Utilization of public and private dental services in Sibu,Sarawak: a sociodemographic appraisal and types of treatment received

This study investigated the sociodemographic profiles of patients attending public and private dental clinics and the types of treatment received. Patients (n=454) were interviewed using a structured questionnaire at two public and four private clinics in Sibu District, Sarawak. Generally, Chinese (74.7%), females (60.0%) and urban dwellers (83.7%) were more likely to visit the dentist. Both clinics had more females and more Chinese but private clinics had a lower percentage of female attendees (53.1% versus 67.0%) but a higher percentage of Chinese (85.0% versus 64.5%). Private attendees were younger (mean age of 31.0 years compared to 41.0 years) and from higher income households (median value of MR 2,000 versus MR 900) than public attendees. Treatments were mostly curative and a third of the visits were associated with painful conditions. Age (p=0.006), gender (p=0.003), ethnicity (p<0.001) and household income (p<0.001) were associated with the type of clinic visited. Choice of clinic was not related to having painful conditions (p=0.970). To ensure a more affordable and equitable distribution of oral healthcare, health planners need to identify disparities in the utilization of services and differences between public and private attendees.     

Dissociation of modular total hip arthroplasty at the femoral head-neck interface after loosening of the acetabular shell following hip dislocation

Modular component dissociation is a potential problem of current modular total hip arthroplasty (THA) systems. We describe a case of dissociation of the modular THA at the femoral head-neck interface after loosening of the acetabular shell during closed reduction for posterior dislocation of THA. The causes of this dissociation and acetabular shell loosening are discussed. Successful treatment was provided with surgical revision of the acetabular and the femoral head components. The present case serves as a graphic reminder that the acetabular shell overhanging the acetabular bone must be avoided when implanting modular THA components.     

Three-day lansoprazole quadruple therapy for Helicobacter pylori-positive duodenal ulcers: a randomized controlled study

AIM: To compare the efficacy and tolerability of a 3-day quadruple therapy with a standard 7-day triple therapy in eradicating Helicobacter pylori infection and healing duodenal ulcers. METHODS: Patients with H. pylori-positive duodenal ulcers were randomized to receive either lansoprazole 30 mg, clarithromycin 500 mg, and metronidazole 400 mg twice daily for 7 days (LCM-7) or lansoprazole 30 mg, clarithromycin 500 mg, metronidazole 400 mg, and bismuth subcitrate 240 mg twice daily for 3 days (LCMB-3). No pre- or post-treatment acid suppression was used. Follow-up endoscopy was performed at week 6. RESULTS: A total of 118 patients were recruited. Sixty patients in the LCM-7 group and 53 patients in the LCMB-3 group returned for endoscopy. Intention-to-treat eradication rates were 87% and 86% (P=0.94) and per protocol eradication rates were 87% and 94% (P=0.29) in the LCM-7 and LCMB-3 groups, respectively. Per protocol and intention-to-treat ulcer healing rates were 98% and 98% in LCM-7 and 100% and 91% in LCMB-3, respectively. There were no significant differences in efficacy in relation to the initial metronidazole and clarithromycin susceptibility. Significant reduction in the duration of side-effects was found in the LCMB-3 group. CONCLUSION: The 3-day quadruple therapy is highly effective, better tolerated and can be considered as a first-line therapy in duodenal ulcer management.     

Potent inactivation of representative members of each PKC isozyme subfamily and PKD via S-thiolation by the tumor-promotion/progression antagonist glutathione but not by its precursor cysteine

We recently established that S-glutathiolation of cPKCalpha fully inactivates the isozyme, at a stoichiometry of approximately 1 mol GSH/mol cPKCalpha. In this report we demonstrate that, in addition to cPKCalpha, six other PKC isozymes that are representative of the three subfamilies within the PKC family (cPKCbeta1, cPKCbeta2 and cPKCgamma, nPKCdelta and nPKCepsilon and aPKC-zeta) are subject to inactivation by S-glutathiolation induced by the thiol-specific oxidant diamide, which induces disulfide bridge formation. Among PKD and the seven PKC isozymes examined in this report only nPKCdelta has been directly implicated as an antagonist of tumor promotion/progression, while several of the kinases have been implicated in the mediation of tumor promotion/progression. We report that of the kinases examined nPKCdelta was the most resistant to inactivation by diamide-induced S-glutathiolation. In the absence of GSH only nPKCdelta activity exhibited a biphasic response to diamide, with low diamide concentrations oxidatively enhancing nPKCdelta activity and higher concentrations inactivating the isozyme; the other seven kinases were subject to monophasic, concentration-dependent, oxidative inactivation by diamide to various extents. The results provide evidence that at least some pro-oxidant environments may support the potent inactivation of nPKCepsilon and other PKC isozymes implicated in tumor promotion/progression by the mechanisms of S-glutathiolation and, in some cases, disulfide bridge formation among the isozyme thiols, without inducing substantial nPKCdelta inactivation. The results also show that neither the seven PKC isozymes examined nor PKD are inactivated by S-cysteinylation under conditions that support potent inactivation by S-glutathiolation. This indicates that the protection that the tumor promotion/progression antagonist GSH may afford against oxidative tumor promotion/progression mechanisms by S-thiolating and inactivating PKC isozymes and PKD cannot be afforded by the metabolic GSH precursor cysteine. These observations support a role for PKC inactivation via S-glutathiolation in the mechanism of tumor promotion/progression antagonism by GSH in pro-oxidant environments.     

Superiority of enoxaparin over heparin in combination with a GPIIb/IIIa receptor antagonist during coronary thrombolysis in dogs

It is known that a low-molecular-weight heparin (LMWH) is more effective than unfractionated heparin in unstable angina/non-Q-wave myocardial infarction (UA/NQMI) and the platelet GPIIb/IIIa receptors play an important role in acute myocardial infarction (AMI). Therefore, enoxaparin might have a similar advantage over heparin when used with a GPIIb/IIIa antagonist (RPR109891) in coronary thrombolysis. After induction of coronary thrombosis in anesthetized dogs, infusion of saline, enoxaparin, heparin, RPR109891, enoxaparin+RPR109891, or heparin+RPR109891 was initiated followed 15 min later by recombinant tissue plasminogen activator (rt-PA). The incidence of reperfusion in the enoxaparin+RPR109891- and the heparin+RPR109891-treated groups was similar, but time to reperfusion tended to be shorter for enoxaparin versus heparin. Only 43% of the vessels reoccluded in the enoxaparin+RPR109891 group, compared to 100% vessels in the heparin+RPR109891 group. Enoxaparin+RPR109891 maintained flow for a significantly longer time compared to saline, enoxaparin, heparin, and heparin+RPR109891. Enoxaparin+RPR109891 and heparin+RPR109891 increased the template bleeding time by 2- and 3-fold and activated partial thromboplastin time (APTT) by 1.3- and 3-fold, respectively. These data suggest that enoxaparin is more effective and potentially safer than heparin when combined with a GPIIb/IIIa receptor antagonist during rt-PA-induced coronary thrombolysis.     

Langerhans cell histiocytosis

Langerhans cell histiocytosis is a rare condition that can affect any organ of the body. Patients of all ages may present to the dermatologist and it is important to make the diagnosis as quickly as possible, because time from presentation to diagnosis is of prognostic importance in adults with the disease. Langerhans cell histiocytosis is now classified as a class I histiocytosis and research into this disease has been very active over the past 10 years. We now know that the disease represents a clonal expansion of a Langerhans cell, which shows phenotypic evidence of activation. The tissue damage induced by the disease appears to be related to local cytokine release. In single system disease, Langerhans cell histiocytosis is responsive to local therapy but, in resistant single system disease or in multisystem disease, etoposide is the most effective monochemotherapy. Some patients will need maintenance treatment with azathioprine or 6-mercaptopurine with or without methotrexate. In such cases, physicians who are used to treating chronic and relapsing diseases and who have experience with these drugs, such as dermatologists, are the most appropriate to manage patients with Langerhans cell histiocytosis.     

Carbon disulfide vasculopathy: a small vessel disease

We present the clinical manifestations of 4 male patients with acute stroke-like symptoms and polyneuropathy after long-term exposure to carbon disulfide (CS2) in a viscose rayon plant. The ages of onset of polyneuropathy ranged from 42 to 45 years with a duration of CS2 exposure between 6 and 21 years. The ages of onset of stroke were from 42 to 48 years. The risk factors for stroke including heart disease and diabetes were denied, except for smoking in 4, hyperlipidemia in 2 and hypertension in 1. At the initial visit in 1992, only 2 patients developed sudden onset of hemiparesis suggesting a lacunar stroke before the diagnosis of CS2 intoxication. Brain computed tomography (CT) scans showed low-density lesions in the basal ganglia in 2 patients, cortical atrophy in 1 and normal in 1. Brain magnetic resonance image (MRI) study disclosed multiple lesions in the corona radiata and basal ganglia on T(2)-weighted images in 3 patients and cortical atrophy in 1. After the diagnosis, they left their jobs for a CS2-free environment, and improvement of the working conditions was noted. During 5 years follow-up period, another 2 patients also developed an acute episode of stroke with hemiparesis. Brain CT and/or MRI follow-up studies in these 2 patients revealed new lesions in the basal ganglia and corona radiata. Intriguingly, a patient with previous stroke also developed new lesions in the bilateral thalami and brainstem. Carotid Doppler scan, transcranial Doppler scan and/or cerebral angiography did not show any prominent stenosis or occlusion in the major intracranial large arteries. We conclude that encephalopathy may occur in patients after long-term CS2 exposure, probably due to impaired cerebral perfusion. The lesions tend to occur in the basal ganglia, corona radiata and even brainstem, particularly involving the small-sized vessels. In addition, the cerebral lesions may progress even after cessation of CS2 exposure. Therefore, we suggest that CS2 exposure may be a risk factor for stroke.