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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.
Carbon monoxide (CO) is a toxic gas produced as a result of incomplete combustion of organic materials. The source of CO production is very common especially in nations that depend on power generating sets for electricity. Chronic disease is non-communicable and usually takes a longer time to manifest. Examples are kidney failure, diabetes mellitus, hypertension, cancer, and cardiac arrest. These diseases are now very common in society, not sparing the youthful population that was rare ab initio. The major difficulty in the containment of chronic diseases is the inability to establish a definitive causative agent. The definite causative agent is important in public health and management of chronic diseases. Preventive medicine is anchored on establishing the causative agent of a disease. Without knowing the causative agent of a disease, the path to prevention becomes very cumbersome.
The knowledge of the causative agent of a disease is the bedrock of preventive medicine and public health. Several reasons such as lifestyle modification, hereditary, climate change, nutrition or aging have been adduced as the cause of chronic diseases. These reasons are quite weak and not definite. The exact causative agent(s) of chronic diseases is a conundrum that needs a deliberate study and review so as to enhance definite diagnosis, preventive measures and appropriate therapeutic intervention. Measurement of biochemical and haematological parameters are employed in disease diagnosis and management. Alterations of these parameters are used to identify chronic diseases and also form part of an alarm system of a potential breakdown of the normal functioning of the body. The effect of chronic CO intoxication on these parameters could be of importance in establishing causative
agent(s) of diseases that are for long opaque and non-definite. This review was therefore designed to interrogate various narratives, meta-analysis, and researches on this subject. Explicit knowledge of the pattern or presentation of biochemical and haematological parameters arising from chronic CO intoxication could be of great importance in preventive medicine, disease diagnosis and appropriate therapeutic intervention.
Biochemical parameters; Haematological parameters; Chronic diseases; Carbon monoxide; Chronic intoxication.
Tramadol is a synthetic centrally acting analgesic used worldwide for pain relief, but now abused as a euphoria generating substance. The short- and long-term implications of tramadol intoxication on blood cells and its components are still hazy and controversial.
Our primary aim was to evaluate the alterative pattern of haematological parameters resulting from acute or chronic tramadol intoxication.
The study was made of acute and chronic phases of sixty male rats (Rattusnorvegicus) randomly pair-divided into established groups of six male rats each. The acute stage consisted of a control group of 6 rats administered with normal saline solution, and a treatment group of 6 rats administered with lethal dose of tramadol. The control group for the chronic stage consisted of 6 rats that were administered normal saline solution. Whereas, the tramadol-dependent groups comprised of 3 groups of 6 rats each administered orally with 50 mg/kg, 100 mg/kg, and 200 mg/kg of tramadol for 90 days respectively. Statistical analyses consisted of the one-way analysis of variance (ANOVA), Student’s t-test, and Pearson’s Correlation using the JMP statistical discovery™ software version 14.1. Blood samples were collected after anesthetic sacrifice by cardiac puncture for the analysis of full blood
count and red cell indices using SYSMEX Automated Blood Count machine (SYSMEX KX-21N ANALYZER) and microscopy for blood film reading.
Results of the acute phase of the study showed that the packed cell volume (PCV) in the treatment group (51.00±2.96%) was significantly higher (t=3.99, p=0.002) than control (37.83±1.43%). Similarly, the haemoglobin concentration (Hb) in the treatment group (14.70±0.46 g/dL) was significantly higher (t=5.10, p=0.005) than control (11.55±0.41 g/dL). The mean cell haemoglobin
concentration (MCHC) was significantly lower (t=2.67, p=0.02) in the control group (28.30±0.52 g/dL) than treatment (30.43±0.61 g/dL). However, that of the chronic phase exhibited a progressive increase in platelet count which was proportional to increasing dosage of treatment (t=8.59, p=0.007).
This study has demonstrated that tramadol administration could cause haematological alterations which could be beneficial if administrated optimally and deleterious, if abused. Therefore, indiscriminate and prolonged use of tramadol should be monitored to avert haemotoxicity.
Tramadol; Intoxication rats; Full blood count; Red cell indices.
brief research report
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