Statins are widely used in the management or inhibition of several processes that lead to the development of cardiovascular diseases. Increased statin therapy has been related to the induction of type II diabetes (DM), a state which predisposes to cardiovascular disease (CVD). Statins are well-known to possess anti-inflammatory properties and the ability to disrupt de novo biosynthesis of cholesterol and lipid homeostasis has been implicated in the induction of inflammatory responses within pancreatic β-cells. Inhibition of β-hydroxy β-methyl glutaryl-CoA (HMG-CoA) results an increased level of low-density lipoproteins (LDL) receptors. Increased LDL receptor numbers will replenish exhausted intracellular supplies, resulting in higher levels of intracellular cholesterol. Therefore, stimulating immunological response and inflammatory reactions, disrupt the functional integrity of the β-cell via oxidation of the plasma-derived low-density lipoprotein. Despite the pleiotropic effects of statins on the pancreatic β-cell, they have also been reported to affect a number of other cell types associated with the development of diabetes. Inhibition of the biosynthesis of isoprenoid by statins has been associated with the down-stream regulation of glucose transporter (GLUT 4) in adipose tissues, which facilitates the uptake of glucose. This effect resulted in increasing resistance to insulin in the liver, muscle, and adipose tissue. Adiponectin, a plasma protein released by adipocytes, alters fatty acids and carbohydrate metabolism both in the muscle cells and liver. This process indirectly influences resistance to insulin by the attendant decrease in hepatic gluconeogenesis and to upregulate muscular β-oxidation and glucose uptake.
A clinical study was conducted to evaluate fingerstick blood as a viable biological matrix for monitoring prescription and illicit drugs in a clinical setting on patients undergoing pain and addiction treatment. The current standard for monitoring patients’ medication use, misuse, and diversion is urine drug testing (UDT).
Materials and Methods
This study compared 632 paired urine and fingerstick blood specimens collected at three pain management clinics and one suboxone clinic for 35 drugs and/or metabolites. Plasma from the fingerstick blood was used for the analysis. The urine and plasma specimens were analyzed by validated liquid chromatography–tandem mass spectrometry (LC-MS-MS) procedures. The urine cutoff used by most pain testing laboratories were used to identify positive and negative drugs in urine. Limit of quantitation was used to identify positive and negative drugs in plasma. Drugs and/or metabolites were quantified in both urine and plasma using deuterium-labeled internal standards.
Results were tabulated for urine and plasma specimens for data analysis. The results showed that 8.7% of plasma specimens detected more drugs compared to the corresponding urine specimens, and 2.2% of the urine specimens detected a drug that was negative in the corresponding plasma specimen. Overall 89.1% of the specimens had complete agreement between urine and plasma specimens for detection. The observed Cohen’s Kappa value for overall drug detection was 0.96 an “almost perfect” agreement as characterized by Landis and Koch.
Based on the observed data, the authors conclude that plasma collected from fingerstick blood is a better matrix to monitor patients currently prescribed pain medications or patients currently undergoing medication-assisted opioid treatment compared to urine drug testing.
Fingerstick blood; Pain management; Prescription drugs; Opioids; Opiates; Illicit drugs.
Decontamination is a critical medical counter measure in reducing toxic exposure following poisoning. Little is known on the effectiveness of this procedure and its impact in the context of preventing secondary exposure of healthcare workers and secondary contamination of facilities. Presented here is a case of dimethoate poisoning that required a prolonged period of skin decontamination to remove residual skin contamination.
A young gardener consumed dimethoate at the workplace witnessed by a colleague who called the emergency services immediately. Paramedics noted the patient to be drowsy with stable vital signs and 100% oxygen saturation. En-route to the hospital the patient vomited multiple times and was drenched in vomitus with a pungent odour. Upon arrival at the emergency department (ED), vital signs remained stable with a Glasgow Coma Scale (GCS) of 10. Due to gross external contamination from the vomitus and pungent odours emanating suggestive of chemical fumes off-gassing, the hospital decontamination shower was activated for patient decontamination. Staff donned protective suits and proceeded to disrobe and bag all the patient’s clothing before showering the patient for 10-minutes using soap and water. Post-decontamination a chemical agent monitor (CAM) were used to screen for residual chemicals following the hospital’s decontamination protocol. The chemical alarm was triggered twice, first around the left mastoid region and again just below the left breast. This required targeted re-showering for a further 10-minutes before patient was finally cleared of contamination. Subsequently, the patient was given atropine (2.4 mg) and pralidoxime (1 g) followed by an infusion at the intensive care unit (ICU). The patient made an uneventful recovery and was discharged 5-days later.
This case of dimethoate poisoning is notable for the prolonged period of skin decontamination to remove residual skin contamination and illustrates potential implications to patient and health care worker safety. Past mass casualty incidents involving
chemicals, such as the sarin attack in Tokyo, highlight the high incidence of secondary exposures amongst healthcare workers due to the lack of casualty decontamination. As a result, many hospitals have developed capacity to conduct rapid and timely decontamination at their premises to prevent further complications from secondary chemical exposure. However, the effectiveness of this process of decontamination needs further evaluation.
Contaminated casualty; Decontamination; Dimethoate; Poisoning; Hazardous material incident; Organophosphorus compounds.
brief research report
Since the Sarin incident in the subways of Tokyo in 1995, there has been an unprecedented increase in the use of chemical agents on civilian populations internationally. This scourge of chemical terrorism has been relentless worldwide and is likely to continue to be a public health issue that needs to be addressed by the relevant authorities as part of national disaster preparedness and response. One aspect of chemical disasters involves the need for mass decontamination of chemically-contaminated casualties from the scene. The traditional role of hazardous materials civil defence experts in providing such decontamination of victims in the pre-hospital setting is limited by many factors. The presence of congestion in densely populated areas in a highly built up environment of modern-day cities, compounds the timeliness of putting up cordons and crowd control and hence delays the prompt set up of such mobile decontamination facilities close to the incident site. The expected side effect is an almost instantaneous influx of contaminated casualties to the nearest hospital in such situations, which drives the need for public hospitals to be ultimately capable of performing mass casualty decontamination as part of hazardous materials disaster preparedness. This review presents an innovatively designed rapidly deployable hospital-based decontamination facility that has served a tertiary care hospital in Singapore for the last 2 decades in being prepared for managing mass casualties arriving from a chemical disaster in a timely manner.
Decontamination; Chemical incident; Industrial disasters; Toxic industrial chemicals; Hazardous materials preparedness; Disaster contingency plans; Emergency preparedness.
Depatment of Pharmacology & Physiology
Oklahoma State University Center for Health Sciences
Tulsa, Oklahoma, USA
Department of Natural Sciences
Southern University at New Orleans
6400 Press Drive
New Orleans, LA. 70126, USA
Department of Human Physiology
West Bengal, India