Tuberculous meningitis in Denmark: a review of 50 cases

<p>Abstract</p> <p>Background</p> <p>Tuberculous meningitis is the most severe manifestation of extrapulmonary tuberculosis with a high mortality rate and a high rate of sequelae among survivors. The aim of this study is to assess the current epidemiology, clinical features, diagnostic procedures, treatment and outcome in patients with tuberculous meningitis in Denmark, a country with a low tuberculosis incidence.</p> <p>Methods</p> <p>A nationwide retrospective study was conducted, comprising all patients notified with tuberculous meningitis (TBM) in Denmark from 2000-2008. Medical records were reviewed using a standardised protocol.</p> <p>Results</p> <p>Fifty patients, including 12 paediatric patients, were identified. 78% of the patients were immigrants from countries of high tuberculosis endemicity. 64% of all patients had a pre-existing immunosuppressive condition; 10% were HIV positive, 48% were HIV seronegative and 42% had an unknown HIV status. Median symptom duration before admission was 14 days in the Danish patient population and 20 days in the immigrant group. Biochemical analysis of cerebrospinal fluid (CSF) samples revealed pleocytosis in 90% with lymphocyte predominance in 66%. Protein levels were elevated in 86%. The most common findings on neuro-radiological imaging were basal meningeal enhancement, tuberculomas and hydrocephalus. Lumbar puncture was performed on 42 patients; 31 of these specimens (74%) had a positive CSF culture for mycobacteria and 9.5% were smear positive for acid-fast bacilli. The overall mortality rate was 19% and 48% of the remaining patients had neurological sequelae of varying degree.</p> <p>Conclusion</p> <p>TBM is a rare but severe manifestation of extrapulmonary TB in Denmark. The clinician must be prepared to treat empirically if the suspicion of TBM has arisen to improve treatment outcome.</p

Second thoughts about implementing routine screening of cancer patients for distress

Recommendations for routine screening of cancer patients for distress lack evidence that screening improves patient outcomes. Settings contemplating screening should consider other options for using the same resources. This article reviews evidence relevant to decision making and calls attention to limits in using screening instruments cross-culturally and for triaging patients for receipt of services. Whether screening is the best option depends on the patient population, culture, and health system

Brain activity and fatigue during prolonged exercise in the heat

The published version of this article can be viewed at the link below.We hypothesized that fatigue due to hyperthermia during prolonged exercise in the heat is in part related to alterations in frontal cortical brain activity. The electroencephalographic activity (EEG) of the frontal cortex of the brain was measured in seven cyclists [maximal O2 uptake ([(V)\dot]O2maxVO2max ) 4.8-0.1 (SE) l min-1] cycling at 60% [(V)\dot]O2maxVO2max in a hot (H, 42°C) and a cool (C, 19°C) environment. Fast Fourier transformation of the EEG was used to obtain power spectrum areas in the ! (8-13 Hz) and # (13-30 Hz) frequencies. The ratio !/# was calculated as an index of arousal level; an elevated !/# index reflects suppressed arousal. In H, subjects fatigued after 34.4-1.4 min coinciding with an oesophageal temperature (Toes) of 39.8-0.1°C, an almost maximal heart rate (HR 192-3 beats·min-1), a rating of perceived exertion (RPE) of 19.0-0.8 and significantly elevated !/# index (188-71% of the value after 2 min of exercise; P<0.05). In C, subjects cycled for a similar period while Toes was below 38°C, HR and RPE were low, and the !/# index was not significantly elevated (59-27% of 2 min value; P=NS). Increases in the !/# index were strongly correlated to increases in Toes (r2=0.98; P=0.0001).This study belongs to a series of studies that were supported by grants from Team Denmark

Aprotinin inhibits the contact, neutrophil, and platelet activation systems during simulated extracorporeal perfusion

Aprotinin reduces blood loss after cardiac operations and decreases the bleeding time. The mechanism of action of aprotinin that produces these effects is not clear. During simulated extracorporeal circulation the contact and complement systems, platelets, and neutrophils are activated. We investigated the effect of aprotinin on kallikrein-C1̄-inhibitor complex and C1̄-C1̄-inhibitor complex formation, neutrophil degranulation, and platelet release and aggregation during simulated extracorporeal circulation. Fresh heparinized human blood was recirculated at 37° C for 2 hours in a spiral coil membrane oxygenator-roller pump perfusion circuit. Changes in platelet count, leukocyte count, platelet response to adenosine diphosphate, and plasma levels of β-thromboglobulin, kallikrein-C1̄-inhibitor complexes, C1̄-C1̄-inhibitor complexes, and neutrophil elastase were measured before and at 5, 30, 60, and 120 minutes of recirculation at 0, 0.015, 0.03, 0.06, and 0.12 mg/ml doses of aprotinin. Platelet counts decreased to 36% ± 12% of control values at 5 minutes and increased to 56% ± 13% at 120 minutes without aprotinin. Aprotinin did not affect platelet counts, but it did prevent the decrease in sensitivity of platelets to adenosine diphosphate and it attenuated β-thromboglobulin release. In the absence of aprotinin, kallikrein-C1̄-inhibitor and C1̄-C1̄-inhibitor complexes increased progressively to 0.53 ± 0.14 U/ml and 2.38 ± 0.33 U/ml, respectively, at 120 minutes. Kallikrein-C1̄-inhibitor complexes were completely inhibited and C1̄-C1β-inhibitor complexes were partially inhibited at aprotinin concentrations of 0.03 mg/ml or greater. Release of neutrophil elastase was partially but not completely inhibited at the highest dose of aprotinin and was 50% inhibited at a dose of 0.03 mg/ml. Because activation of the fibrinolytic system does not occur in this system, the changes were independent of the inhibition of plasmin. We conclude that aprotinin in high doses completely inhibited kallikrein-induced activation of neutrophils and partially inhibited complement-induced activation. Aprotinin did not directly affect platelet adhesion or aggregation, but it indirectly preserved platelet sensitivity to agonists and also attenuated release of α-granule contents. The data indicate that in the presence of aprotinin platelet function was partially preserved, kallikrein production was totally inhibited, complement activation was partially inhibited, and neutrophil release was partially inhibited, thus attenuating the 'whole body inflammatory response' associated with cardiopulmonary bypass

Absorption of mercuric chloride and mercuric sulphide and their possible effects on tissue glutathione in mice

10.1007/BF01699416Bulletin of Environmental Contamination and Toxicology422307-314BECT