Two metabolites of the tobacco-specific transplacental carcinogen NNK can be detected in the urine from newborns of mothers who smoked cigarettes during pregnancy.

Serum lactate dehydrogenase (LDH), aspartate aminotransferase (ASAT), and hydroxybutyrate dehydrogenase (HBDH) activities are significantly elevated in asphyxiated newborns within the first days of life. The approach of the present study was to evaluate firstly if serum levels of these enzymes correlate with the development of hypoxic-ischemic encephalopathy (HIE) and periventricular-intraventricular hemorrhage (PIVH) in full-term and premature asphyxiated newborns, and secondly if postnatally elevated enzyme activities could be predictive for these disorders. ASAT, LDH and HBDH activities were measured in 98 asphyxiated newborns. Blood samples were taken serially at five fixed times: 0 (cord), 12, 24, 72, and 144 hours post partum. All newborns were examined for the development of HIE and PIVH using standardized scoring systems. Fifty percent of the newborns were full-term and 50% were premature. Ten of the full-term (20.4%) and 21 (42.8%) of the premature newborns developed HIE. Nineteen newborns (19.4%) suffered PIVH (full-term/premature, 7/12). The full-term asphyxiated newborns with HIE or PIVH showed significantly elevated ASAT, LDH, and HBDH activities within the first 72 hours of life. In case of the premature asphyxiated newborns, the enzyme activities did not differ significantly between the study groups. The overall predictive values showed a high sensitivity (HIE/PIVH, 90.0%/71.4%), a high specificity (71.0%/88.1%), an acceptable negative predictive value (44.9%/50.0%), and a high positive predictive value (96.5%/94.9%) for the development of HIE and PIVH in full-term asphyxiated newborns. It is concluded that measurements of ASAT, LDH, and HBDH activities are reliable predictors for the development of HIE and PIVH in full-term asphyxiated newborns.(ABSTRACT TRUNCATED AT 250 WORDS)

Traumatic dural lesions (caused by major or minor head injuries, iatrogenic damage to the dura) can go undetected for many years until clinical symptoms such as meningitis, cerebral abscess, and/or cerebrospinal fluid (CSF) rhinorrhea supervene.1 It is known from the traumatologic literature that late meningitis occurs in 3%-50% of unrepaired dural injuries of the anterior skull base.2-6 Without surgical repair, the resulting dural scar is often too thin to provide an adequate barrier against infection.2,7-12 The possibility of an occult dural lesion should always be considered in patients with endocranial complications of unknown origin. It can be very difficult to prove occult dural lesions and to locate their site exactly, but it is a prerequisite for surgical repair in order to prevent endocranial complications. Different diagnostic tools such as high-resolution CT, fluorescein nasal endoscopy, CT cisternography, and MRI were highlighted in the literature to search for CSF leaks. These methods were judged to be of different value for location of a dural lesion.In this article, the authors review their expierences in detecting occult traumatic dural lesions in 23 patients.

Little is known about the kinetics of most serum enzymes during the first hours of life, and even less about the effect on such enzyme activities of perinatal hypoxia-ischaemia. It was the aim of the present study to evaluate the serum kinetics of seven differently located cell enzymes in healthy and asphyxiated newborns during the 1st week of life. The serum activities of cytoplasmic and mitochondrial [aspartate aminotransferase (ASAT), creatine kinase (CK), glutamate dehydrogenase (GLDH), lactate dehydrogenase (LDH), and hydroxybutyrate dehydrogenase (HBDH)] and membrane-bound (γ-glutamyltransferase and leucine arylaminidase) enzymes were prospectively measured in full-term asphyxiated (n = 49) and healthy (n = 87) newborns during the first 144 h of life. The blood samples were taken serially at five fixed times; 0 (cord), 12,24,72, and 144 h postpartum. The asphyxiated newborns had significantly increased serum activities of ASAT, LDH, and HBDH up to 72 h postpartum, whereas healthy newborns showed higher CK and GLDH activities. Only the activities of ASAT, LDH, and HBDH seemed to depend on the oxygen supply of the fetus or newborn. If other causes of increased serum enzyme activities, e.g. liver diseases, haemolytic disorders, tumours, or inborn errors of metabolism, are excluded, elevated serum activities of ASAT, LDH, and HBDH should draw one’s attention to a perinatal hypoxic-ischaemic insult of the newborn.

An aneurysmal cyst of the petrosal bone presenting as hearing loss and recurrent bacterial meningitis is reported. None