Phytotherapy in psychiatry: why psychiatrists should know about it.

There is a substantial use of Complementary and Alternative Medicine (CAM) among both the general population and psychiatric patients, with only a minority of these users disclosing this information to their healthcare providers, including physicians and psychiatrists. This widespread use of CAM can impact positively or negatively on the clinical outcomes of psychiatric patients, and it is often done along with conventional medicines. Among CAM, phytotherapy has a major clinical relevance due to the introduction of potential adverse effects and drug interactions. Thus, the psychiatrist must learn about phytotherapy and stay up-to-date with solid scientific knowledge about phytotherapeutics/herbal medicines to ensure optimal outcomes for their patients. Furthermore, questions about herbal medicines should be routinely asked to psychiatric patients. Finally, scientifically sound research must be conducted on this subject.

Nonvitamin K Anticoagulants: Risk of Bleeding When Interacting With Other Medications: A Cohort Study From Medicare.

INTRODUCTION: Patients on nonvitamin K antagonist (NVKA) are usually taking other drugs. Potential interaction may increase the gastrointestinal (GI) bleeding risk associated with NVKA. METHODS: Observational cohort study using Medicare data from 2017 to 2020. Participants receiving a NVKA were included. A concomitant overlapping period while on NVKA was assessed for nonsteroidal anti-inflammatory drugs (NSAIDS), selective serotonin reuptake inhibitors (SSRI), antiplatelets, glucocorticoids, aspirin and proton pump inhibitors (PPI). A logistic regression predicting either any bleeding or GI bleeding was conducted estimating the odds ratio (OR) and 95% confidence interval (CI). RESULTS: A total of 102 531 people on NVKA with mean age 77 years (SD = 9.8) and 55% females (N = 56 671) were included. Previous history of GI bleeding occurred in 2 908 (2.8%) participants, concomitant exposure to PPI occurred in 38 713 (38%), SSRI in 16 487 (16%), clopidogrel in 15 795 (15.4%), NSAIDs in 13 715 (13.4%) and glucocorticoids in 13 715 (13.4%). Risk for any bleeding was shown for clopidogrel (OR: 1.37, 95% CI: 1.30, 1.44), prasugrel/ticagrelor (OR: 1.36, 95% CI: 1.18, 1.58), glucocorticoids (OR: 1.26, 95% CI: 1.19, 1.34), and SSRIs (OR: 1.13, 95% CI: 1.07, 1.19). GI bleeding risk was shown for clopidogrel (OR: 1.44, 95% CI: 1.34, 1.55), prasugrel/ticagrelor (OR: 1.47, 95% CI: 1.20, 1.79), SSRIs (OR: 1.09, 95% CI: 1.01, 1.17) and glucocorticoids (OR: 1.33, 95% CI: 1.23, 1.44). PPI use was correlated with both NSAID (r = 0.07, p ≤ 0.0001) and SSRI use (r = 0.09, p ≤ 0.0001). CONCLUSION: NVKA concomitantly taken with antiplatelets, glucocorticoids, and SSRIs showed an increased risk for any bleeding and GI bleeding.

Rhabdomyolysis associated with concomitant use of colchicine and statins in the real world: identifying the likelihood of drug-drug interactions through the FDA adverse event reporting system.

Background: Currently, there remains substantial controversy in research regarding whether the concomitant use of colchicine and statins increases the occurrence of rhabdomyolysis, warranting further substantiation. Objective: This study aimed to identify the likelihood drug-drug interactions (DDIs) for the co-administration of colchicine and statins resulting in rhabdomyolysis. Methods: A disproportionality analysis was conducted by using data sourced from the US Food and Drug Administration Adverse Event Reporting System (FAERS) to detect rhabdomyolysis signals associated with the combined use of colchicine and statins. The association between (colchicine/statins/colchicine and statins) and rhabdomyolysis were evaluated using information component (IC). DDI signals were calculated based on the Ω shrinkage measure and Bayesian confidence propagation neural network (BCPNN) method. Furthermore, stratification was performed based on colchicine and individual statins agents. Results: In total, 11,119 reports of rhabdomyolysis were identified in the FAERS database, 255 (2.29%) involved both colchicine and statins. Our analysis showed potential DDI signals of rhabdomyolysis (Ω025 = 1.17) among individuals concurrent use of colchicine and statins. Moreover, further drug-specific analysis suggests DDI signals in the colchicine-atorvastatin pair (Ω025 = 1.12), and colchicine-rosuvastatin pair (Ω025 = 1.05), along with a higher proportion of rhabdomyolysis (IC025 = 5.20) and (IC025 = 4.26), respectively. Conclusion: The findings suggest that concomitant use of colchicine and statins may increase the risk of rhabdomyolysis, particularly when combined with atorvastatin or rosuvastatin. Therefore, healthcare professionals should pay special attention to life-threatening AE such as rhabdomyolysis, when co-prescribing colchicine statins.

Effect of Danhong injection on pharmacokinetics and pharmacodynamics of rivaroxaban in rats.

BACKGROUND AND OBJECTIVES: Rivaroxaban is often used in combination with DHI to treat thromboembolic disease. Whether the combination causing HDIs is still unknown. The purpose of this study was to evaluate effects of DHI on pharmacokinetics and pharmacodynamics of rivaroxaban in rats and effects on CYP3A2. METHODS: Plasma concentration of rivaroxaban with or without DHI was determined by HPLC. Pharmacokinetics parameters were calculated. Effect of DHI on pharmacodynamics of rivaroxaban was investigated by APTT, PT, TT, FIB, INR, length of tail thrombosis, vWF, t-PA, PAI-1, IL-1ß, TNF-α and histopathological sections. Effect of DHI on CYP3A2 in rats was investigated by probe drug method. RESULTS: Cmax and AUC of rivaroxaban increased significantly in combination group (P < 0.05). APTT, PT, INR and TT increased (P < 0.05), length of tail thrombosis, FIB, vWF, PAI-1, IL-1ß and TNF-α of combination group decreased significantly (P < 0.05) compared with rivaroxaban or DHI alone. Histopathologic section of tail thrombus had significant improvement. Cmax and AUC of dapsone increased (P < 0.05) in DHI group. CONCLUSION: In summary, DHI is an inhibitor of CYP3A2 and could significantly affect pharmacokinetics and pharmacodynamic of rivaroxaban, enhance anticoagulant and antithrombotic efficacy in rats. However, the combination of rivaroxaban and DHI might lead to potential HDIs. The dosage of rivaroxaban should be adjusted in clinical.

Assessment of co-ingestion effects on poisoning patterns, drug-drug interactions, and adverse outcomes in acute toxic exposure.

Multiple toxic exposures are increasing nowadays. In cases of acute poisoning involving multiple agents, there is a potential for additional toxicity that goes beyond the effects and toxicity of each drug. Very scarce studies have investigated the problem of multiple toxic exposures where the information on drug-drug interactions (DDIs) originates from clinical experience, which is inconclusive and cannot be generalized to patients. Therefore, the current study aimed to explore the influence of co-ingestion on the clinical presentation of exposed patients and to identify the common associated DDIs and their effect on poisoning outcomes, including the need for mechanical ventilation (MV), intensive care unit (ICU) utilization, and prolonged hospital stay. The current study is a retrospective cross-sectional study that was conducted using medical records of 169 adult patients admitted to a poison control center and diagnosed with acute drug poisoning. Of them, 40.8 % were exposed to multiple drugs. The total number of drugs reported in the current study was 320 preparations, with an average of 1.9 drugs per patient. There were about 726 potential DDIs; more than half of these interactions were significant (n = 486). Antidepressants and psychotropics showed the highest total number of DDIs. Patients with multiple ingestion were significantly older and this pattern of exposure was more frequent among suicidal attempters, substance abusers, cardiac patients, and patients diagnosed with neurological and psychological problems. Moreover, patients with multiple ingestions showed severe presentations indicated by higher grades of Poison Severity Score and lower Glasgow Coma Scale. Multiple ingestion was associated with higher liability for MV, ICU admission, and prolonged length of hospital stay (p < 0.001). There was a significant moderate direct correlation between the number of drugs consumed and the number of resulting DDIs (r = 0.542, p < 0.001). There was a significant direct correlation between the occurrence of significant chronic/chronic drug interactions from one side and the history of substance abuse (r = 0.596, p = 0.041) and psychological illness (r = 0.662, p = 0.019) from the other side. Moreover, significant acute/acute drug interactions were correlated with being male (r = 0.969, p < 0.001) of older age (r = 0.672, p = 0.024). Similarly, significant acute/chronic drug interactions were moderately correlated with being a male (r = 0.692, p = 0.013). The presence of epilepsy and psychological problems were the main significant predictors of multiple acute toxic exposures. Among the patients exposed acutely to more than one agent who were on long-term treatment, exposure to three drugs or more could significantly predict the need for MV with excellent area under the curve (AUC) of 0.896 and 77.0 % accuracy. Moreover, and it was a fair predictor of ICU admission (AUC = 0.625), with an 88.9 % ability to exclude patients unlikely to need ICU admission. Particular attention should be paid to the patients at risk of potential DDIs. When prescribing drugs, the minimum number of drugs with the lowest effective doses, and minimal potential DDIs should be prioritized.

Therapeutic drug monitoring in Parkinson's disease.

A patient-tailored therapy of the heterogeneous, neuropsychiatric disorder of Parkinson's disease (PD) aims to improve dopamine sensitive motor symptoms and associated non-motor features. A repeated, individual adaptation of dopamine substituting compounds is required throughout the disease course due to the progress of neurodegeneration. Therapeutic drug monitoring of dopamine substituting drugs may be an essential tool to optimize drug applications. We suggest plasma determination of levodopa as an initial step. The complex pharmacology of levodopa is influenced by its short elimination half-life and the gastric emptying velocity. Both considerably contribute to the observed variability of plasma concentrations of levodopa and its metabolite 3-O-methyldopa. These amino acids compete with other aromatic amino acids as well as branched chain amino acids on the limited transport capacity in the gastrointestinal tract and the blood brain barrier. However, not much is known about plasma concentrations of levodopa and other drugs/drug combinations in PD. Some examples may illustrate this lack of knowledge: Levodopa measurements may allow further insights in the phenomenon of inappropriate levodopa response. They may result from missing compliance, interactions e.g. with treatments for other mainly age-related disorders, like hypertension, diabetes, hyperlipidaemia, rheumatism or by patients themselves independently taken herbal medicines. Indeed, uncontrolled combination of compounds for accompanying disorders as given above with PD drugs might increase the risk of side effects. Determination of other drugs used to treat PD in plasma such as dopamine receptor agonists, amantadine and inhibitors of catechol-O-methyltransferase or monoamine oxidase B may refine and improve the value of calculations of levodopa equivalents. How COMT-Is change levodopa plasma concentrations? How other dopaminergic and non-dopaminergic drugs influence levodopa levels? Also, delivery of drugs as well as single and repeated dosing and continuous levodopa administrations with a possible accumulation of levodopa, pharmacokinetic behaviour of generic and branded compounds appear to have a marked influence on efficacy of drug treatment and side effect profile. Their increase over time may reflect progression of PD to a certain degree. Therapeutic drug monitoring in PD is considered to improve the therapeutic efficacy in the course of this devastating neurologic disorder and therefore is able to contribute to the patients' precision medicine. State-of-the-art clinical studies are urgently needed to demonstrate the usefulness of TDM for optimizing the treatment of PD.

Interactions of human serum albumin with phosphate and Tris buffers: impact on paclitaxel binding and nanoparticles self-assembly.

AIM: To investigate the conformational changes in human serum albumin (HSA) caused by chemical (CD) and thermal denaturation (TD) at pH 7.4 and 9.9, crucial for designing controlled drug delivery systems with paclitaxel (PTX). METHODS: Experimental and computational methods, including differential scanning calorimetry (DSC), UV-Vis and intrinsic fluorescence spectroscopy, mean diameter, polydispersity index (PDI), ζ-potential, encapsulation efficiency (EE), in vitro release and protein docking studies were conducted to study the HSA denaturation and nanoparticles (NPs) preparation. RESULTS: TD at pH 7.4 produced smaller NPs (287.1 ± 12.9 nm) than CD at pH 7.4 with NPs (584.2 ± 47.7 nm). TD at pH 9.9 exhibited high EE (97.3 ± 0.2%w/w) with rapid PTX release (50% within 1h), whereas at pH 7.4 (96.4 ± 2.1%w/w), release only 40%. ζ-potentials were around -30 mV. CONCLUSION: Buffer type and pH significantly influence NP properties. TD in PBS at pH 7.4, provided optimal conditions for a stable and efficient drug delivery system.

Assessing pharmacokinetics and drug-drug interactions of the combination therapy of myelofibrosis with ruxolitinib and lenalidomide by a new eco-friendly HPLC method for their simultaneous determination in plasma.

Ruxolitinib (RUX), a Janus kinase 2 (JAK2) inhibitor, and lenalidomide (LEN), an immunomodulatory agent, have recently been proposed as a combined treatment for myelofibrosis (MF). This combination has demonstrated improved efficacy, safety, and tolerability compared to monotherapy. To further refine these findings, an efficient analytical tool is needed to simultaneously determine RUX and LEN concentrations in blood plasma. This tool would enable the study of their pharmacokinetics, drug-drug interactions, and therapeutic monitoring during MF therapy. Unfortunately, such a method has not been existed in the literature. This study presents the first HPLC method with UV detection for the simultaneous quantitation of RUX and LEN in plasma. The method was validated according to the ICH guidelines for bioanalytical method validation. It exhibited linearity in the concentration ranges of 10 to 3150 ng mL- 1 for RUX and 80 to 5200 ng mL- 1 for LEN. The limits of quantitation were determined to be 25 and 90 ng mL- 1 for RUX and LEN, respectively. All other validation parameters were satisfactory. The HPLC-UV method was successfully employed to study the pharmacokinetics and drug-drug interactions of RUX and LEN in rats following oral administration of single doses. The results demonstrated that the pharmacokinetics of both drugs were changed substantially by their coadministration. LEN exhibited synergistic effects on the maximum plasma concentration (Cmax) and total bioavailability of RUX, meanwhile it exhibited diminishing effect on the values of volume of distribution (Vd) and clearance (CL). Additionally, RUX decreased the Cmax and total bioavailability of LEN, meanwhile it increased its Vd and CL. These data suggest that the use of RUX, as a combination with LEN, is a better therapeutic approach for MF, compared with RUX as a monotherapy. The effects of LEN on the pharmacokinetics of RUX should be considered and can be useful in determining the appropriate RUX dosage and dosing regimen to achieve the desired therapeutic effect when used as a combination therapy with LEN. The method's environmental friendliness was confirmed through three comprehensive tools. This method represents a valuable tool for determining the appropriate dosage and dosing regimen of RUX in combination therapy with LEN to achieve the desired therapeutic effect. Furthermore, it can aid in predicting drug distribution in different patients and assessing the drug accumulation or insufficient drug levels in specific body compartments.

Characterization of Expression-Based Gene Clusters Gives Insights into Variation in Patient Response to Cancer Therapies.

Background: Transcriptomics can reveal much about cellular activity, and cancer transcriptomics have been useful in investigating tumor cell behaviors. Patterns in transcriptome-wide gene expression can be used to investigate biological mechanisms and pathways that can explain the variability in patient response to cancer therapies. Methods: We identified gene expression patterns related to patient drug response by clustering tumor gene expression data and selecting from the resulting gene clusters those where expression of cluster genes was related to patient survival on specific drugs. We then investigated these gene clusters for biological meaning using several approaches, including identifying common genomic locations and transcription factors whose targets were enriched in these clusters and performing survival analyses to support these candidate transcription factor-drug relationships. Results: We identified gene clusters related to drug-specific survival, and through these, we were able to associate observed variations in patient drug response to specific known biological phenomena. Specifically, our analysis implicated 2 stem cell-related transcription factors, HOXB4 and SALL4, in poor response to temozolomide in brain cancers. In addition, expression of SNRNP70 and its targets were implicated in cetuximab response by 3 different analyses, although the mechanism remains unclear. We also found evidence that 2 cancer-related chromosomal structural changes may impact drug efficacy. Conclusion: In this study, we present the gene clusters identified and the results of our systematic analysis linking drug efficacy to specific transcription factors, which are rich sources of potential mechanistic relationships impacting patient outcomes. We also highlight the most promising of these results, which were supported by multiple analyses and by previous research. We report these findings as promising avenues for independent validation and further research into cancer treatments and patient response.

Ticagrelor alters the membrane of Staphylococcus aureus and enhances the activity of vancomycin and daptomycin without eliciting cross-resistance.

Infections with multidrug-resistant bacteria pose a major healthcare problem which urges the need for novel treatment options. Besides its potent antiplatelet properties, ticagrelor has antibacterial activity against Gram-positive bacteria, including methicillin- and vancomycin-resistant Staphylococcus aureus (MRSA and VRSA). Several retrospective studies in cardiovascular patients support an antibacterial effect of this drug which is not related to its antiplatelet activity. We investigated the mechanism of action of ticagrelor in Staphylococcus aureus and model Bacillus subtilis, and assessed cross-resistance with two conventional anti-MRSA antibiotics, vancomycin and daptomycin. Bacillus subtilis bioreporter strains revealed ticagrelor-induced cell envelope-related stress responses. Sub-inhibitory drug concentrations caused membrane depolarization, impaired positioning of both the peripheral membrane protein MinD and the peptidoglycan precursor lipid II, and it affected cell shape. At the MIC, ticagrelor destroyed membrane integrity, indicated by the influx of membrane impermeable dyes, and lipid aggregate formation. Whole-genome sequencing of in vitro-generated ticagrelor-resistant MRSA clones revealed mutations in genes encoding ClpP, ClpX, and YjbH. Lipidomic analysis of resistant clones displayed changes in levels of the most abundant lipids of the Staphylococcus aureus membrane, for example, cardiolipins, phosphatidylglycerols, and diacylglycerols. Exogeneous cardiolipin, phosphatidylglycerol, or diacylglycerol antagonized the antibacterial properties of ticagrelor. Ticagrelor enhanced MRSA growth inhibition and killing by vancomycin and daptomycin in both exponential and stationary phases. Finally, no cross-resistance was observed between ticagrelor and daptomycin, or vancomycin. Our study demonstrates that ticagrelor targets multiple lipids in the cytoplasmic membrane of Gram-positive bacteria, thereby retaining activity against multidrug-resistant staphylococci including daptomycin- and vancomycin-resistant strains.IMPORTANCEInfections with multidrug-resistant bacteria pose a major healthcare problem with an urgent need for novel treatment options. The antiplatelet drug ticagrelor possesses antibacterial activity against Gram-positive bacteria including methicillin-resistant and vancomycin-resistant Staphylococcus aureus strains. We report a unique, dose-dependent, antibacterial mechanism of action of ticagrelor, which alters the properties and integrity of the bacterial cytoplasmic membrane. Ticagrelor retains activity against multidrug-resistant staphylococci, including isolates carrying the most common in vivo selected daptomycin resistance mutations and vancomycin-intermediate Staphylococcus aureus. Our data support the use of ticagrelor as adjunct therapy against multidrug-resistant strains. Because of the presence of multiple non-protein targets of this drug within the bacterial membrane, resistance development is expected to be slow. All these findings corroborate the accumulating observational clinical evidence for a beneficial anti-bacterial effect of ticagrelor in cardiovascular patients in need of such treatment.

Drug-drug interactions in HIV-infected patients receiving chemotherapy.

INTRODUCTION: Coadministration of antiretrovirals and anti-cancer medications may present many complex clinical scenarios. This is characterized by the potential for drug-drug interactions (DDIs) and the challenges that arise in patient management. In this article, we investigate the potential for DDIs between antiretrovirals, including protease inhibitors (PIs), non-nucleoside reverse transcriptase inhibitors, nucleoside reverse transcriptase inhibitors (NRTIs), integrase strand transfer inhibitors (INSTIs), and anti-cancer medications. AREAS COVERED: PubMed, Google Scholar, and Clinicaltrials.gov were searched for relevant articles in April 2024. Our review highlights PIs and NNRTIs as particularly prone to DDIs with anticancer agents, with implications for efficacy and toxicity of concomitant cancer therapy. We explain the mechanisms for interactions, emphasizing the significance of pharmacokinetic effects and enzyme induction or inhibition. We discuss clinical challenges encountered in the management of patients receiving combined ART and cancer therapy regimens. EXPERT OPINION: Data are lacking for potential DDIs between antiretroviral and anti-cancer agents. While some interactions are documented, others are theoretical and based on the pharmacokinetic properties of the medications. Awareness of these interactions, inter-collaborative care between healthcare providers, and standardized treatment guidelines are all crucial for achieving optimal treatment outcomes and ensuring the well-being of patients with HIV/AIDS and cancer comorbidities.

Plasma and urinary CP I and CP III concentrations in chimeric mice with human hepatocytes after rifampicin administration.

The interest in transporter-mediated drug interactions has been increasing in the field of drug development. In this study, we measured the plasma and urinary concentrations of coproporphyrin (CP) I and CP III as endogenous substrates for organic anion-transporting polypeptide (OATP) using chimeric mice with human hepatocytes (PXB mice) and examined the influence of an OATP inhibitor, rifampicin (RIF). CP I and CP III were actively taken up intracellularly, and RIF inhibited the uptake in a concentration-dependent manner for both CP I and CP III in human hepatocytes (PXB-cells). Single doses of RIF at 10 and 30 mg/kg were orally or intravenously administered to PXB mice and wild-type ICR mice. Plasma concentrations (AUC0-8h) of CP I increased in both mice. However, a marked increase in CP III was only observed in ICR mice, after intravenous administration of RIF at 30 mg/kg. The IC50 values of RIF for intracellular CP I/III uptake and the unbound plasma concentrations of RIF suggested that the increase in plasma CP I is associated with the exposure of RIF to OATPs. The 24-h cumulative urinary excretions of CP I and CP III increased in both mice, but more markedly in PXB mice. Thus, RIF increased the plasma and urinary concentrations of CP I and CP III in the mice, as reported in humans, and CP I may be a more sensitive biomarker of OATP-mediated drug interactions in PXB mice.

Physical Compatibility Between Intravenous Magnesium Sulfate and Potassium or Sodium Phosphate in a Pediatric Intensive Care Unit.

Objective:To evaluate the physical compatibility between intravenous magnesium sulfate and potassium and sodium phosphate, a common electrolyte intravenous supplementation in pediatric intensive care units. Study design: Magnesium sulfate was mixed separately with potassium phosphate and sodium phosphate at ratios of 1:1, 1:4, and 4:1. Binary mixtures were prepared, in triplicate and under sterile conditions, by permuting the order of addition. The undiluted pure drugs were used as controls for possible sequence effects. Visual changes, turbidity, and pH were assessed immediately after mixing (baseline) and at 4 and 24 hours. Two observers performed visual changes by naked-eye visual inspection in order to search visible haze, particulate matter, gas formation, or color change. Turbidity was measured by nephelometry and incompatibility was defined as an increase of ≥0.5 nephelometric turbidity units (NTU) from baseline. pH was measured using a portable pH meter and incompatibility was defined as a variation of >1 pH unit during the observation period. Results: None of the admixtures exhibited visual changes or significant variations in turbidity (increases of ≥0.5 in nephelometric turbidity units) or pH (changes of >1 unit) during the observation period and neither compared with baseline. Conclusion: In this study, no visual changes were observed, and turbidity and pH evaluated by instrumental methods remained within acceptable limits and showed no significant variations from baseline, therefore no physical incompatibility between magnesium sulfate and potassium or sodium phosphate was found.

Metformin-associated lactic acidosis: a serious complication of a common drug.

Metformin-associated lactic acidosis (MALA) is a rare and potentially life-threatening complication of metformin use. It typically occurs in patients who are diabetic and also have other risk factors for lactic acidosis, including kidney and liver conditions, malignancy, or use of certain medications. We report a case of MALA in a man in his 70s with diabetes who presented with gradually worsening gastrointestinal symptoms, including severe abdominal pain and nausea. He reported these symptoms in the setting of metformin use with an acute kidney injury (AKI), likely brought on by poor oral intake and excessive antibiotic use for a urinary tract infection. He was promptly started on intravenous fluids with a bicarbonate drip to concurrently treat his prerenal AKI and lactic acidosis, which resulted in rapid resolution of his symptoms. Renal function normalised within 12 days of admission. Since diabetic patients commonly use metformin and are also at higher risk of renal dysfunction, this case highlights the vulnerability of this group of patients and the need for increased knowledge and awareness of MALA.

Foundations for a Personalized Psycho-Oncology: The State of the Art.

Personalized psycho-oncology represents a major challenge for the holistic care of cancer patients. It focuses on individualized psychotherapeutic and psychiatric interventions to address specific psychological needs. This narrative review summarizes the current literature on personalized psycho-oncology and highlights the prevalence and impact of psychiatric/psychological disorders in cancer patients. Personalized approaches, including tailored interventions and interdisciplinary collaboration, have been shown to be effective in improving mental health and overall quality of life. The integration of inflammatory biomarkers into treatment plans is a promising but challenging way to alleviate mental health problems. In addition, there is a need for specific diagnostic tools and treatment guidelines that take into account the specific psychological impact of different types of cancer. Future research should aim to refine these personalized strategies, improve diagnostic accuracy, and evaluate the cost-effectiveness of these interventions to improve both the psychological well-being and treatment outcomes of cancer patients.