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Urine of a person with rhabdomyolysis and the characteristic brown urine discoloration as a result of myoglobinuria and odor like chicken liver (private experience).
Source publication
Objectives:
The goal of this clinical trial was to determine the incidence of undesirable side effects, and to ascertain any occurrence of genetic polymorphisms.
Material and methods:
Clinically, we looked for manifestations of a benign myositis and of serious rhabdomyolysis. We observed a group 198 patients treated with statins, primarially flu...
Context in source publication
Citations
... One case of rhabdomyolysis occurred in a patient who received rosuvastatin in combination with gemfibrozil. 19 Furthermore, a phase 1 clinical trial study was conducted to evaluate the safety of rosuvastatin (1-8 mg/kg/day) and erlotinib (150 mg/day) in treating advanced solid malignancies; one case of rhabdomyolysis was reported. 12 Lastly, other studies did not list the type or dose of statins used. ...
... Additionally, they had CK levels above normal at more than 2000 U/L or 10 times the upper limit of normal (ULN). 5,12,19 Moreover, their urine samples change to a darker color. 19 However, some of the studies did not specifically list the symptoms experienced by patients and the laboratory test results. ...
... 5,12,19 Moreover, their urine samples change to a darker color. 19 However, some of the studies did not specifically list the symptoms experienced by patients and the laboratory test results. Goss et al reported a rhabdomyolysis-related death. ...
Nisa Safitri,1 Maya Fadila Alaina,1 Dian Ayu Eka Pitaloka,1,2 Rizky Abdulah1,2 1Department of Pharmacology and Clinical Pharmacy, Faculty of Pharmacy, Universitas Padjadjaran, Sumedang, 45363, Indonesia; 2Center of Excellence in Higher Education for Pharmaceutical Care Innovation, Universitas Padjadjaran, Sumedang, 45363, IndonesiaCorrespondence: Dian Ayu Eka Pitaloka Tel +62 22-84288812Email dian.pitaloka@unpad.ac.idAbstract: Although statins are effective for treating hypercholesterolemia, they can have various side effects, including rhabdomyolysis, a potentially fatal condition. This review evaluated the incidence and underlying molecular mechanism of statin-induced rhabdomyolysis and analyzed its risk factors, prevention, and management. We focused on the clinical and randomized clinical trials of statin monotherapies and combinations with other drugs. The primary mechanism of statin therapy-induced rhabdomyolysis is believed to be a decrease in ubiquinone (coenzyme Q) produced by the HMG-CoA pathway. Additionally, different types of lipophilic and hydrophilic statins play a role in causing rhabdomyolysis. Although statin-induced rhabdomyolysis has a low incidence, there is no guarantee that patients will be free of this side effect. Rhabdomyolysis can be prevented by reducing the risk factors, such as using CYP3A4 inhibitors, using high-dose statins, and strenuous physical activities.Keywords: statin, hypercholesterolemia, adverse effect, rhabdomyolysis, risk factor
... The mechanism through which the bee venom might have partially prevented the simvastatin-induced myopathy is not clear as the proposed mechanisms of its induction of myopathy are multiple including inflammatory mitochondrial impairment and oxidative stress [35], passing through multifactorial induction of apoptosis [36] and autoimmune triggered myopathy [37], even genetic predisposition is hypothesized [38]. On the other hand, the bee venom has several components with different mechanisms of action and different therapeutic effects. ...
Background
Statin-induced myopathy is the most common adverse effect of statins. Bee venom provides a potential mean of controlling immune responses and inflammatory reactions; the proposed mechanisms for statin-induced myopathy.
Objective
The present study aimed at clarification of the role of the bee venom in prevention of statin-induced myopathy.
Materials and methods
It was carried out on 30 Sprague-Dawley female rats. Rats were randomly classified into 3 groups: control group, statin group which received statins for 2 weeks, and venom group that was exposed to alternate day actual bee sting concurrent to statins administration for 2 weeks. Quantitative electromyography (QEMG) was performed as well as serum creatine kinase (CK) and cholesterol levels, in addition to in vitro muscle contractility tests.
Results
QEMG and contractility tests showed significant changes in the statin group compared to both control and venom groups. Serum cholesterol level decreased with increase in CK levels in the statin and venom groups compared to controls; however, the CK level was significantly lower in the venom group as compared to the statin group.
Conclusion
Bee venom therapy offers a simple and available means of prophylaxis against the myopathic effects induced by statins in animal model. However, it partly restricts the therapeutic effect of statins.
... The main side effect of statins is myopath found in 5-25 percent of cases take statins. The number of patients at risk of statin-associated myopathy may reach millions in western countries (Drobny et al, 2014;Patel et al, 2015;Zhong et al, 2018). ...
... They have been currently used to treat hypercholesterolemia in order to prevent cardiovascular diseases. 14 However, they have a number of undesirable sideeffects including muscle damage and skeletal muscle disorder 15,16 and abnormalities in liver enzymes tests 17 and increases the risk of diabetes. Besides, in the eld of food science, scientic studies have focused on the search of natural sources (such as phenolic component, caroténoide, ellagitannin). ...
This study was carried out to investigate the hypolipidemic, cardioprotective and anticoagulant properties of fish goby protein hydrolysates (GPHs) in rats fed a high fat and fructose diet (HFFD). Wistar rats were fed with HFFD for 2 months, coupled with the oral administration of GPHs and undigested goby protein (UGP). Compared with the standard diet, HFFD induced dyslipidemia and liver structure alterations, and increased pancreatic lipase activity. In addition, HFFD caused a significant increase in body weight. Interestingly, administration of UGP and GPHs to HFFD fed rats was efficacious in lowering serum total cholesterol (TC), triglyceride (TG) and low-density lipoprotein cholesterol (LDL-c) as well as hepatic TC and TG, and increased the serum high density lipoprotein cholesterol (HDL-c) content. Moreover, all treatments significantly decreased the atherogenic index and coagulant factor levels (thrombin and prothrombin). UGP and GPH administration also significantly decreased pancreatic lipase activity, which mitigates lipid accumulation. Similarly, UGP and its hydrolysates showed cardioprotective potential revealed by decreasing the risk of atherogenic and coronary artery disease and improving the liver architecture. The ex vivo plasma clotting test showed that GPHs exert a great therapeutic anticoagulant potential. The overall results demonstrated that GPH supplementation can counteract high-fat/fructose diet-induced obesity.
Muscle cramps are sustained, painful contractions of muscle and are prevalent in patients with and without medical conditions. The objective of this review is to present updates on the mechanism, investigation and treatment of neurogenic muscle cramps. PubMed and Embase databases were queried between January 1980 and July 2014 for English-language human studies. The American Academy of Neurology classification of studies (classes I-IV) was used to assess levels of evidence. Mechanical disruption, ephaptic transmission, disruption of sensory afferents and persistent inward currents have been implicated in the pathogenesis of neurogenic cramps. Investigations are directed toward identifying physiological triggers or medical conditions predisposing to cramps. Although cramps can be self-limiting, disabling or sustained muscle cramps should prompt investigation for underlying medical conditions. Lifestyle modifications, treatment of underlying conditions, stretching, B-complex vitamins, diltiezam, mexiletine, carbamazepine, tetrahydrocannabinoid, leveteracitam and quinine sulfate have shown evidence for treatment.
Delirium is a serious but potentially avoidable complication in critically ill patients. Various pathophysiological processes have been associated with delirium development; however, neuroinflammation hypothesis and pleiotropic effects are the reasons why HMG-CoA reductase inhibitors have been evaluated for delirium prevention. Statin therapy is associated with favorable outcomes in critically ill patients, but significant variability of results exists in patients who received these agents postoperatively. Study design methodological weaknesses, inconsistent delirium assessment, and lack of information on sedation regimens may have confounded these outcomes. Furthermore, no evidence exists on the type of statin, lipophilic or non-lipophilic, that is associated with the most benefit or when therapy with a statin should be initiated. Thus, the efficacy of HMGM-CoA reductase inhibitors on delirium prevention has not been fully established and non-pharmacological methods should remain mainstay of therapy.
