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Biomedical subjects

K Dalhoff

Publications and source records attributed to K Dalhoff.

At least 109 records · Page 6Linked to original sources

[Generalized nocardiosis with meningoencephalitis in a nonimmunosuppressed female patient].

Four weeks after an attack of pneumonia of unknown aetiology a 40-year-old woman was hospitalized because of a nonpurulent, predominantly basal meningoencephalitis and infratentorial abscesses. She had dysarthria, mild right-sided motor hemiparesis and central paresis affecting the 7th cranial nerve. An area of fluctuating resistance, about 3 cm in diameter, was noticed over the left thigh. Serology indicated inflammatory disease, but there was no immunodeficiency. The CSF showed lymphocytic pleocytosis with mild protein increase but no evidence of infective agent. As tubercular meningitis was suspected she was treated with rifampicin (300 mg i.v. twice daily), isoniazid (300 mg i.v. once daily), streptomycin (800 mg i.m. once daily), cefotaxime (2.0 g i.v. three times daily), fluconazole (200 mg i.v. once daily) and dexamethasone (16-8-8 mg i.v.). She suddenly died two days after admission, probably as the result of central regulatory failure. Generalized nocardiosis involving lung, subcutaneous tissue and brain was revealed at autopsy. Although nocardiosis occurs predominantly in patients under immunosuppression, this infection should be considered in the differential diagnosis of treatment-resistant pneumonia and meningoencephalitis without obvious predisposition.

Adult↗

Simultaneous measurements of glutathione and activated sulphate (PAPS) synthesis rates and the effects of selective inhibition of glutathione conjugation or sulphation of acetaminophen.

The aim of the present study was to examine the effects of the hepatotoxic drug acetaminophen (AA) on the synthesis rates of glutathione (GSH), activated sulphate (PAPS; adenosine 3'-phosphate 5'-phosphosulphate) and the AA metabolites AA-GSH and AA-sulphate after selective inhibition of GSH biosynthesis or sulphation in isolated rat hepatocytes. Selective inhibition of the two interdependent metabolic pathways was accomplished by buthionine sulphoximine (BSO) and 2,6-dichloro-4-nitrophenol (DCNP). The synthesis rates of GSH and PAPS were determined simultaneously by a previously described method based on trapping of radioactivity (35S) in the pre-labelled GSH and PAPS pools. Pre-incubation with 10 mM BSO for 30 min depleted GSH by 38% (P < 0.05) and PAPS by 27% (P < 0.05). The depletion resulted in increased PAPS synthesis at low, non-toxic [5-19 nmol/(10(6) cells.min)] (P < 0.05) and at high, toxic [7-30 nmol/10(6) cells.min)] (P < 0.05) AA concentrations. In both cases sulphur is diverted from GSH biosynthesis to sulphoxidation and PAPS synthesis, thereby maintaining the PAPS pool and preserving the sulphation capacity. This corresponds to the finding that AA sulphation was unaffected by BSO irrespective of AA concentration [6 vs 5 and 20 vs 17 nmol/(10(6) cells.hr), respectively]. Even though the GSH synthesis was halved after BSO pre-incubation, the GSH conjugating capacity of AA was well preserved. Incubation with 200 microM DCNP and 5 mM AA diminished PAPS synthesis from 24 to 10 nmol/(10(6) cells.min) (P < 0.02) and reduced AA-sulphate synthesis by 67% compared to experiments without DCNP incubation [4.8 vs 14.7 nmol/(10(6) cells.hr)] (P < 0.05). GSH and AA-GSH synthesis rates did not change compared to control experiments in which sulphation was not inhibited [1165 vs 1487 nmol/(10(6) cells.min), respectively] and [1.7 vs 1.7 nmol/(10(6) cells.hr), respectively]. This indicates that increased sulphur availability due to decreased PAPS synthesis is unable to raise the cysteine pool and stimulate the gamma-glutamyl cycle and GSH synthesis.

Acetaminophen↗

[Extrathoracic prolapse of the pulmonary parenchyma after a bout of coughing with spontaneous serial rib fractures].

A 54-year-old man with an feverish infection of the lower respiratory tract developed severe pain in the lateral and basal part of the left thorax after a severe coughing bout. A haematoma occurred at the site and it looked as though tissue evaginated at that spot on coughing and pressing. The clinical diagnosis was pneumonia and abnormal mobility of the eighth to tenth rib on the left with crepitations. The chest radiograph demonstrated fractures of these ribs and extrathoracic sickle-shaped collection of air in the left laterobasal area. Computed tomography additionally showed prolapse of pulmonary tissue on pressing. This was thus a case of "cough fracture", complicated by herniation of lung tissue. There was no evidence of incarceration of lung tissue and, as the patient was very obese, surgery was not indicated. Symptoms and signs of infection regressed on symptomatic and antibiotic treatment. The rib fractures healed as pseudoarthroses. Lung tissue prolapse on pressing was still present 3 months later.

Cough↗

Inhibition of acetaminophen oxidation by cimetidine and the effects on glutathione and activated sulphate synthesis rates.

The aim of the present study was to examine the effects of the hepatotoxic drug, acetaminophen, on the synthesis rates of glutathione, activated sulphate (PAPS, adenosine 3'-phosphate 5'-phosphosulphate) and the acetaminophen metabolites, acetaminophen-glutathione and acetaminophen-sulphate after inhibition of cytochrome P-450 drug oxidation by cimetidine in isolated rat hepatocytes. The synthesis rates of glutathione and PAPS were determined simultaneously by an established method based on trapping of radioactivity (35S) in the prelabelled glutathione and PAPS pools. Preincubation of the hepatocytes with 60 micrograms/ml cimetidine for 30 min. did not affect PAPS (1.71 versus 1.78 nmol/10(6) cells) nor glutathione concentration (16.0 versus 16.4 nmol/10(6) cells). The subsequent incubation with 5 mM acetaminophen resulted in decreased PAPS synthesis in the cimetidine treated cells [0.79 x 10(3) versus 0.92 x 10(3) nmol/(10(6) cells.hr)] (P < 0.05). There was no difference in PAPS concentration or acetaminophen-sulphate synthesis [1.73 versus 1.79 nmol/10(6) cells and 13.0 versus 12.9 nmol/(10(6) cells.hr), respectively]. Decreased PAPS synthesis may be related to decreased ATP supply or may be the result of a feed-back regulation due to diversion of sulphur from glutathione synthesis to sulfoxidation. The glutathione synthesis was not significantly affected by cimetidine treatment [57 x 10(3) versus 27 x 10(3) nmol/(10(6) cells.hr)]. As expected acetaminophen-glutathione synthesis decreased by 38% [1.66 versus 2.68 nmol/(10(6) cells.hr)] (P < 0.01). Also the glutathione concentration was lower in cimetidine treated cells [15.2 versus 15.9 nmol/10(6) cells] (P < 0.05). We have previously shown that glutathione synthesis was reduced if substrate availability decreased (acetaminophen concentration lowered).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetaminophen↗

Intercellular adhesion molecule 1 (ICAM-1) in the pathogenesis of mononuclear cell alveolitis in pulmonary sarcoidosis.

BACKGROUND: Alveolitis in pulmonary sarcoidosis is characterised by an accumulation of highly activated macrophages and CD4+ lymphocytes in the alveolar compartment. The role of intercellular adhesion molecule 1 (ICAM-1) expression on alveolar cells has been studied in this context. METHODS: Using a sandwich ELISA technique, ICAM-1 expression on alveolar macrophages from 17 consecutive untreated patients with pulmonary sarcoidosis and six healthy normal volunteers was quantified. In addition, parameters of macrophage activation (tumour necrosis factor alpha (TNF alpha) and superoxide anion release) were evaluated. RESULTS: Significantly elevated expression could be demonstrated on alveolar macrophages from patients with pulmonary sarcoidosis compared with healthy controls (mean (SD) 0.74 (0.24) ELISA units (EU) v 0.46 (0.12) EU). On subdividing the patients into those with active and those with inactive disease, only the former showed increased ICAM-1 levels on alveolar macrophages (0.82 (0.27) EU) compared with control alveolar macrophages. No differences were detected in serum levels of soluble ICAM-1 between patients and controls. ICAM-1 expression on alveolar macrophages from patients with sarcoidosis correlated with the spontaneous release of TNF alpha but not with the release of the superoxide anion by the activated macrophages. There was no correlation with the percentage of lymphocytes or the absolute number of CD4+ cells in bronchoalveolar lavage fluid. CONCLUSIONS: Increased ICAM-1 surface expression on alveolar macrophages reflects disease activity in the pulmonary compartment. Considering the significance of adhesion molecules during antigen presentation and lymphocyte activation, ICAM-1 expression on alveolar macrophages may have an important role in the immune process of pulmonary sarcoidosis.

Adult↗

No net splanchnic release of glutathione in man during N-acetylcysteine infusion.

Glutathione and amino acid concentrations were measured in arterial and hepatic vein plasma in four healthy volunteers and two patients with cirrhosis. There was no significant splanchnic efflux of glutathione (95% confidence limits, -0.501 to 0.405 mumol/min). After infusion of N-acetylcysteine (NAC) in a high dose (150 mg/kg body weight primer plus 15 mg/(h x kg BW), corresponding to treatment of acetaminophen overdose, there was no change in the splanchnic glutathione efflux (95% confidence limits, -0.531 to 0.375 mumol/min). NAC increased hepatic plasma flow rate from 0.90 +/- 0.531 min-1 to 0.97 +/- 0.11 (mean +/- SEM; p < 0.05). The effects of NAC treatment on plasma amino acids corresponded to an increased load on hepatic metabolic N conversion and transamination among nonessential amino acids. Splanchnic uptake of serine, alanine, cystine, isoleucine, and phenylalanine increased after NAC compatible with stimulated hepatic glutathione synthesis. In contrast to the rat, plasma glutathione in man probably originates mainly from extrahepatic tissues.

Acetylcysteine↗

Drug metabolism and genetic polymorphism in subjects with previous halothane hepatitis.

To test the hypothesis that halothane hepatitis is caused by a combination of altered drug metabolism and an immunoallergic disposition, the metabolism of antipyrine, metronidazole, sparteine, phenytoin, and racemic R- and S-mephenytoin was investigated in seven subjects with previous halothane hepatitis. The HLA tissue types and the complement C3 phenotypes were also determined. The metabolism of antipyrine and metronidazole was within normal range in all subjects, and they were all fast or extensive metabolizers of sparteine, mephenytoin, and phenytoin. HLA tissue types were unremarkable. Five of the seven subjects had complement C3 phenotypes F or FS. In the general population phenotype S is the most common, but the difference in complement C3 phenotypes is not statistically significant (p = 0.07). We conclude, although in a limited number of patients, that subjects with previous halothane hepatitis do not appear to be different from controls with regard to drug metabolism and HLA tissue type. The possibility of a higher frequency of complement C3 phenotype F and FS needs further investigation.

Adult↗

Effects of cysteine and acetaminophen on the syntheses of glutathione and adenosine 3'-phosphate 5'-phosphosulfate in isolated rat hepatocytes.

The aim of the present study was to introduce and validate a radioactive tracer method in which adenosine 3'-phosphate 5'-phosphosulfate (PAPS) and glutathione (GSH) are measured simultaneously in isolated hepatocytes. PAPS and GSH are co-substrates in sulphation and GSH conjugation, and both are dependent on sulphur deriving from cysteine. The effect of cysteine on the syntheses was investigated at non-toxic and toxic concentrations of the hepatotoxic drug acetaminophen (AA). Administration of AA trapped radioactivity (35S) in the pre-labelled PAPS and GSH pools by formation of the metabolites, AA-sulphate and AA-GSH. Turnover rates were determined from the decline of AA-sulphate and AA-GSH specific activity. Syntheses of PAPS and GSH were calculated by multiplying the rates with the concentrations of the respective co-substrates. Increasing AA concentration from non-toxic to toxic levels resulted in increased median PAPS and GSH syntheses (8 to 11 and 311 to 2218 nmol/10(6) cells/min, respectively) (P less than 0.05). Addition of cysteine did not alter median PAPS synthesis (5 to 3 nmol/10(6) cells/min) but decreased median GSH synthesis (666 to 261 nmol/10(6) cells/min) (P less than 0.05) in experiments with non-toxic AA concentrations. In experiments with toxic AA concentrations opposite effects of cysteine were seen, i.e. median PAPS synthesis was reduced (3 to 2 nmol/10(6) cells/min) (P less than 0.05) while median GSH synthesis was unchanged (23 to 16 nmol/10(6) cells/min). The present method provides a tool in which two important detoxification pathways can be measured simultaneously and the data suggest that the two pathways are regulated by substrate availability.

Acetaminophen↗

[Oxygen radical formation in pulmonary sarcoidosis. The signs of early macrophage activation].

Oxygen radical formation of alveolar macrophages (by luminogenic substrate-intensified chemiluminescence) and the concentrations of phagocyte products myeloperoxidase, elastase and lactoferrin, as well as alpha-proteinase inhibitor and albumin were measured in bronchoalveolar lavage fluid of 28 patients with pulmonary sarcoidosis. There were 15 men and 13 women (mean age 41 [18-62] years), 10 of them with sarcoidosis I, 10 with clinically active sarcoidosis II and 8 with inactive sarcoidosis II. Six healthy persons served as controls. The purpose of the study was to demonstrate the extent of correlation between macrophage activity and stage of sarcoidosis. Patients in stage I had significantly higher luminescence (346 +/- 253 relative light units [RLU] per second) than the controls (117 +/- 29 RLU/s; P less than 0.02). But the difference between controls and patients in clinically active stage II (294 +/- 75 RLU/s) was not significant and the luminescence in patients with clinically inactive stage II was within normal range (119 +/- 33 RLU/s). The concentrations of proteins measured in the lavage fluid was increased, independent of the site of formation. These data indicate that in pulmonary sarcoidosis there exists, early and independent of stage, a marked activation of alveolar macrophages with increased production of oxygen radicals and a resulting increase in permeability of the alveolo-capillary membrane.

Adolescent↗

DNA polymorphism of HLA class II genes in primary biliary cirrhosis.

We investigated the DNA restriction fragment length polymorphism of the major histocompatibility complex class II genes: HLA-DRB, -DQA, -DQB, DPA, -DPB, the serologically defined HLA-A, B, C, DR antigens, and the primed lymphocyte typing defined HLA-DP antigens in 23 Danish patients with primary biliary cirrhosis (PBC) and in healthy Danes. The following genetic markers were found with increased frequencies in PBC: HLA-B8 (relative risk, RR = 2.4, P less than 0.05, 'corrected' P greater than 0.05), HLA-DR3 (RR = 3.4, P less than 0.01, 'corrected' P less than 0.05), the DRB3*01/02/03 (DRw52) associated DRB Bgl II 9.1 kilobase (kb) fragment (RR = 2.9; P less than 0.05, 'corrected' P greater than 0.05), the DQA1*0501 associated DQA Taq I 4.8 kb fragment (RR = 3.1; P less than 0.05, 'corrected' P greater than 0.05), the DQB1*0201 (DQw2) associated DQB Hin dIII 11.5 kb fragment (RR = 3.1; P less than 0.05, 'corrected' P greater than 0.05). No DNA fragments specific for DRB1*0301 (DR3) could be identified. The frequencies in PBC of other genetic markers including DRw8, DRB1*08, HLA-DP antigens, DPA, and DPB genes did not differ significantly from those in controls. The associations between PBC and B8, DR3, DQA1*0501, and DQB1*0201, which are frequently found together on the same haplotype, are at variance with recent reports on associations between PBC and Drw8. The discrepancy suggests that PBC is genetically heterogenous.

Genes, MHC Class II↗

Cerebrospinal fluid beta-2-microglobulin in adult patients with acute leukemia or lymphoma: a useful marker in early diagnosis and monitoring of CNS-involvement.

Beta-2-microglobulin (B2m) was measured in the cerebrospinal fluid (CSF) and serum from 18 adults with acute lymphoblastic leukemia, acute myeloblastic leukemia or lymphoma in order to detect early central nervous system (CNS) involvement or relapse. Six had CNS-involvement documented by neurologic symptoms and tumor cells in the CSF. Their CSF-B2m-concentrations were significantly higher before intrathecal chemotherapy than in those without this complication (P less than 0.01). During therapy CSF-B2m levels fell rapidly to normal values on repeated measurements. The study demonstrates that serial determination of CSF-B2m alone may be a useful and sensitive marker of CNS-dissemination in acute leukemia and malignant lymphoma. Using the criteria of CSF-B2m greater than 160 nmol/l as a positive diagnostic test the sensitivity of the test was 100%, the specificity was 76%. The same values for the CSF/serum-ratio greater than 1 were 75% and 64%, respectively.

Adult↗

Glutathione treatment of hepatocellular carcinoma.

This prospective study was undertaken to substantiate observations that glutathione (GSH) inhibits or reverses tumor growth in humans with hepatocellular carcinoma (HCC), a neoplasm with an extremely poor prognosis. Eight patients with biopsy-proven HCC not amenable to surgery were given 5 g of GSH daily from the time of diagnosis. Two patients withdrew shortly after receiving GSH due to intolerable side-effects. Of the six eligible patients, two had mildly advanced tumors and four moderately advanced tumors. At 1-2-month intervals the liver was CT and ultra-sound scanned to assess the growth status of the tumor (progression, stagnation or regression). All the patients, except a male with a fibrolamellar type of HCC, died within 1 year after diagnosis. Two women with moderately advanced tumors survived almost 1 year, tumor growth stopped or regressed and in one of the women an initially abnormal alfa-1-fetoprotein (AFP) returned to normal after GSH treatment. AFP remained normal throughout the treatment period in the other women. These observations indicate that GSH may have a sex-dependent effect on HCC. However, further studies involving more patients are required to pursue this hypothesis.

Adult↗

[Myeloperoxidase, lactoferrin and elastase in bronchoalveolar lavage and plasma in pneumonia].

Neutrophilic granulocytes in the lower respiratory tract are of decisive importance for the elimination of pathogenic germs in bacterial pneumonia. On the other hand, the liberation of phagocyte products (e.g. elastase) can result in tissue damage in the parenchyma of the lungs. For this reason, we determined in patients suffering from acute pneumonia (n = 21), in patients with acute pneumonia associated with immunosuppression (n = 12), in patients who had overcome their pneumonia (n = 9) and in controls (n = 17) in bronchoalveolar lavage (BALF) and in plasma, the concentration of the locally produced granulocyte products myeloperoxidase (MPO), lactoferrin (LF) and elastase-alpha 1 proteinase complex (ELA) as well as of the alpha 1 proteinase inhibitor (alpha 1 Pi) and alpha 2 proteinase inhibitor (alpha 2 Pi) via chemoluminescence immunoassay, and compared the same with the differential cell count in the BALF. The protein concentrations were referred to the albumin concentration (Alb) for standardisation. This concentration did not differ significantly between the various patients and control groups. The BALF concentration of ELA in the group with pneumonia (median: 86.3 micrograms/l or 8.5 micrograms/mg Alb) was about eight times higher than in the group of patients suffering from pneumonia with immunosuppression (median: 16 micrograms/l or 1.0 micrograms/l Alb, p less than 0.001) or in whom the pneumonia was no longer present (17.6 micrograms/l or 0.5 micrograms/mg), and approximately 40 times higher than in the control group (3 micrograms/l or 0.2 micrograms/mg, respectively). Similar results were obtained for LF (61 micrograms/mg Alb vs. 11.3; 16.8 and 5.9 micrograms/mg; p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Pharmacokinetics of paroxetine in patients with cirrhosis.

In a 14-day multiple-dose study the pharmacokinetics of paroxetine was investigated in 12 patients with alcoholic cirrhosis and in 6 subjects without liver disease. The dose of 20-30 mg paroxetine daily was adjusted to the reduction in liver function, as assessed by the galactose elimination capacity. Accordingly, all but two of the cirrhotic patients received 20 mg, while all six control subjects received 30 mg. Dose-corrected, trough drug concentration at steady state (CSSmin) and dose-corrected AUC24h were significantly higher in the patients with liver diseases than in the control subjects [3.4 vs 1.5 ng.ml-1 per mg paroxetine and 89 vs 43 h (ng).ml-1 per mg paroxetine]. The elimination t1/2 was prolonged [83 vs 36 h], but the difference was not statistically significant, and the cirrhotic patients were still able to clear almost all the paroxetine by metabolism. All but two patients with cirrhosis experienced nausea during the first two or three days after the first dose, while none of the controls had this symptom. The study showed slower elimination of paroxetine and consequently higher plasma levels in patients with cirrhosis, suggesting that in the latter the dose of paroxetine should be in the lower end of the therapeutic range.

Adult↗

Restriction fragment length polymorphism of two HLA-B-associated transcripts genes in five autoimmune diseases.

The restriction fragment length polymorphism of the two human HLA-B-associated transcripts (BATs) genes, BAT1 and BAT2, identifying polymorphic bands of 12, 8, 2.5, and 1.1 kb, and at 3.3, 2.7, 2.3, and 0.9 kb, respectively, was investigated in patients with primary biliary cirrhosis (PBC), systemic lupus erythematosus (SLE), pauciarticular juvenile rheumatoid arthritis (P-JRA), rheumatoid arthritis (RA), and primary Sjögren's syndrome (pSS), and in healthy Danes. The BAT2/RsaI 2.7-kb band fragment was more frequent in PBC, pSS, and SLE than in controls, but the p values did not reach significance when corrected for multiple comparisons. For pSS and SLE, the associations may be secondary to primary associations with HLA-B8 because the BAT2/RsaI 2.3-kb band, which is allelic to the BAT2/RsaI 2.7-kb band, is strongly negatively associated with HLA-B8 and HLA-DR3. The only significance obtained shows that the HLA-B8 frequency is increased in BAT2/RsaI 2.7-kb positive pSS patients as compared to the corresponding controls indicating that the HLA-B8 association may be strongest. No missing or extra DNA fragments were observed in the disease groups when compared with controls indicating that gross deletions or duplications of the BAT1 and BAT2 genes in the patients are unlikely. In conclusions, it cannot be excluded that the BAT2/RsaI 2.7-kb band may contribute to the susceptibility to PBC, pSS, and SLE.

Autoimmune Diseases↗

Acute ethanol administration reduces the antidote effect of N-acetylcysteine after acetaminophen overdose in mice.

1. The combined antidote effect of N-acetylcysteine and ethanol on the toxicity of acetaminophen was investigated. 2. Fed male mice were given acetaminophen i.p. (600 mg kg-1) and after 5 min in addition ethanol i.p. (0.2 ml, 19% v/v), N-acetylcysteine i.p. (1.2 g kg-1, 0.2 ml), N-acetylcysteine + ethanol i.p. (same doses as given individually) or saline i.p. (0.4 ml). Survival rates were determined after 24, 48, 72 and 96 h. 3. In the N-acetylcysteine group the survival rate was 85%. This rate was significantly reduced to 43% in the N-acetylcysteine + ethanol group (P = 0.0001). In the groups given ethanol or saline alone only 7% and 3%, respectively, survived 96 h. 4. The data suggest that the protective effect of N-acetylcysteine on acetaminophen-induced toxicity in fed mice is reduced by concomitant administration of ethanol. This may explain the clinical observation that ingestion of ethanol worsens the prognosis after acetaminophen intoxication.

Acetaminophen↗

Fractional excretion of beta-2-microglobulin in the urine of patients with normal or reduced renal function and hepatic coma.

The purpose of this prospective study was to evaluate beta-2-microglobulin (beta 2m) as a differential diagnostic indicator between hepatic nephropathy (HN) and acute tubulointerstitial nephropathy (ATIN) in patients with reduced renal function and hepatic coma, and to determine whether beta 2m excretion could be used as a marker of renal impairment before increased serum creatinine (S-Cr) concentration or decreased creatinine clearance (Cr-Cl). Finally, the use of beta 2m as a prognostic indicator was investigated. Eighteen patients in hepatic coma grade III-IV were entered in the study and were divided into two groups in accordance with their renal function (serum creatinine above/below 180 mumol/l). The fractional excretion of beta 2m (FE-beta 2m) was used to monitor beta 2m elimination. The study failed to show any distinction in FE-beta 2m between HN and ATIN patients, presumably owing to the small number of patients. FE-beta 2m could not predict the development of renal failure earlier than the increase in S-Cr or decrease in Cr-Cl. However, a few patients who survived paracetamol intoxication had increased FE-beta 2M in the beginning of the coma and normal S-Cr and Cr-Cl. Patients who died as a result of paracetamol intoxication had both abnormal FE-beta 2m and abnormal S-Cr and Cr-Cl, suggesting that if therapy had been initiated earlier, when only FE-beta 2m was affected, these patients might have survived. All patients who survived, except three paracetamol- and one aminoglycoside-intoxicated patient, had normal FE-beta 2m in the beginning of the coma.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetaminophen↗

[Bronchoscopic diagnosis of pneumonia with quantitative microbial count determination].

Micro-organism counts of bronchoalveolar lavage (BAL) and microbrush swabs were obtained from 40 immunocompetent (group A) and 23 immunosuppressed (group B) patients with nosocomial pneumonia, and a control group consisting of 40 patients with noninfectious pulmonary infiltrates. The sensitivity of BAL was high: 77.5% for group A and 85% for group B, while microbrush swabs gave many false-negative results. Microorganism counts were at or above 10(5) cfu/ml in 32 of 44 examinations (bacterial or mycotic pneumonia), but in only one case of the control group. Lower counts were obtained with localized infection and microorganisms difficult to culture (Aspergilla and Legionella). Granulocytosis in the lavage fluid was demonstrated in 38 of 41 patients with bacterial pneumonia and thus proved useful in the differential diagnosis. In 16 of 40 immunocompetent and 13 of 23 immunosuppressed patients with pneumonia the results were therapeutically of importance. Thus, invasive diagnosis is indicated especially in complicated or treatment-resistant nosocomial infections.

Adult↗