How do multimorbidity and lifestyle factors impact the perceived health of adults with intellectual disabilities?

BACKGROUND: Adults with intellectual disability (ID) have poorer physical and perceived health than the general population. Knowledge of perceived health predictors is both limited and important for guiding the development of preventive actions. The aims of this study were to investigate (1) the associations between perceived health and demographics, degree of ID, physical health conditions, and weight and physical activity level and (2) lifestyle factors and multimorbidity as predictors for perceived health adjusted for age, gender, and level of ID. METHOD: The North Health in Intellectual Disability study is a community based cross-sectional survey. The POMONA-15 health indicators were used. Univariate and multivariate logistic regression analyses with poor versus good health as the dependent variable were applied. RESULTS: The sample included 214 adults with a mean age 36.1 (SD 13.8) years; 56% were men, and 27% reported perceiving their health as poor. In univariate analyses, there were significant associations between poor health ratings and female gender, lower motor function, number of physical health conditions and several indicators of levels of physical activity. In the final adjusted model, female gender [odds ratio (OR) 2.4, P < 0.05], level of ID (OR 0.65, P < 0.05), numbers of physical health conditions (OR 1.6, P < 0.001) and lower motor function (OR 1.5 P < 0.05) were significant explanatory variables for poor perceived health, with a tendency to independently impact failure to achieve 30 min of physical activity daily (OR 2.0, P = 0.07). CONCLUSION: Adults with ID with female gender, reduced motor function and more physical health conditions are at increased risk of lower perceived health and should be given attention in health promoting interventions. A lack of physical activity tends to negatively influence perceived health.

[Can we rely on electronic reporting of laboratory results?]. / Kan vi stole på elektronisk meldingsformidling av laboratorieresultater?

BACKGROUND: Electronic result reporting from two laboratories to physicians in primary health care through electronic data interchange (EDI) has been used as a supplement to the printed reports. The aim of the study was to see if the quality of the electronic reporting could be improved so that the printed reporting could be cut out without any loss of data. MATERIAL AND METHODS: Staff members in 20 selected offices were interviewed and error messages on file in the computer systems were studied. RESULTS: During a period of four months, the laboratories sent 10,740 electronic messages to the selected offices. Error messages arose from 71 of these messages (0.7%). 49 of the errors were discovered and corrected by the staff, but 22 errors were not noticed, and the result reports were lost. INTERPRETATION: If electronic result reporting should become the only reporting routine, it would be necessary to change several routines both in the laboratories and in the physician's offices. Patients must be identified by using official identifiers. The physicians must control in the computer system that all requested results are received, and the programs used for controlling the messages before they are entered into the electronic patient journal, must be improved.

[Prostate-specific antigen. A new biological serum marker for prostatic adenocarcinoma]. / Prostataspesifikt antigen. En ny biologisk serummarkør ved adenokarsinom i prostata.

Prostate-specific antigen (PSA) was measured by polyclonal radioimmunoassay in 45 untreated patients with prostatic cancer and 14 patients with benign prostatic hyperplasia. Prostatic acid phosphatase (PAP) was determined in 35 patients with prostatic cancer and 14 patients with benign hyperplasia. Serum PSA was raised in 42 patients with cancer of the prostate, but only 14 of 35 patients showed increased serum levels of PAP. Half the patients with benign prostate hyperplasia had PSA greater than 4 micrograms/l and one third had PSA greater than 10 micrograms/l. PAP was slightly elevated in two patients with benign prostatic hyperplasia. Serum PSA increased with the clinical stage of prostatic cancer. However, preoperative levels of PSA were not sufficiently reliable to predict the final pathological stage for each individual patient. After radical prostatectomy for cancer confined to the prostate, serum PSA fell to an undetectable level.

Induction of cytosolic clofibroyl-CoA hydrolase activity in liver of rats treated with clofibrate.

Among subcellular fractions of liver homogenates of rats, the clofibroyl-CoA hydrolase activity is found mainly in the cytosolic fraction. It is here shown that the subcellular distribution of clofibroyl-CoA hydrolase appears to be different from the distribution of palmitoyl-CoA hydrolase activity. Thus, in contrast to the case with palmitoyl-CoA, no hydrolysis of clofibroyl-CoA was catalysed by the microsomal fraction. Furthermore, the hydrolysis of palmitoyl-CoA and clofibroyl-CoA in the cytosolic fraction seemed to be catalyzed by two different enzymes. Rats treated with clofibrate (0.3%, w/w) showed a significant increased clofibroyl-CoA hydrolase activity where the cytosolic hydrolase was increased 3.5-fold. Clofibrate administration also elevated the specific clofibroyl-CoA hydrolase activity by factors of 1.7 and 1.5 in the mitochondrial and the light-mitochondrial fractions, respectively. Thus, it is possible that clofibroyl-CoA hydrolase has also a multiorganelle localization.

Separation and measurement of clofibroyl coenzyme A and clofibric acid in rat liver after clofibrate adminstration by reversed-phase high-performance liquid chromatography with photodiode array detection.

A method to identify and quantitate clofibric acid and clofibroyl coenzyme A (CoA) products in rat liver was developed using reversed-phase high-performance liquid chromatography. The system was developed with baseline separation of clofibroyl-CoA from clofibric acid using isocratic elution, with a mobile phase consisting of 52% methanol and 28 mM potassium phosphate buffer (pH 4.2). With this high methanol concentration, the large amount of UV-absorbing materials present in the liver extracts were eluted earlier than the investigated compounds. Clofibroyl-CoA has a characteristic absorbance spectrum with distinct peaks at 260 and 230 nm, while clofibric acid showed only a distinct peak at 230 nm. Using an on-line photodiode array detector, the spectra could be recorded during analysis without interrupting the flow of the mobile phase. This spectral analysis identification possibilities and evaluation of the purity of the chromatographic peaks. In a perchloric extract of rat liver, the recovery of clofibric acid and clofibroyl-CoA added to the liver extract ranged from 70 to 80%. A linear relationship was observed between clofibric acid and clofibroyl-CoA concentration and the area of their peaks in the chromatogram. The detection limit of the method was lower than 5 pmol for both compounds when the absorbance was recorded at 230 nm. The method could be used without modification for the estimation of clofibroyl-CoA and clofibric acid in biological extracts.

Cerebrospinal fluid enzymes in neurological diseases.

The activities of adenylate kinase, creatine kinase and lactate dehydrogenase were measured in cerebrospinal fluid and serum from 127 patients admitted to the Department of Neurology. All cerebrospinal fluid samples with hemoglobin greater than 1 mg/l were excluded. Upper reference limits for the enzyme determinations were established, using samples from patients without objective criteria of organic involvement of the nervous system. High enzyme activities did not correlate to any particular group of diseases and were also found in patients without organic brain diseases. We conclude that determination of the three enzymes in cerebrospinal fluid is of limited value in the diagnosis of neurological diseases.

Changes in fatty acid composition of myelin cerebrosides after treatment of the developing rat with methylmercury chloride and diethylmercury.

Suckling rats were exposed to methylmercury chloride or diethylmercury in order to induce chronic sublethal intoxication during the period of active myelination. Doses of 5 mg Hg/kg body weight were injected every second day from 5-25 days of age. The rats were killed at 27-28 days of age, and the brains contained about 1 microgram Hg/g wet weight. No changes in brain weight, myelin content of proteins or phospholipids were found, whereas the cholesterol and galactolipid levels were slightly reduced. The most significant change observed was a decrease in the ratio between alpha-hydroxy fatty acid and the nonsubstituted fatty acid in the myelin cerebrosides. The biochemical changes were less pronounced in the animals given diethylmercury than in animals receiving methylmercury.