Biomedical subjects

W Koelfen

Publications and source records attributed to W Koelfen.

21 records · Page 2Linked to original sources

PubMedDate not supplied

[Intrathecal production of neopterin in meningitis in childhood].

A major activator of antigen presenting cells (APC) is gamma interferon a product of activated T-lymphocytes. CNS is not well studied and represents a unique system with respect to the immune reactions. Neopterin is an indirect marker of gamma interferon deliberation and may give some new information on the role of APC in CNS. Neopterin in serum and cerebrospinal fluid (CSF) was determined by specific RIA in children who were lumbar punctured to exclude meningitis. Neopterin was found in various concentrations in serum and CSF of all patients (n = 47). Bacterial meningitis (group 3) was diagnosed in 12 and aseptic meningitis in 18 children (group 2). CSF was drawn in 17 children with febrile convulsions (group 1). Elevated serum neopterin in childhood was only reported in children with an atypical PKU, while data on CSF neopterin were published only in a few cases of adults with CNS involvement. The results show that the APC is stimulated rapidly in childhood similar as in adults following severe viral or bacterial infections. Furthermore neopterin in CSF is not only explained by alteration of the blood-brain barrier but also it may reflect local intrathecal response with activation of accessory cells (APC) in the CNS itself. Between the stimulation of the cellular immune system indicated by increased levels of neopterin and the severity of the disease seems to be a positive correlation.

Antigen-Presenting Cells↗

PubMedDate not supplied

[High frequency oscillatory ventilation of infants with severe respiratory disorders: possibilities, risks and limits].

By pediatricians the high frequency oscillatory ventilation (HFOV) is used almost only in the neonatal period. We report on the administration of HFOV in infants with pulmonary insufficiency after failure of conventional ventilatory support. 6 infants (aged 2-7 months, all former preterm babies) were referred to our hospital due to severe pneumonia after unsuccessful conservative management. Indications for HFOV were hypoxia (mean paO2 41.8 mm Hg with FiO2 = 0.95 and mean airway pressure = 16.6 cm H2O) and/or air leak syndrome. In all cases a sufficient oxygenation could be achieved by HFOV, followed then by stepwise reduction of FiO2 and MAP. The air leaks receded. After 12-178 h on HFOV a successful switchback to conventional ventilatory support (at FiO2 = 0.48 and MAP < 12 cm H2O) was possible, all infants were extubated 6-15 days later. Possible risks of HFOV are air leaks, a necrotizing tracheobronchitis and hemodynamic changes due to compression of the heart and great vessels. With the at the moment in Germany available oscillatory ventilators HFOV as a rescue therapy must be limited for infants with a body weight below 5-6 kg.

Female↗

PubMedDate not supplied

Severe hepatotoxicity during valproate therapy: an update and report of eight new fatalities.

Since our last report on valproate (VPA)-related hepatotoxicity in 1988, 8 other children have died of VPA-associated liver failure in Germany and Switzerland. We compared the clinical course of these children with that of 6 children with a reversible outcome of severe hepatotoxicity related to VPA. Thirty-five percent of patients with fatal liver failure were normally developed, 23.5% were receiving VPA monotherapy, and 35.3% were aged < or = 2 years. The initial clinical symptoms of VPA-related hepatotoxicity were nausea, vomiting, apathy or coma, and increasing seizures in more than 50% of patients, in combination with febrile infections at onset of symptoms. As compared with the series of German patients reported in 1988, one third of the fatalities occurred after the first 6 months of therapy as compared with 6% in the 1988 series. Clinical symptoms and laboratory findings were the same in patients with reversible and with fatal outcome. Early or immediate withdrawal of VPA after the first signs of VPA-associated hepatotoxicity may be responsible for the increased number of children who recovered after VPA-related severe liver failure. The pathogenesis of liver failure during VPA treatment remains unknown; metabolic defects and cofactors such as polypharmacy or infections have become increasingly likely to contribute by depleting intracellular CoA. Worldwide, 132 patients have died of VPA-associated liver failure and/or pancreatitis. Because a group at risk for fatalities with VPA cannot be defined precisely, patients treated with VPA and their families must be made well aware of the clinical symptoms of hepatotoxicity such as apathy, vomiting, or increased seizure frequency, especially in the presence of febrile infections. Laboratory tests and clinical controls during the first 6 months of therapy should not be neglected.

Adult↗