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J P Ungerer

Publications and source records attributed to J P Ungerer.

15 recordsLinked to original sources
PubMed2001

Significance of cerebrospinal fluid adenosine deaminase isoenzymes in tuberculous (TB) meningitis.

Adenosine deaminase (ADA) exists as two isoenzymes, ADA(1) and ADA(2). It appears that the ADA(2) isoenzyme originates mainly from monocytes and macrophages. In tuberculous pleural effusions most of the ADA activity consists of ADA(2). The aim of this prospective study was to analyse ADA isoenzymes in the CSF of patients with meningitis to investigate whether the expected rise of the ADA(2) isoenzyme would occur in tuberculous meningitis. ADA isoenzyme analysis was performed on the CSF of 15 patients with tuberculous and 11 patients with bacterial meningitis by an automated kinetic enzyme coupled assay in the presence and absence of a specific ADA inhibitor. The ratio of ADA(2)/ADA(Total) was > 0.8 in 14/15 patients with tuberculous meningitis. In bacterial meningitis the ratio was > or =0.8 in 10/11 patients. The ADA(2) isoenzyme is the major contributor to increased ADA activity in the CSF of patients with tuberculous meningitis, probably reflecting the monocyte-macrophage origin of the ADA.

Adenosine Deaminase↗
PubMed1999

Elevated adenosine deaminase activity in patients with HIV and tuberculous peritonitis.

OBJECTIVE: To evaluate the diagnostic potential of the ADA(T), ADA isoenzymes (ADA1 and ADA2) and the interferon-gamma (IFN-gamma) test in HIV-seropositive patients with tuberculous peritonitis. METHODS: Ascitic ADA(T), ADA1, ADA2 and IFN-gamma were prospectively evaluated in HIV-seronegative patients with tuberculous peritonitis (n = 17), HIV-seropositive patients with tuberculous peritonitis (n = 6) and in patients with cirrhosis (n = 22) and malignancy (n = 5). RESULTS: ADA(T) and ADA2 isoenzyme activities of HIV-seronegative (ADA(T) = 109 U/l; ADA2 = 94 U/l) and HIV-seropositive (ADA(T) = 109.5 U/l; ADA2 = 95.5 U/l) patients with tuberculous peritonitis, respectively, were significantly different (P < 0.001) from patients with cirrhosis (ADA(T) = 10.5 U/l; ADA2 = 8 U/l) and malignancy (ADA(T) = 13 U/l; ADA2 = 11 U/l). There was no significant difference in ADA(T) and ADA2 activities between HIV-seropositive and seronegative patients with tuberculous peritonitis. There was no significant correlation between ADA, its isoenzymes and IFN-gamma. CONCLUSIONS: The diagnosis of tuberculous peritonitis can be made by a sensitive, relatively non-invasive procedure in both HIV-seronegative and seropositive patients with minimal risk to the patient and the investigator. The diagnostic value of ADA(T) is not enhanced by measuring ADA isoenzymes or IFN-gamma.

AIDS-Related Opportunistic Infections↗
PubMed1996

Adenosine deaminase isoenzymes in typhoid fever.

The activity of serum adenosine deaminase and its isoenzymes (ADA1 and ADA2) was measured in the sera of 55 patients with clinically diagnosed typhoid fever, 46 of whom were seropositive for Salmonella typhi infection. At presentation 95% of the serologically positive patients had increased serum adenosine deaminase activity. The increase in activity was greater than that of other frequently measured enzymes. Isoenzyme ADA2 accounted for 84% of the activity, indicating a monocyte/macrophage origin. Results show that in patients with typhoid fever, serum adenosine deaminase, particularly its isoenzyme ADA2, may be regarded as a marker for monocyte/macrophage activation and could be valuable in diagnosis.

Adenosine Deaminase↗
PubMed1994

Significance of adenosine deaminase activity and its isoenzymes in tuberculous effusions.

Adenosine deaminase (ADA) activity is increased in effusions caused by certain clinical conditions including tuberculosis and bacterial infections. In this study, the ADA isoenzyme patterns in tuberculous and parainfective effusions were investigated to determine the isoenzyme responsible for this increase in activity. Fifty-one tuberculous effusions and six parainfective effusions were investigated. All effusions had increased ADA activity (median values of 126 and 127 units/L, respectively). In the tuberculous effusions, ADA2 isoenzyme was found to be primarily responsible for total activity, with a median contribution of 88 percent. The ADA1 (both ADA1m and ADA1c isoenzymes) was the major isoenzyme in the parainfective effusions with a median contribution of 70 percent. The ADA2 isoenzyme activity most likely reflects monocyte-macrophage turnover or activity, while ADA1 probably originates from lymphocytes or neutrophils. It is therefore essential to determine the isoenzyme profile when interpreting ADA activity levels in effusions. The measurement of the individual isoenzymes will enhance the diagnostic utility of ADA activity determinations in pleural effusions.

Adenosine Deaminase↗
PubMed1993

An enzymatic assay of inorganic phosphate in serum using nucleoside phosphorylase and xanthine oxidase.

We have developed a new enzymatic assay for the determination of inorganic phosphate (Pi) in serum, using nucleoside phosphorylase (NP) and xanthine oxidase (XOD). Pi and inosine react to form hypoxanthine and ribose-1-phosphate. The hypoxanthine is oxidized to xanthine, which is further oxidized to uric acid. In these two reactions 2,6-dichlorophenol-indophenol (DCIP) is reduced to a colourless compound and the decrease in colour is measured spectrophotometrically at 600 nm. The assay is automated with an RA-XT analyser. The precision of the automated assay is acceptable (C.V. < 3.5%) and results are accurate and linear across a range of values from 0.2-2.5 mmol/l. The assay correlates well with molybdate methods carried out on SMAC III and RA-XT analysers (r values 0.99 and 0.98, respectively), and seems to be less prone to non-specific sample interference than the usual RA-XT method. The enzymatic assay described seems to be suitable for the routine determination of serum Pi.

Humans↗
PubMed1993

Kinetic determination of serum adenosine deaminase.

A new kinetic method for the determination of serum adenosine deaminase (EC 3.5.4.4) is described, with adenosine as the substrate and nucleoside phosphorylase and xanthine oxidase as the reaction enzymes. Inosine is produced, which is converted to hypoxanthine. The hypoxanthine is oxidized to xanthine, which is further oxidized to uric acid. In these two reactions, blue 2,6-dichlorophenolindophenol is reduced to a colorless compound and the decrease in color is measured spectrophotometrically at 606 nm. The assay was automated by using a Cobas Mira analyzer. The automated assay had a CV of < 7%, and the calibration curve was linear from 10 to 120 U/L. The assay correlates well with an established method, based on detection of liberated NH3 with Berthelot's reaction. The reference interval (mean +/- 2 SD) was 14-34 U/L (mean 24 U/L, n = 84). The enzymatic method described is easily automated and seems to be suitable for the routine determination of adenosine deaminase in serum.

2,6-Dichloroindophenol↗
PubMed1993

Determination of the functioning of autotransplanted parathyroid tissue in muscle.

Twenty dialysis and renal transplant patients with parathyroid hyperplasia underwent a total parathyroidectomy and an autotransplantation in forearm muscle. Twelve patients were available for investigation of the function of the transplanted parathyroid tissue. Differential studies of the two arms revealed functioning of the transplanted tissue in all cases. This was more readily demonstrated by determining the intact hormone in both arms.

Calcium↗
PubMed1992

Using changes in attributable risk to predict long-term efficacy of simvastatin treatment.

It is a common perception that coronary heart disease (CHD) deaths will decline by 2% for every 1% decrease in serum total cholesterol (TC). We investigated the changes in serum TC concentrations obtained with simvastatin, an inhibitor of hydroxymethylglutaryl-CoA reductase, in 70 hypercholesterolemic subjects. Although simvastatin reduced serum TC concentrations by 30% after 6 months, calculations from age- and risk-related TC quintiles show that the absolute difference in attributable CHD deaths would be just > 1%. These results are reminiscent of the experience from several large prospective primary drug trials that demonstrated impressive relative benefit ratios but much smaller absolute differences (< 2%) in CHD endpoints between the treated and untreated groups. This epidemiologically based approach of assessing efficacy and potential long-term benefit of a lipid-lowering drug may be more appropriate and potentially less misleading than just the percentage change of TC (or other lipoproteins) so frequently reported in short-term drug trials.

Adult↗
PubMed1992

Serum adenosine deaminase: isoenzymes and diagnostic application.

Human adenosine deaminase (ADA; EC 3.5.4.4) consists of three isoenzymes: ADA1, ADA1+CP, and ADA2. We developed an electrophoretic technique to distinguish between these three isoenzymes. The isoenzyme pattern was studied in tissue and cell homogenates, as well as in serum from normal subjects and from patients with increased serum ADA who had either hepatitis, infectious mononucleosis, tuberculosis, pneumonia, rheumatoid arthritis, or acute lymphoblastic leukemia (ALL). The highest ADA activity was found in lymphocytes and monocytes. ADA2 could be detected only in monocytes (18% of total ADA activity). It was also the predominant isoenzyme in the sera of controls and all disease groups, except for ALL--the only condition evaluated that is not of an inflammatory nature. We conclude that serum ADA reflects monocyte/macrophage activity or turnover in most diseases studied. The exception is ALL, where serum ADA most probably originates from lymphocyte precursors.

Adenosine Deaminase↗
PubMed1991

Ethnic immunity to coronary heart disease?

Dietary fat intake is often regarded as a major determinant of coronary heart disease (CHD) rate and it has been deemed unnecessary to invoke racial or other factors to explain the differences in CHD rates among different ethnic groups. Despite a high prevalence of CHD risk factors such as hypertension, obesity, and smoking, CHD remains a rarity in westernized black Africans. Cord blood total cholesterol (TC), low density lipoprotein cholesterol (LDLC) and apolipoprotein B (apo B) levels were measured and found to be respectively 12.1%, 18.3% and 22.4% lower in black neonates when compared to white neonates. These differences were again studied in a group of young black African males and a comparable group of age-matched whites who had been exposed to the same environment and western diet for at least 2 years. Although the body mass indices and serum albumin concentrations in the adult males were not significantly different, serum levels of TC, LDLC and apo B were 10.7%, 18.7% and 39.7% lower in the blacks, respectively. Furthermore, high density lipoprotein cholesterol (HDLC) and Apolipoprotein AI were 20.2% and 9.5% higher, homocysteine 45.6% lower and coagulation factor VII 26.6% lower in the adult black Africans. It is concluded that blacks are biochemically less responsive to an atherogenic diet than whites and these differences are already present at birth.

Adult↗
PubMed1990

Discordance between measured and calculated total carbon dioxide.

Recent studies on the agreement and correlation between measured and calculated total CO2 (TCO2) have yielded conflicting results. Pre-analytical variation could have been partially responsible. While keeping such variables at an absolute minimum, we found excellent correlation (r = 0.98) in 88 samples, with only a small variation in agreement between measured and calculated TCO2 values (SD = 1.1 mmol/L), which could be a function of variation in apparent pK (pK'). A subsequent evaluation of 913 consecutive samples, routinely analyzed, yielded similar results. These results suggest that some of the discrepancies reported in the literature could be ascribable to differences in sample types and sample handling. Rigid control of pre-analytical procedures is therefore a prerequisite in studies on this topic. The two methods were found to agree over a wide range of values, such that either of them could be used to evaluate clinical acid-base status accurately.

Acid-Base Equilibrium↗
PubMed1988

Molecular forms of adenosine deaminase in pleural effusions.

The molecular forms of adenosine deaminase (ADA) were studied in pleural effusions with high ADA activity. The molecular forms were separated by polyacrylamide gel electrophoresis (PAGE), and the molecular masses estimated by gel filtration. Effusions investigated were: tuberculosis (TB) (20 cases), lymphoma (3 cases), chronic myelogenous leukemia (1 case) and empyema (6 cases). Two ADA forms were identified, a small form (Smf-ADA) and a large form (Lmf-ADA). Without exception, the tuberculous effusions have shown only Lmf-ADA. All the other effusions contained both forms, the Smf-ADA being predominant. This was also the ADA pattern seen in normal lymphocytes. These findings may indicate different mechanisms of ADA release or origins of ADA in the various effusions. The Lmf-ADA may be secreted by activated T cells in TB, which would confirm the notion that ADA activity reflects cellular immunity. In contrast, in the nontuberculous cases the ADA probably leaked from damaged lymphocytes or neutrophils, hence the reflection of the cellular ADA pattern. The PAGE pattern may also be of value in distinguishing between TB and these other causes of high pleural fluid ADA.

Adenosine Deaminase↗