Validity and reliability of the Patient Activation Measure® (PAM®)-13 Malay version among patients with Metabolic Syndrome in primary care.

INTRODUCTION: The Patient Activation Measure (PAM) is one of the most extensively used, widely translated, and tested instruments worldwide in measuring patient activation levels in self-management. This study aimed to determine the validity and reliability of the PAM-13 Malay version among patients with Metabolic Syndrome (MetS) attending a primary care clinic. METHODS: This work is a cross-sectional validation study among patients with MetS attending a university primary care clinic in Selangor. The PAM-13 Malay version underwent a validation process and field testing. Psychometric properties were examined using principal component analysis (PCA) with varimax rotation, scree plot, Monte Carlo simulation, internal consistency, and test-retest reliability analyses. RESULTS: The content of the PAM-13 Malay version and the original version were conceptually equivalent. The questionnaire was refined after face validation by 10 patients with MetS. The refined version was then field-tested among 130 participants (response rate 89.7%). The Kaiser-Meyer-Olkin test was 0.767, and Bartlett's test of sphericity was ≤0.001, indicating sampling adequacy. Two factors were identified and labeled as (1) Passive and Building Knowledge, and (2) Taking Action and Maintaining Behavior. These labels were chosen as they were conceptually consistent with the items representing the levels of activation in PAM-13. The validated PAM-13 Malay version consisted of 13 items, framed into two domains. The overall Cronbach's α was 0.79, and the intraclass correlation coefficient was 0.45. CONCLUSIONS: The PAM-13 Malay version is valid, reliable, and fairly stable over time. This questionnaire can be used to evaluate the levels of activation among patients with MetS in primary care in Malaysia.

Pleuritic chest pain and fever: An unusual presentation of aortic dissection.

It remains a challenge to diagnose aortic dissection in primary care, as classic clinical features are not always present. This case describes an atypical presentation of aortic dissection, in which the patient walked in with pleuritic central chest pain associated with a fever and elevated C-reactive protein. Classic features of tearing pain, pulse differentials, and a widened mediastinum on chest X-ray were absent. This unusual presentation highlights the need for a heightened level of clinical suspicion for aortic dissection in the absence of classic features. The case is discussed with reference to the literature on the sensitivity and specificity of the classic signs and symptoms of aortic dissection. A combination of the aortic dissection detection risk score (ADD-RS) and D-dimer test is helpful in ruling out this frequently lethal condition.

Changes in uptake of vitamin B(12) and trace metals in brains of mice treated with clioquinol.

Clioquinol is a hydroxyquinoline antibiotic that has been associated with severe side-effects in the CNS. The syndrome caused by clioquinol treatment, subacute myelo-optic neuropathy (SMON), is considered as one of the worst drug disasters of this century. The precise biochemical mechanism behind SMON is not fully understood. Clioquinol can form strong lipophilic chelates with divalent cations and therefore it has been speculated that the drug may disturb the retention of vitamin B(12) through chelation of Co(2+). In the present study, the tissue distribution and uptake capacity of [57Co]cyanocobalamin were estimated in mice treated with clioquinol or saline. The concentrations of some trace metals were also determined in brain tissue. Accumulation of vitamin B(12) in the brain and its concentration in blood were decreased by clioquinol treatment. The mean concentrations of several trace metals were also lowered in the brain while the concentration of cobalt in the brain was not affected, suggesting that clioquinol does not bind to the cobalt in vitamin B(12). Moreover, a significant decrease in the levels of S-adenosylmethionine (SAM) was observed in the brain after clioquinol treatment. This may be a consequence of decreased vitamin B(12) levels. From these results, it can be concluded that chronic treatment with clioquinol may alter the tissue homeostasis of vitamin B(12) in the brain.

Transmethylation reactions and autoradiographic distribution of vitamin B12: effects of clioquinol treatment in mice.

The catastrophic epidemic of subacute myelo-optic neuropathy (SMON) affected Japan around 1970 with thousands of victims. The cause was attributed to high doses of locally acting oxyquinolines. It has been speculated that oxyquinoline derivatives of the clioquinol type can disturb the retention of vitamin B12 through chelation of Co2+. In the present paper, possible effects of clioquinol on the uptake and tissue distribution of [57Co]-cyanocobalamin have been studied in mice. In vivo experiments showed markedly decreased accumulation of radiolabelled vitamin B12 in the kidney and skin in animals that were pre-treated with clioquinol. The chloroform:water partition coefficients for [57Co]-cyanocobalamin in the presence or absence of clioquinol were also determined. No statistically significant alterations in the partition coefficient for [57Co]-cyanocobalamin in the presence of clioquinol was evident, indicating that clioquinol does not bind cobalt. In addition, transmethylation reactions in the CNS in mice treated with clioquinol were studied. Specific activities of methionine adenosyltransferase, and S-adenosylhomocysteine levels were not affected. In contrast, clioquinol treatment caused a significant increase in the levels of S-adenosylmethionine in the brain. The data of the present study show that clioquinol treatment can affect the accumulation of vitamin B12 in the kidney and the skin but not in the brain. These results do not support the hypothesis that clioquinol causes its damage to the nervous system by a direct chemical interaction with vitamin B12.

Inhibitors of catecholamine metabolizing enzymes cause changes in S-adenosylmethionine and S-adenosylhomocysteine in the rat brain.

Previous studies have shown that the biochemical changes that occur in parkinsonism are associated with disturbances in methylation reactions. Therefore, our hypothesis was that MAO and COMT inhibitors, which inhibit the metabolism of dopamine, might affect the methylation reaction. In the present study, we analyzed levels of S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH) in brain homogenates from rats which had received a one-week treatment with tolcapone or phenelzine, inhibitors of COMT and MAO, respectively. Tolcapone treatment caused an increase in the levels of SAM (130% as compared with control animals, p < 0.001). In animals treated with phenelzine, the SAM levels were 78% of those of the controls (p < 0.05). SAH levels were slightly increased (115% as compared with controls, p < 0.05) in the phenelzine group, while they were unchanged in the tolcapone treated animals. Treatment with tolcapone decreased the catalytic activity of methionine adenosyltransferase (MAT) (from 15.4 +/- 1.6 to 11.3 +/- 1.4 pmol mg-1 min-1, p < 0.0001) while phenelzine treatment had no significant effect. In addition the transmethylation ratio (SAM/SAH) were significantly increased with tolcapone (120%, p < 0.05) and decreased with phenelzine (71%, p < 0.05) as compared to the controls. The essential finding of this paper was that brain SAM levels were reduced by MAO inhibition and enhanced by COMT inhibition.

A histochemical demonstration of altered cytochrome oxidase activity in the rat brain by neuroleptics.

Regional alterations in neuronal functional activity were examined in the rat brain using cytochrome-c oxidase (COX) histochemistry following chronic neuroleptic treatment. Haloperidol, fluphenazine, and clozapine were administered to animals for 28 days after which profiles of COX activity were generated. Significant increases in COX activity were evident in area 2 of the frontal cortex of all treated animals. Clozapine and fluphenazine, but not haloperidol, caused significant increases in COX activity in the caudate nucleus, nucleus accumbens, septum, and pontine nucleus. Statistically significant increases in COX activity were also observed in hippocampal CA2 and CA3 subfields in clozapine treated animals. Results offer support for the concept that neuroleptics achieve their therapeutic effects primarily via an enhancement of brain function in the frontal cortex, but also point to other brain regions which may be involved in the actions of these drugs.

Neuroleptic-induced mitochondrial enzyme alterations in the rat brain.

For years, it has been known that neuroleptics have the capacity to interfere with the mitochondrial respiratory chain in vitro. We report that haloperidol and fluphenazine, classical neuroleptics, cause a generalized reduction in the activity of NADH: ubiquinone oxidoreductase (complex I) in the rat brain in vivo, an effect that was not observed with the atypical neuroleptic, clozapine. MPTP, which bears significant structural similarities with haloperidol, also demonstrated a significant reduction in complex I activity after low-dose, chronic administration. Interestingly, an increase in the activity of cytochrome-c oxidase (complex IV), probably reflecting enhanced functional neuronal activity, was observed in the frontal cortex of all chronically treated animals, an effect that is unlikely to result from compensation for the inhibition of complex I. Results suggest that previous findings, in which a reduction in the activity of cytochrome-c oxidase was observed in postmortem brain samples from schizophrenics, are not dependent on treatment with neuroleptics.

Normalization of cytochrome-c oxidase activity in the rat brain by neuroleptics after chronic treatment with PCP or methamphetamine.

Previous studies, primarily involving the use of positron emission tomography (PET), have contributed to the hypothesis that a state of hypometabolism may underlie schizophrenia. The chronic use of methamphetamine (MAP) or phencyclidine (PCP), both of which have been shown to enhance dopaminergic function in the brain, leads to a psychotic state in man which has prompted the suggestion that these compounds may have utility as models of schizophrenia. In the present study, regional alterations in energy metabolism were examined in the rat brain using cytochrome-c oxidase (COX) and succinate dehydrogenase (SDH) histochemistry following chronic treatment with PCP and MAP. PCP and MAP were administered alone or in the presence of fluphenazine or clozapine to animals for 28 days, after which mitochondrial enzyme activities were estimated. Both PCP and MAP produced profoundly similar decreases in COX activity in a broad spectrum of regions. Most prominent in this regard were the caudate-putamen, nucleus accumbens and septum. No changes were noted in sections stained for SDH activity, suggesting that results were dependent upon neither a generalized mitochondrial dysfunction nor mitochondrial loss. Cell counts and TUNEL histochemistry also failed to reveal any significant differences between control and treated animals, implying that reductions were not a result of cell loss. Both clozapine and fluphenazine offered varying degrees of protection from the effects of PCP and MAP. The results provide evidence which implicates dopaminergic hyperactivity in the finding of reduced energy metabolism in the brains of schizophrenics.

Latex allergy in hospital employees.

To investigate the incidence of latex IgE-mediated hypersensitivity, 224 hospital employees were interviewed and prick skin tests were performed to six common aeroallergen extracts, one non-latex "synthetic" glove extract, and four different latex glove extracts. Of the 224 subjects, there were 136 nurses, 41 laboratory technicians, 13 dental staff, 11 physicians, 6 respiratory therapists, and 17 housekeeping and clerical workers. All 224 subjects tested negative for the nonlatex glove (Tactylon) extract but 38 (17%) tested positive for latex extracts. The incidence ranged from 0% in housekeeping staff to 38% in dental staff. Eighty-four percent of the latex skin test-positive employees complained of itching and 68% of rash upon exposure to latex, whereas the latex skin test-negative employees reported these symptoms in 29% and 17%, respectively. Urticaria was a symptom in 55% of the latex skin test-positive and 0.5% of the skin test negative-subjects. Anaphylaxis occurred in 10.5% of the skin test-positive and in none of the skin test-negative employees. Symptoms of sneezing (34% vs 7%), nasal congestion (39% vs 7%), and lacrimation and ocular itching (45% vs 6%) were also significantly different between the latex skin test-positive and latex skin test-negative subjects. We conclude that the incidence of latex IgE-mediated allergy in hospital employees is 17%. The symptoms of anaphylaxis and hives when using latex gloves are sensitive predictors of IgE-mediated latex allergy.

Evaluation of latex allergy in patients with meningomyelocele.

Seventy-six patients with meningomyelocele were evaluated for latex sensitivity by medical history and epicutaneous skin testing. Four different latex glove extracts, two nonlatex glove extracts, cornstarch, selected inhalant antigens, and negative and positive controls were used for skin testing. Forty-nine patients (64.5%) were skin test positive to latex extracts (latex-positive group). Twenty-four patients (49%) of the latex-positive group and none of the latex-negative group had histories of immediate reactions to latex products (P less than .001). The latex-positive group had a higher mean number of surgical procedures, 12.67 +/- 11.27, compared with 6.89 +/- 6.55 (P less than .001) in the latex-negative group. Twenty-three of the latex-positive patients (47%) used latex products daily compared to seven patients (26%) in the latex-negative group (P = .073). Twenty latex-positive patients (41%) had atopy compared with five patients (19%) of the latex negative group (P = .041). There was no significant difference between the two groups in age, sex, daily catheterization, or positive skin tests to cornstarch. All 76 patients tested negative to the nonlatex glove extracts. Ten control subjects tested negative for all latex and nonlatex glove extracts.