Corticosteroid therapy does not prevent nephritis in Henoch-Schönlein purpura

Nephritis occurs in 20%–50% of children with Henoch-Schönlein purpura (HSP), and the onset of renal involvement may be delayed for weeks or months in a substantial proportion of patients. The present study was performed to determine whether corticosteroid therapy was effective in preventing delayed nephritis in children with HSP. The medical records of 69 children with HSP were reviewed. Nineteen patients had acute nephritis occurring from 1–12 days after the onset of other signs and symptoms. The remaining 50 patients had no evidence of acute renal involvement. Of these 50 patients, 20 were treated during the acute phase of the illness with corticosteroids, while 30 never received corticosteroid therapy. Delayed nephritis (>3 weeks following an initial normal urinalysis) occurred in 4 of 20 (20%) patients who received prior corticosteroid treatment, and in 6 of 30 (20%) patients who were not treated. These results indicate that early corticosteroid therapy does not prevent delayed nephritis in children with HSP.     

A simplified method for detecting cytomegalovirus by polymerase chain reaction from histologic sections of small biopsies.

Using a simplified procedure, we have extracted DNA from unstained paraffin sections of needle biopsies of kidney and liver transplants and identified the presence of CMV using the polymerase chain reaction. This method utilizes oligonucleotide primers for two genes shown to be specific for cytomegalovirus (CMV) as well as an internal control gene (hemoglobin) in a single reaction. Utilizing nested PCR amplification with agarose gel electrophoresis, CMV can be detected without radioisotopes to a level of sensitivity equivalent to one one-hundredth of a cytomegalic virocyte per cm2 of a 3-microM paraffin section. This method is applicable to situations where only scarce paraffin-embedded tissue is available.     

Micro1-opioid antagonist naloxonazine alters ethanol discrimination and consumption.

The endogenous opioid system is implicated in excessive ethanol-drinking behavior. However, the role of individual opioid receptor subtypes in the mechanism underlying excessive ethanol-drinking behavior is not yet well understood. Therefore, we investigated the ability of a selective micro1-opioid antagonist, naloxonazine, to modulate ethanol-drinking behavior and ethanol discrimination in a rat model with the use of ethanol self-administration and drug discrimination paradigms. The effects of naloxonazine (0.001-10 mg/kg) on ethanol intake were examined in Sprague-Dawley rats under conditions of limited access to 10% (wt./vol.) ethanol and ad libitum access to food and water. Pretreatment with high doses of naloxonazine (1-10 mg/kg) significantly reduced ethanol consumption. When the effects of naloxonazine on food intake in free-feeding male rats were examined, naloxonazine (1.8-10 mg/kg) significantly suppressed 24-h food intake. Another group of rats was trained to discriminate ethanol (1.25 g/kg, i.p.) from saline on a fixed-ratio schedule (FR 10), and ethanol dose-response tests were conducted once rats had acquired ethanol-saline discrimination. Injections were given 15 min before ethanol dose-response tests were conducted, and after characterization of the ethanol dose-response curve, the effects of naloxonazine on ethanol discrimination were assessed by administering naloxonazine (0.001-10 mg/kg, i.p.) 15 min before ethanol administration. Treatment with naloxonazine (0.001-1.8 mg/kg, i.p.) before the ED(100) dose of ethanol partially antagonized the discriminative stimulus of ethanol without having any effect on the response rate. The results support the suggestion of involvement of micro1-opioid receptors in the discriminative effects of ethanol and ethanol-drinking behavior.     

Short-term lack of cerebral perfusion with good outcome. Advantages of early intracranial pressure monitoring

A 21-year-old man was injured by a tailboard of a truck. He suffered a severe head injury with bilateral depressed skull fractures necessitating surgical decompression. On admission to the hospital the patient showed bending to pain stimuli (Glasgow Coma Score 5). Anisocoria was noticed from the beginning. Initial intracranial pressure (ICP), measured 3 hours after injury, was 30 mm Hg, and the cerebral perfusion pressure (CPP) was 70 mm Hg. During surgical elevation of the skull fracture on the right side an unexplainable rise of ICP to values of 100 mm Hg occurred, which corresponded to the mean arterial blood pressure (MAP). At the same time both pupils were dilated and fixed indicating a lack of cerebral perfusion. Due to immediate trephination of the opposite side, the ICP was lowered to values below 20 mm Hg, and sufficient cerebral perfusion (above 50 mm Hg) was regained. The patient showed a good recovery and was transferred to a rehabilitation center 5 weeks after injury.This case report emphasizes the importance of early and continuous intracranial pressure monitoring for adequate therapy in neurosurgical emergencies.