amino acid phenylalanine. This results from a mutation in the gene responsible for phenylalanine hydroxylase, an enzyme that converts phenylalanine into tyrosine. When this enzyme is deficient, phenylalanine builds up in the blood, leading to symptoms such as vomiting, rashes, seizures, growth deficiency, and severe mental retardation. An early diagnosis and a diet restricting phenylalanine intake...
Drug Dosing: Infants and Children01:29

Drug Dosing: Infants and Children

Pediatric patient dosages diverge from adults due to disparities in body surface area, total body water, and extracellular fluid per kilogram of body weight. The dosing regimen considers the variations in pharmacokinetics and pharmacology across distinct age groups, encompassing preterm newborns, infants, young children, older children, and adolescents. Calculation of pediatric patient doses is predicated on determining body surface area, which exhibits a superior correlation with the child's...
Insulin: Dosing Regimen and Adverse Effects01:16

Insulin: Dosing Regimen and Adverse Effects

Insulin-replacement therapy usually includes both long-acting insulin (basal) and short-acting insulin (to cater to postprandial needs). In a diverse group of type 1 diabetes patients, the average daily insulin dose is typically 0.5-0.7 units/kg body weight. However, obese patients and pubertal adolescents may need more due to insulin resistance.
The basal dose constitutes about 40%-50% of the total daily dose, with the rest as premeal insulin. The mealtime insulin dose should mirror...
Oral Hypoglycemic Agents: Glinides01:06

Oral Hypoglycemic Agents: Glinides

Repaglinide (Prandin) and Nateglinide (Starlix), known as glinides, are oral insulin secretagogues that stimulate insulin release from pancreatic β cells by closing the ATP-sensitive potassium channels (KATP channel). Repaglinide controls insulin release from pancreatic β cells by managing potassium efflux. It shares two binding sites with sulfonylureas and also has a unique site, indicating overlapping mechanisms of action. With a rapid onset and a 4-7 hour duration, it effectively manages...
Hyperglycemia01:29

Hyperglycemia

Hyperglycemia is an abnormally high blood glucose level. It is diagnosed by fasting glucose ≥126 mg/dL, 2-hour oral glucose tolerance test (or OGTT) ≥200 mg/dL, random glucose ≥200 mg/dL with symptoms, or HbA1c ≥6.5%. However, HbA1c results may be unreliable in certain conditions, such as anemia or hemoglobinopathies, and the diagnosis should be confirmed unless classic symptoms are present. Postprandial hyperglycemia is typically considered significant when glucose levels exceed 180 mg/dL two...