1/213. Congenital unilateral fusion of the maxilla and mandible. We present an uncommon severe first branchial arch congenital malformation, in which complete unilateral bony fusion between the maxillary and mandibular processes was found in a newborn exposed to carbamazepine medication all through pregnancy. This condition interferes with oral feeding, intubation, growth and development. In a review of previously reported cases it was found that this anomaly was commonly associated with other abnormalities. The etiology of this malformation was uncertain in our case, as carbamazepine was not proven to be the definite cause. ( info) |
2/213. Transient hypertrophic cardiomyopathy in the newborn following multiple doses of antenatal corticosteroids. Postnatal exposure to steroids has been associated with hypertrophic cardiomyopathy (HCM) in the newborn. Such an effect has not been described in infants born to mothers who received antenatal steroids. We report three newborns whose mothers were treated with betamethasone prenatally in different doses, duration of time, and who developed various degrees of HCM diagnosed by echocardiography. There was no maternal evidence of diabetes except for one infant whose mother had a normal fasting and post-prandial blood glucose prior to steroid therapy, but an abnormal one hour postprandial glucose after 8 weeks of betamethasone therapy, with a normal HbA1 C level. There was no family history of HCM, no history of maternal intake of other relevant medications, and no hypertension in all three newborns. Follow-up echocardiography revealed complete resolution of the HCM changes in all infants. We suggest that repeated antenatal maternal steroid intake may cause changes of HCM in the newborn. These changes appear to be dose- and duration-related and are mostly reversible. Further prospective controlled studies to evaluate these observations and to investigate potential mechanisms are warranted. ( info) |
3/213. fertility and its complications in a patient with salt losing congenital adrenal hyperplasia. A report is made concerning fertility and its complications in a patient with salt losing congenital adrenal hyperplasia. fertility with a successful outcome of pregnancy has rarely been reported in women with salt losing congenital adrenal hyperplasia. Problems which have been identified in the past include non-compliance, poor endocrine follow up, secondary polycystic ovarian disease with menstrual irregularity, anovulation and problems related to sexual function. There has been only one report in the literature of a woman with salt losing congenital adrenal hyperplasia who has had two pregnancies with live births. There has been no previous report of subsequent problems with neonatal management of these children. This case highlights some of the long term hazards of management of salt losing congenital adrenal hyperplasia and reports for the first time neonatal complications possibly consequent upon prenatal maternal therapy. ( info) |
4/213. Suicidal paracetamol poisoning of a pregnant woman just before a delivery. The aim of the paper is to present a case of self-poisoning with paracetamol, overdosed just before a delivery. A 21-year-old woman was admitted to Obstetric and gynecology Ward of local hospital in the second stage of physiological delivery, more than 6 hours after she had ingested 19 g of acetaminophen for self-poisoning. She delivered a normal infant weighing 3520 g who had Apgar scores of 10, and then both infant and mother were sent in an emergency ambulance to the nearest poison centre. Blood samples for toxicological examination were taken on admission to toxicological intensive care unit i.e. 11 hours post maternal ingestion. acetaminophen levels of both patients were above the acetaminophen overdose nomogram line and the antidote treatment, i.v. N-acetylcysteine was administered according to the protocol: the mother within 11 hours post-ingestion and approximately 4 hours after a delivery; the neonate within 11 hours post maternal ingestion and 4 hours of life. Higher paracetamol concentration in the blood of infant compared to the mother's was noted in the first and then control toxicological examination performed within 35 hours post maternal ingestion. Peak maternal aspartate aminotransferase (AST) activity was 326 U/L within 35 hours and alanine aminotransferase (ALT) activity was 262 U/L within 56 hours post-ingestion. The highest neonatal enzyme activity was noted within 11 hours post maternal ingestion of paracetamol, and the elevation was not high. Except moderate anaemia in the mother, no clinical or biochemical symptoms of renal, cardiovascular or CNS injury were stated in the mother or infant. Normalisation in the maternal enzymes activity was stated within 226 hours, while in the neonatal within 58 hours post maternal ingestion. The woman recovered without sequelae and was discharged from hospital on the 11th day following paracetamol overdosing. No evidence of the liver injury was found in the infant either. ( info) |
5/213. Neonatal end-stage renal failure associated with maternal ingestion of cyclo-oxygenase-type-1 selective inhibitor nimesulide as tocolytic. Cyclo-oxygenase-type-2 (COX-2) enzyme is fundamental for nephrogenesis, upregulated on fetal membranes and myometrium at parturition. Fetal COX-2 inhibition, due to maternal nimesulide assumption, can be responsible for neonatal chronic renal failure. ( info) |
6/213. Neonatal mydriasis due to effects of atropine used for maternal Tik-20 poisoning. A neonate was born to a mother who had consumed an organophosphorus(OPC) compound with suicidal intent. The mother was administered atropine and this caused mydriasis in the neonate without any other pharmacological effects. There was no evidence of placental dysfunction. There are no case reports of OPC consumed in pregnancy and its effect on neonates or of effects of massive doses of atropine in the mother and its effects on the fetus or the newborn. ( info) |
7/213. Perinatal vasoconstrictive renal insufficiency associated with maternal nimesulide use. A full-term newborn developed oliguric renal failure at 24 hr of life, which persisted for several days. Her mother ingested therapeutic doses of nimesulide, a non-steroidal anti-inflammatory (cyclo-oxygenase-2 inhibitor) drug, during the last 2 weeks of pregnancy. She was found at delivery to have developed oligohydramnion, esophagitis, and a bleeding peptic ulcer. The infant's fractional excretion of sodium was very low (0.5%) pointing for a severe vasoconstrictive mechanism involved. Renal sonogram showed hyperechogenic medullary papillae, which resolved during convalescence. This case emphasizes the importance of renal prostagandins in the control of vascular tone and sodium homeostasis. This is the first report of an adverse effect of fetal renal circulation by maternal ingestion of nimesulide. ( info) |
8/213. Cloverleaf skull and multiple congenital anomalies in a girl exposed to cocaine in utero: case report and review of the literature. The case of a girl with cloverleaf skull (CLS) and multiple congenital anomalies is reported. Both parents have a history of drug use. Maternal cocaine abuse during the first trimester of pregnancy was obvious, and other drugs, such as marihuana and alcohol, were also taken by the mother. Many central nervous system malformations have been reported in association with cocaine abuse, the most severe being midline defects and neural tube defects. To our knowledge this is the first case reported of CLS anomaly associated with drug exposure. We also describe other anomalies not previously reported in association with CLS. ( info) |
9/213. Multimodal cancer chemotherapy during the first and second trimester of pregnancy: a case report. This paper reports treatment with combined chemotherapy during pregnancy. A 39-year-old woman with breast cancer was given adjuvant chemotherapy including cyclophosphamide, methotrexate and 6-fluorouracil from the 6th to the 24th week of gestation. The possibility of teratogenic effects on the fetus was explained to the patient however she refused to terminate the pregnancy. A 30-week male infant with only a minor malformation was delivered. The authors reviewed the literature regarding chemotherapeutic agents given during the first trimester of pregnancy. Most cytotoxic drugs have teratogenic effects on experimental animal subjects. However, actual data on human fetuses are sparse because of the variety of therapeutic regimens and the rarity of administering chemotherapy during pregnancy. The long-term effects of exposure to cytotoxic drugs in utero, needs further research. ( info) |
10/213. Disorders of maternal calcium metabolism implicated by abnormal calcium metabolism in the neonate. Normal fetal and neonatal calcium homeostasis is dependent upon an adequate supply of calcium from maternal sources. Both maternal hypercalcemia and hypocalcemia can cause metabolic bone disease or disorders of calcium homeostasis in neonates. Maternal hypercalcemia can suppress fetal parathyroid function and cause neonatal hypocalcemia. Conversely, maternal hypocalcemia can stimulate fetal parathyroid tissue causing bone demineralization. We report two asymptomatic women, one with previously unrecognized hypoparathyroidism and the other with unrecognized familial benign hypercalcemia, who were diagnosed when their newborn infants presented with abnormalities of calcium metabolism. J.B. was born at 34 weeks' gestation with transient hyperbilirubinemia and thrombocytopenia. At 1 month of age he had severe bone demineralization, cortical irregularities, widening and cupping of the metaphyses, and lucent bands in the scapulae. The total serum calcium and phosphorus were normal with an ionized calcium of 5.4 mg/dL (4.6-5.4). His alkaline phosphatase, parathyroid hormone, and 1,25-dihydroxyvitamin D levels were all increased. P.B., mother of J.B., had no symptoms of hypocalcemia either prior to, or during this pregnancy. She had severe hypocalcemia and hyperphosphatemia, laboratory values typical of hypoparathyroidism. J.N. presented at 6 weeks of age with new onset of seizures and tetany secondary to severe hypocalcemia. The serum phosphorus, creatinine, alkaline phosphatase, and parathyroid hormone levels were normal. At 15 weeks of age his calcium was slightly elevated with a low fractional excretion of calcium. P.N., mother of J.N., had no symptoms of hypercalcemia either prior to, or during this pregnancy. Her serum calcium was 12.7 mg/dL and urine calcium was 66.5 mg/24 hr, with a low fractional excretion of calcium ranging from 0.0064 to 0.0073. P.N. has a brother who previously had parathyroid surgery. Both J.N. and P.N. meet the diagnostic criteria for familial benign hypercalcemia. These cases illustrate the important relationships between maternal serum calcium levels and neonatal calcium homeostasis. They emphasize the need to assess maternal calcium levels when infants are born with abnormal serum calcium levels or metabolic bone disease. ( info) |