Chronical Kidney Disease (CKD) causes deterioration of renal function with reduction of glomerular filtration (GFR). Drugs which are mainly excreted through the kidney have reduced renal elimination (Clrenal) in CKD. For decades dosage adjustments for these drugs have been computed based on GFR and clearance measurement of biomarker serum creatinine (Clcr), respectively, and according to the rule of Dettli [1-3] where the appropriate dose D compared to the normal dose (Dnorm) may be assessed through the individual elimination fraction Q:
Introduction: Pain alleviation is the primary intervention in promoting quality of life. Among the compounds used in management of pain are opioids. Codeine is mostly used as antitussive and is commonly present in cough syrups. Tramadol and Morphine are used as analgesics based on severity of pain. Although these drugs provide instant pain relief, they are associated with many side effects and the most worrying once are addiction, respiratory depression and tolerance. Methods: Codeine, Tramadol, and Morphine were used as query compounds to generate similar compounds using SwissSimilarity. Similar compounds were docked to mu, kappa, and delta receptors and those that showed better docking scores to mu receptor and lower scores to kappa and delta were analyzed for toxicity profiles using ProTox II and pharmacokinetics profiles using SwissADME. Results: ZINC13831510; 0.992, ZINC03629718; 0. 995; ZINC03870350; 0.993; ZINC28256912; 0.992; and ZINC71774151; 0.977 showed highest binding score to mu receptors and lower to both kappa and delta. All compounds were predicted to inhibit CYP2D6 enzyme. All compounds permeated Blood Brain Barrier with the exceptions of ZINC04102208; 0.992; and ZINC13831510; 0.992. Tramadol, its zinc compounds and ZINC03629718; 0.995. were not substrates for P-glycoprotein. Tramadol and ZINC03639132; 0.976; were predicted immunoactive. All compounds conformed to Lipinski rule of five. Conclusion: In conclusion, ZINC13831510; 0.992; showed the highest binding score to morphine. ZINC02509756; 0.986; and ZINC26259212; 0.995; were considered the safest as compared to Tramadol and Codeine and their zinc compounds respectively. Further invitro studies are recommended for the following promising compounds ZINC13831510; 0.992, ZINC03629718; 0. 995; ZINC03870350; 0.993; ZINC28256912; 0.992; and ZINC71774151; 0.977 ZINC02509756; 0.986; and ZINC26259212; 0.995;.
In COPD, chronic inflammation and exposure to irritants, such as cigarette smoke, lead to the thickening of bronchial walls. This results from increased deposition of collagen and other extracellular matrix components, contributing to the narrowing of airways. Nevertheless, it is widely recognized that COPD is an inflammatory disorder marked by partially reversible airflow limitation wherein genetic factors interact with the environment. In recent years, numerous investigations have substantiated the correlation between gene polymorphisms and COPD. SUMF1 has been implicated in diverse cellular processes, including lysosomal function and extracellular matrix maintenance, both of which play pivotal roles in respiratory health. The genetic variations in SUMF1 could lead to an imbalanced sulfation in the extracellular matrix of lung tissue, potentially playing a role in the onset of COPD. Recent studies have uncovered a potential link between dysregulation of SUMF1 and COPD progression, shedding light on its involvement in the abnormal sulfatase activity observed in COPD patients. Through a comprehensive review of current literature and experimental findings, this article aims to contribute to the growing body of knowledge surrounding the genetic intricacies concerning sulfation of airway remodeling and possible pharmacological applications in COPD and asthma management.
1,4-napthoquinone and its derivatives possess significant anticancer, antinociceptive and antimicrobial activities and thus modification of 1,4-napthquinonone might result in generation of a lead compound for the development of more effective drug therapy against cancer, pain disorders and bacterial infections. In the present study, 2-methylamino-{3-[2-(4-morpholinyl)-ethyl]-amino}-1,4- Naphthoquinone was synthesized and then evaluated for cytotoxic, antimicrobial and antinociceptive activity. In MTT-based cytotoxicity assay, the compound exhibited strong cytotoxic activity against HeLa cell line with a LD50 value of 17.5μg/ml. In antimicrobial susceptibility test performed by agar disc diffusion method, the compound exhibited promising antibacterial activity against both Grampositive and Gram-negative bacteria with 17-20mm of diameter of zone of inhibition suggesting that the synthesized compound possesses a broad spectrum of antibacterial activity. The compound also demonstrated promising antifungal activities against Saccharoromyces cerevisiae, Candida albicans and Aspergillus nigar. In the acetic acid-induced writhing test in mice, at a dose of 50 mg/kg body weight, the compound displayed significant analgesic activity with 68.3% writhing inhibition which was comparable to that of the standard aceclofenac. These results suggested that the synthesized napthoquionone analog possesses remarkable cytotoxic, antinociceptive and antimicrobial activities and thus could be a potential lead for the development of drug against cancer, infections and pain disorders.
Objective: Determine the distribution and longitudinal changes in antihypertensive medication regimens in the Systolic Blood Pressure Intervention Trial (SPRINT). Methods: We used antihypertensive medication data collected by pill bottle review at each visit to categorize antihypertensive regimens by medication class. Free text string variables of medication names were independently reviewed by two clinical pharmacists to create standardized generic medication names and classes. Results: Figure 1 illustrates longitudinal changes in class combinations and number of drugs at the randomization, 6, 12, and 18-month visits. Fifty-six percent of participants modified their initial regimen by the 6-month visits; 43% of participants made additional modifications to their regimens from the 6-month to the 18-month visit. The most common initial regimens, and least likely regimens to be changed over time, were combinations with an ACEI/ARB and diuretics ± other classes (42% of initial regimens). Participants in the intensive arm added a mean (standard deviation) of 0.6 (0.9) medications to their initial regimens in the first 18-months compared to -0.1 (0.9) in the standard arm. Conclusion: Intensive blood pressure treatment requires more medication complexity in terms of class and dose. Further study of distinct regimens may reveal if certain class and dose combinations provide better SBP control, safety, or patient satisfaction.
In 2012, RET rearrangements are observed in 1-2% of Non-Small-Cell Lung Cancer (NSCLC) patients and result in the constitutive activation of downstream pathways normally implied in cell proliferation, growth, differentiation and survival. Several compounds have been reported, including some traditional kinases inhibitors and the discovery of some new structure of natural products. Cabozantinib and vandetanib are multikinase inhibitors have been explored in the clinic for NSCLC patients. As a result of the nonselective nature of these multikinase inhibitors, patients had off-target adverse effects. Then, the discovery and clinical validation of highly potent selective RET inhibitors such as pralsetinib and selpercatinib demonstrating improved effificacy and a more favorable toxicity profile. However, acquired resistance mediated by secondary mutations in the solvent-front region of the kinase (e.g. G810C/S/R) becomes a major challenge for selective RET inhibitor therapies. In this review, we will highlight typical RET inhibitors developed during these years and provide a reference for more potential RET inhibitors exploration in the future.
Rats were used to test the potential of cannabis to reduce mechanical hypersensitivity, or mechanical allodynia, which was brought on by vincristine chemotherapy. After that, action sites were located. Method of experimentation: After ten daily injections of vincristine, mechanical hypersensitivity developed in comparison to those that received saline at the same periods. The effects on chemotherapy-induced neuropathy were assessed for the CB1/CB2 receptor agonist WIN55, 212-2, the receptor-inactive enantiomer WIN55, 212-3, the CB2-selective agonist (R,S)-AM1241, the opiate agonist morphine, and vehicle. To determine the locations of action, WIN55, 212-2 was injected either locally in the hind paw or intrathecally (i.t.). By employing competitive antagonists for either CB1 (SR141716) or CB2 receptors (SR144528), pharmacological selectivity was demonstrated. Vincristine-evoked mechanical allodynia was decreased when WIN55, 212-2, but not WIN55, 212-3, were administered systemically. A change in the dose-response curve to the left was noticed after WIN55, 212-2 in comparison to morphine therapy. Antibodies of CB1 (SR141716) and CB2 (SR144528) inhibited WIN55, 212-2’s anti-allodynic actions. Via a CB2 mechanism, (R,S)-AM1241 reduced c-induced mechanical hypersensitivity. Without causing catalepsy, both cannabinoid agonists reduced the mechanical hypersensitivity brought on by vincristine. Cannabis-induced neuropathy may be modulated by cannabinoids at spinal sites of action. When delivered intraperitoneally, WIN55, 212-2 but not WIN55,212-3 inhibited vincristine-evoked mechanical hypersensitivity at dosages that were inert after local hindpaw injection. Spinal co-administration of CB1 and CB2 antagonists inhibited WIN55,212-2’s anti-allodynic effects.By activating CB1 and CB2 receptors, cannabinoids inhibit the maintenance of vincristine-induced mechanical allodynia. The spinal cord is involved in the mediation of these anti-allodynic actions, at least partially.
Numerous cellular processes, including the release of neurotransmitters and the contraction of muscles, are largely triggered and regulated by Ca2+ inflow via Ca2+ permeable ion channels. In addition, Ca2+ influx regulates cellular migration and proliferation, two mechanisms linked to cancer. This study focuses on calcium influx in breast cancer cells and discusses how future drugs for breast cancer therapy may be pharmacological modulators of particular Ca2+ influx channels. Certain breast tumors have altered expression of particular calcium permeable ion channels. Such alterations may occasionally be connected to the prognosis and subtype of breast cancer. These days, models both in vivo and in vitro have assisted in identifying particular Ca2+ channels that are crucial for the growth and invasiveness of of cancerous breast cells. Nonetheless, additional research is still needed to fully understand several features of Ca2+ influx in breast cancer. These include figuring out the processes behind the changed expression and the best treatment plan to target breast cancer cells via particular Ca2+ channels. In the upcoming ten years, research should concentrate on the function of Ca2+ influx in mechanisms other than the migration and proliferation of breast cancer cells.
Planar patch-clamp is an effective screening tool in pharmacology, institutionalized in molecular microbiology over 15 years ago [1]. The creation of planar polymer patch-clamp electrodes and silicon substrates in the 2000s [2,3] and the creation of microfluidic chips and perfusable chambers corresponding to this pharmacological screening technology, although works on the development of microfluidic chips for planar patch-clamp were already being published in the early to mid-2000s, and the first "benchmark study" of a chip for planar patch-clamp dates back to 2003 [4,5]. At the moment, there are automated and robotic schemes for planar patch-clamp, including those available for sale and maintenance [6-8]. In the CIS, this method is not widespread, however, devices such as the "Patchliner" with planar patch-clamp, capable of recording up to 8 cells synchronously, are available [9-11]. Patch-clamp tools can be used in the development of drugs and antimicrobial agents, screening of which can be performed on E. coli, etc. [12-14]. The response of the organism mediated by lysosomes can also be the subject of using this method, as lysosomal ion currents can also be measured in planar patch-clamp systems [PMID: 21139138].
Context: Standard and intensive Systolic Blood Pressure (SBP) interventions would be contextualized by describing the antihypertensive medication regimens used in the SPRINT (Systolic Blood Pressure Intervention Trial). This information may also help future implementation efforts to meet population-wide intensive SBP goals. Methods: At the rerandomization and 12-month visits, we provided SPRINT participants with comprehensive medication data. The class of antihypertensive medications was used to categorize regimens. The analyses were divided into groups based on the kind of treatment (intensive target SBP <120 mm Hg versus standard goal SBP <140 mm Hg) Findings: The median number of classes used at the rerandomization visit was 2.0 for 7860 individuals (83.7% of 9361 randomized), and 2.0 for the standard and intensive groups (P=0.559). After a year, the intensive and conventional groups used a median of 3.0 and 2.0 classes, respectively (P<0.001). In the intensive and standard groups, the most common regimens were rerandomization, Angiotensin-Converting Enzyme inhibitor (ACE), or Angiotensin-II Receptor Blocker (ARB) monotherapy (12.6% versus 12.2%). After a year, 5.3% of participants in the intense group and 14.7% of participants in the normal group still used ACE/ARB monotherapy. The following multidrug regimens were utilized at 12 months by both the intensive and regular participants: a calcium channel blocker and thiazide (12.2% and 7.9%) combined in an ACE/ARB thiazide, and calcium channel blocker (11.4% and 4.3%); an ACE/ARB, thiazide, calcium channel blocker, and beta-blocker (6.5% and 1.2%); and 6.2% and 6.8% of each category. Conclusions: Compared to ACE/ARB monotherapy, SPRINT investigators preferred combining ACEs or ARBs, thiazide diuretics, and calcium channel blockers to aim SBP <120 mm Hg.
Background and Aims: Heart failure is one cardiovascular condition that might progress due to mitochondrial dysfunction. In chronic heart failure, 3hydroxy-3-methylglutaryl CoA reductase inhibitors (statins), which prevent the production of ROS, have cardioprotective benefits. However, it is still unknown how statins can protect the mitochondria in heart failure Experimental Strategy: Angiotensin II (1.5 mg/kg/day) or co-administered simvastatin (oral, 10 mg/kg/day) were given to rats for 14 days, after which the treatment was withdrawn. Wheat germ agglutinin staining and echocardiography were used to analyze the structure and function of the heart. Transmission electron microscopy was used to analyze the shape of the mitochondria as well as the numbers of lipid droplets, lysosomes, autophagosomes, and mitophagosomes. After stimulating human cardiomyocytes, flow cytometry was used to assess changes in intracellular ROS and mitochondrial membrane potential (m). and, respectively, JC1 staining. By using immunohistochemistry and western blotting, apoptotic proteins that are associated to autophagy, mitophagy, and mitochondrial regulation were identified. Key outcomes Simvastatin mitigated the disruption of m and dramatically decreased ROS generation. Simvastatin stimulated autophagy and mitophagy, caused lipid droplets to accumulate, and provided energy for maintaining mitochondrial function and impeded apoptosis that was mediated by mitochondria. According to these results, simvastatin-mediated mitochondrial protection prevents heart failure by modifying antioxidant status and enhancing energy sources for autophagy and mitophagy, which prevent mitochondrial damage and cardiomyocyte apoptosis. Final Thoughts and Implications Mitochondria are crucial in controlling the course of heart failure. Simvastatin reduced angiotensin II-induced heart failure through mitochondrial preservation and may offer a new treatment for heart failure prevention.
Metformin is a biguanide oral hypoglycemic agent used for non-insulin dependent diabetes mellitus. Lactic acidosis still the most important and dangerous side effect of acute and chronic metformin use, its mortality can reach up 50%. Metformin poisoning in children remains rare and is very rarely reported in the literature. The curative treatment is based on early extrarenal purification by haemodialysis or haemodiafiltration. However, the prognosis of high doses of metformin can be fatal. We are reporting the case of a 14-year-old female patient who intentionally overdosed on metformin, resulting in lactic acidosis and death.
The consumption of chia seed (Salvia hispanica L.) has increased in recent years due to its high content of omega-3 and omega-6 fatty acids and dietary fibre. This seed also has a high concentration of proteins and essential amino acids, becoming a promising source of bioactive compounds such as chlorogenic acid, caffeic acid, myricetin, quercetin and kaempferol with the major phenolic acid being rosmarinic acide. Owing to the rich nutritional profile, chia seeds provide numerous health benefits such as cardiac and hepatic protective effects, anti-aging and anti-carcinogenic properties. The high amounts of dietary fibres present in the seeds also confer benefits by preserving good glycemic control thus helping in controlling diabetes mellitus. In addition to the food industry for the development of various baked products, production of biodegradable edible films, use as emulsifiers and stabilizers among other uses. In this article we have focused on drafting a technical description of the chia.
Introduction: Colorectal cancer is one of the common causes of hospitalizations, readmission, and poor quality of life due to disability, pain, and death. Most drugs identified to provide chemoprevention in colorectal cancer, such as NSAIDs, have a high level of toxicity. There is need to find novel drugs targeting colorectal cancer with favorable clinical profiles. Objective: The study aimed to identify possible colorectal cancer prevention drugs by comparing the docking scores (representing potential biologic activity) of Aspirin, Sulindac, and Celecoxib with their structurally similar analogs. Materials and Methods: Ligand-based virtual screening and structure-based virtual screening were done for aspirin, sulindac and celecoxib to identify potential drug-like compounds. Compounds that passed the screening, pharmacokinetic profiling, and toxicity testing were considered possible drugs for colorectal cancer chemoprevention. Results: The study identified 7 drug-like compounds from the ZINC database. ZINC02570895, with a better docking score than celecoxib coupled with favorable toxicity and metabolic profiles, was the most appropriate drug candidate for the inhibition of PDK-1. ZINC22309227, with a better docking score and favorable pharmacokinetic profile than sulindac was the most appropriate compound for further development into a MAP Kinase inhibitor. ZINC39406706, ZINC26469982, ZINC01847506, ZINC3382343, and ZINC01682308 had favorable toxicity profiles compared to aspirin and were most suitable for development of cyclooxygenase inhibitors in colorectal cancer prevention. Conclusion: In-vivo and in-vitro tests are needed to ascertain the biological activity, synthesizability and clinical use of the compounds.
The current study identified small molecule inhibitors targeting IL-1β receptor in inhibiting the atherosclerosis. IL-1β plays an important role in the progression of atherosclerosis by binding to the IL-1R1 receptor. IL-1β secreted by the macrophage induces the expression of cell adhesion molecules on the endothelial cell which causes recruitment of immune cells to the intimal site, promoting the atherosclerosis progression. It also releases IL-6 and MMPs which helps in thrombus formation. Thus, targeting IL-1β can help in limiting the recruitment of immune cell to the intimal site. IL-1RA is an antagonist which binds to the IL-1R1 receptor and limit its interaction with the IL-1β. Thus, critical residues on the IL-1R1 interacting with both the IL-1β and IL-1RA were analyzed. A total of 17 residues were found to be common between both the complexs in the 4A region. Further, in-vitro study suggests 12 critical residues on the IL-1R1 mediating the interaction with the IL-1β. Thus, small molecule inhibitors were used to target the critical residues on the IL-1R1 receptor binding with the IL-1β. Virtual screening in Schrodinger and Auto Dock Vina suggested six compounds interacting with most of the critical residues on the IL-1R1 receptor. Further, physicochemical and ADMET analysis of those compounds suggested good values in all the parameters. Thus, the screened compounds hold good potential to act as an anti-IL-1β inhibitor in limiting the progression of atherosclerosis. Further studies would be to check the efficacy and effectivity of the compounds at the in-vitro and in-vivo levels.
Background and Objective: Aging and age-related diseases have become a global concern. There may be a lot of room for the development of TRADITIONAL CHINESE MEDICINE (TCM) in the future. However, it has yet to fully form a system. Therefore, this study aims to explore the material basis and rules of TCM anti-aging based on network pharmacology and data mining. Methods: In this study, potential targets were searched using the HAGR and Aging Atlas databases, followed by compounds and traditional Chinese herbs from the TCMSP database. On this basis, the target-compound network, compound-Chinese herb network and target-compound-herb network were constructed and visualized using Cytoscape 3.7.2. These networks were used to identify potential targets, compounds and herbs. Finally, the rules of Chinese herbs were summarized by the analysis of properties, flavors, and meridian tropism. Results: A total of 25 potential targets, 210 candidate small compounds and 135 kinds of herbs were obtained. The top five targets included PTGS2, AR, ESR1, GSK3B and CCNA2, and diosgenin, formononetin, tanshinone IIA, phaseolin and phaseollidin were identified as the top 5 compounds. In addition, five core herbs (Huluba, Tiandong, Danshen, Kushen and Shandougen) were confirmed. Moreover, according to the frequency statistics, the Chinese herbs that interfere with aging were mainly bitter, acrid, and sweet, had both cold and warm properties, and belonged to the liver and lung meridians. Conclusion: We explored the potential mechanisms of TCM anti-aging by using network pharmacology and summarized the general rules of traditional Chinese herbs medicine. TCM has great potential in the treatment of aging, and this study provides a new approach and idea for the clinical application of integrated Chinese and Western medicine in the treatment of aging.
Alcohol consumption is a significant risk factor for gastrointestinal cancers that may be controlled. The risk of cancer increases with the amount and duration of drinking. Even occasional drinking can raise cancer risk; 100 g or less per week is presently thought to be the upper limit for low-risk consumption. Alcohol is causally linked to colorectal cancer, hepatocellular carcinoma, gastric cancer, oesophageal squamous cell cancer, and most likely also pancreatic cancer. Alcohol can have a multiplicative effect on the development of gastrointestinal cancer when paired with tobacco usage or being overweight. The recent rises in the incidence of early-onset gastrointestinal cancers in various Western nations may have been influenced by alcohol use. It is important to encourage those who use alcohol in a harmful way to enroll in cancer screening programmes. Eliminating alcohol consumption seems to be effective in lowering the elevated cancer risk that alcohol causes.
2,3,5,4'-Tetrahydroxystilbene-2-O-Β-D-Glucoside (TSG), a main bioactive component of polygonum multiflorum Thumb, exerts anti-oxidant, antitumor, anti-inflammatory effects. However, the protective effects of TSG on hepatocytes through anti-inflammatory effects have rarely been investigated. Mouse liver macrophages (Kupffer cells, KUP5 cells) were primed with various concentrations of TSG before Lipopolysaccharide (LPS) treatment, and AML12 hepatocytes were cultured with the supernatants of KUP5 cells. The results showed that TSG inhibits the expression of iNOS in KUP5 cells. Meanwhile, Tumor Necrosis Factor-a (TNF-a) and interleukin-1Β (IL-1Β) expression in KUP5 cells were reversed after TSG treatment. Additionally, the expression of Peroxisome Proliferators-Activated Receptors-γ (PPAR-γ) was up-regulated while the phosphorylation of p65 and IκB-a were decreased in KUP5 cells after TSG treatment. Furthermore, GW9662 (PPAR-γ antagonist) treatment could eliminate the anti-inflammatory effects of TSG. In AML12 hepatocytes, the level of AST, ALT, and apoptosis was decreased after being cultured with the supernatants of KUP5 cells pretreated with TSG. Moreover, TNF-a neutralization of KUP5 cells supernatants could decrease the level of AST, ALT, and AML12 hepatocyte apoptosis. These results indicate that TSG activates PPAR-γ, thereby decreasing nuclear factor kappa-B (NFκB) activation and reducing the release of TNF-a in macrophages to protect hepatocytes from injury. Our study may help further understand the protective effects of TSG on hepatocytes by suppressing liver inflammation.
Objective: To assess the bioequivalence of 200mg Cefixime tablets after oral administration to healthy adults under fasting condition. Method: This study was an open-label, balanced, randomized singledose, two-treatment, two-sequence, two-period, crossover oral bioequivalence study in healthy adult, human subjects under fasting condition. Subjects were fasted overnight for at least 10.00 hours before scheduled time of start of dosing. Investigational Product, one tablet of the test formulation or one tablet of reference formulation (allocated as per the randomization schedule) was administered orally to each subject. The pharmacokinetic parameters maximum plasma concentration (Cmax), area under the plasma concentration-time curve (AUC0-t), AUC extrapolated to infinity (AUC0-8) was estimated to prove bioequivalence. Acceptance range for bioequivalence was 80.00%-125.00% for 90% confidence intervals of the geometric least square means ratio for Cmax, AUC0-t and AUC0-8. Results: For the test formulation, the Cefixime Mean Cmax was 3891.31ng/ mL (vs. 3676.32ng/mL for reference), AUC0-t was 33299.52ng•h/mL (vs. 32182.07ng•h/mL) and AUC0-8 was 34234.88ng•h/mL (vs. 33162.95ng•h/mL). The 90% confidence intervals for the Geometric Least Squares Means ratios for Cefixime were 105.85% (90% CI: 98.73%-113.48%), 103.47% (90% CI: 96.34%-111.13%) and 103.23% (90% CI: 96.28%-110.69%) for Cmax, AUC0-t and AUC0-8 respectively, which are within the acceptance range of 80.00% to 125.00% for pharmacokinetic parameter Cmax, AUC0-t and AUC0-8 required for concluding bioequivalence between the test and reference formulations. There were no deaths or serious adverse events during the conduct of the study. Conclusion: Test product when compared with the reference product meets the bioequivalence criteria in terms of rate and extent of absorption of cefixime after administration of single dose under fasting condition.
Background: Lithium is an effective medication used as first-line therapy for bipolar disorder. Due to its narrow therapeutic index, frequent monitoring is highly recommended. Objective: This study was designed to validate the atomic absorption spectrophotometric method for serum and saliva lithium determination and examine its application for lithium therapeutic monitoring in patients with bipolar affective disorder. Methods: The atomic absorption spectrophotometer (AAS) apparatus (Rayleigh, China) analyzes lithium in human blood and saliva samples. Precision, Recovery % (Accuracy), Detection Limit, and Specificity were evaluated to validate the used analysis method. The patient's study design was based on an observational study, where four patients with bipolar disorders type 1 and 2 (adults with bipolar disorder and on lithium therapy for one month) aged 32 to 64 years and weighing from 56 to 92 kg participated in this study. Four samples were collected from each patient, two samples of blood and another two of saliva. Results: A linear relationship between the absorbance and lithium concentrations was obtained in 0.175 - 7 μg/mL with an R2 of 0.99. Precision, Recovery % (Accuracy), Detection Limit, and Specificity are within the accepted limits. Ratio analysis of (Saliva/Blood) of Cmin, Cmax, and Cpss were 2.64, 3.77, and 3.54, respectively. The salivary lithium therapeutic range was 2.83- 4.25 mmol/L, which is much higher than blood. Only lithium Cmax in saliva was slightly affected by Body mass index (BMI), age, and creatinine clearance (CLcr), suggesting insignificant effects on lithium levels in general. Conclusions: The AAS method used in this study is reliable and accurate for determining serum and saliva lithium concentrations. A higher correlation coefficient between lithium in saliva and blood suggests that saliva is an excellent candidate to replace blood for lithium therapeutic drug monitoring.
