Risks of congenital malformations and perinatal events among infants exposed to calcium channel and beta-blockers during pregnancy.
Summary of "Risks of congenital malformations and perinatal events among infants exposed to calcium channel and beta-blockers during pregnancy."
Calcium channel blockers and beta-blockers (BBs) are widely used during pregnancy, but data on their safety for the developing infant are scarce. We used population-based data from 5 HMOs to study risks for perinatal complications and congenital defects among infants exposed in-utero.
We studied women older than 15 years delivering an infant between 1/1/96 and 12/31/00, who had been continuously enrolled with prescription drug coverage for ≥1 year prior to delivery. Information on prescription drug dispensings, inpatient, and outpatient diagnoses and procedures was obtained from automated databases at each HMO.
There were 584 full-term infants exposed during pregnancy to BBs and 804 full-term infants exposed to calcium-channel blockers, and over 75 000 unexposed mother-infant pairs with ≥30 days follow-up. Infants exposed to BBs in the third trimester of pregnancy had over threefold increased risk for hypoglycemia (RR 3.1; 95% CI 2.2, 4.2) and an approximately twofold increased risk for feeding problems (RR 1.8; 95% CI 1.3, 2.5). Infants exposed to calcium-channel blockers in the third trimester had an increased risk for seizures (RR 3.6 95% CI 1.3, 10.4). Chart review confirmed the majority of the exposed seizure and hypoglycemia cases. There were no increased risks for congenital anomalies among either group of infants, except for the category of upper alimentary tract anomalies; this increased risk was based on only two exposed cases.
Infants whose mothers receive BBs are at increased risk for neonatal hypoglycemia, while those whose mothers take calcium-channel blockers are at increased risk for neonatal seizures. Copyright © 2010 John Wiley & Sons, Ltd.
Center for Health Research, Kaiser Permanente Georgia, Southeast, Atlanta, Georgia, USA.
This article was published in the following journal.
Name: Pharmacoepidemiology and drug safety
Medical and Biotech [MESH] Definitions
A spectrum of congenital, inherited, or acquired abnormalities in BLOOD VESSELS that can adversely affect the normal blood flow in ARTERIES or VEINS. Most are congenital defects such as abnormal communications between blood vessels (fistula), shunting of arterial blood directly into veins bypassing the CAPILLARIES (arteriovenous malformations), formation of large dilated blood blood-filled vessels (cavernous angioma), and swollen capillaries (capillary telangiectases). In rare cases, vascular malformations can result from trauma or diseases.
Softening or loss of brain tissue following CEREBRAL INFARCTION; cerebral ischemia (see BRAIN ISCHEMIA), infection, CRANIOCEREBRAL TRAUMA, or other injury. The term is often used during gross pathologic inspection to describe blurred cortical margins and decreased consistency of brain tissue following infarction. Multicystic encephalomalacia refers to the formation of multiple cystic cavities of various sizes in the cerebral cortex of neonates and infants following injury, most notably perinatal hypoxia-ischemic events. (From Davis et al., Textbook of Neuropathology, 2nd ed, p665; J Neuropathol Exp Neurol, 1995 Mar;54(2):268-75)
Congenital defects of closure of one or more vertebral arches, which may be associated with malformations of the spinal cord, nerve roots, congenital fibrous bands, lipomas, and congenital cysts. These malformations range from mild (e.g., SPINA BIFIDA OCCULTA) to severe, including rachischisis where there is complete failure of neural tube and spinal cord fusion, resulting in exposure of the spinal cord at the surface. Spinal dysraphism includes all forms of spina bifida. The open form is called SPINA BIFIDA CYSTICA and the closed form is SPINA BIFIDA OCCULTA. (From Joynt, Clinical Neurology, 1992, Ch55, p34)
A congenital disorder that is characterized by a triad of capillary malformations (HEMANGIOMA), venous malformations (ARTERIOVENOUS FISTULA), and soft tissue or bony hypertrophy of the limb. This syndrome is caused by mutations in the VG5Q gene which encodes a strong angiogenesis stimulator.
Malformations Of Cortical Development
Abnormalities in the development of the CEREBRAL CORTEX. These include malformations arising from abnormal neuronal CELL PROLIFERATION or APOPTOSIS; abnormal neuronal migration; and abnormal establishment of cortical organization via neurite extension, synaptogenesis, or neuronal maturation. As well as mutations effecting these developmental processes directly, there are a variety of inborn metabolic errors, such as PEROXISOMAL DISORDERS and mitochondrial and pyruvate metabolic disorders which effect them secondarily and also exhibit these malformations. They are common causes of EPILEPSY and developmental delay and are often a component of multiple congenital anomalies.
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