Systemic Anti Cancer Drug Therapy Essay
Systemic Anti Cancer Drug Therapy Essay
Questions:
2. What conclusions can the researchers from this type of experiments?
3. What are the limitations of this technique?
4. What is the difference between a Pre-Clinical Study and a Clinical Study? Are they both necessary? Why or why not?
5. Summarize the key steps of the procedure used in this experiment, and the purpose behind these steps.
6. Consider Which of the panels represent the control group? Which of the panels represent the experimental group?
7. What does the change in Ki-67 expression indicate? What is the meaning of the change in caspase-3? Systemic Anti Cancer Drug Therapy Essay.
8. What does indicate about temozolomide treatment?
9. Has this approach been useful to other researchers? Share the citation and abstract here. Search the PubMed Database. For help in using PubMed go to the Quick Start Guide.
Answers:
Hypothesis And Rationale
Gliomas refer to a type of tumor that begin in the glial cells of the brain and the spinal cord. They comprise of more than 30% of all kinds of tumors in the central nervous system, of which 80% are malignant. These malignant gliomas are termed as rapidly progressive brain tumors that are made up of anaplastic astrocytoma, anaplastic oligodendroglioma, and mixed anaplastic oligoastrocytoma. Furthermore, its incidence is quite high with approximately 35–45% of them representing primary brain tumors (Goodenberger & Jenkins, 2012). The research was based on the idea that existing therapies for malignant gliomas have palliative effect. This can be attributed to the fact that although malignant gliomas are lethal, chemotherapy is the mainstay of treatment for patients suffering from this condition (Ciechomska et al., 2013). The primary aim of palliative chemotherapy has been associated with prolonging the rates of disease survival.Systemic Anti Cancer Drug Therapy Essay. However, this treatment fails to cure the tumor (Qin et al., 2013). Another major factor that formed the rationale for the research can be attributed to recent research studies that elaborated on the drawbacks and discrepancies of drug efficacy tests on patients with malignant glioma (Miura et al., 2013).
High failure rates of drug based trials called for the need of conducting studies with greater reliability. The authors also focused on the genetic, phenotypic and epigenetic changes of carcinoma cells that are brought about in in vitro tumor cell cultures. This made them formulate the research plan for demonstrating a novel method that relied on the use of specific malignant glioma surgical specimens, in the form of undissociated tumor blocks, subjected to the use of temozolomide (TMZ), a first line chemotherapeutic agent (Joshi et al., 2011).
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Conclusions Drawn
The research findings suggested that in vitro cell cultures were found to specifically expand different types of tumor cells, regardless of the conditions of cell culture. Furthermore, they represent only a certain subpopulation of the complete tumor. The researchers also found that phenotypic and genetic transformation of artificial cell expansion occurs subsequently in long term cell culture experiments. They identified tumor heterogeneity or distinct phenotypic and morphological profiles of tumor cells as a major barrier that prevents proper treatment of such conditions (He et al., 2010). Thus, the researchers concluded that selectively enriching tumor cell population, regardless of their type is not a feasible and reliable method for determining the effectiveness of any chemotherapeutic agent on the tumor cells.
The authors were also of the view that animal models of brain tumors that have been derived from specific tumor subpopulation have the potential of illustrating the characteristic features of the subpopulation only, and not the entire tumor. Systemic Anti Cancer Drug Therapy Essay. Thus, it was concluded from the experiment that use of tumor tissue explant method might hold the potential of accelerating the identification of novel chemotherapeutic drugs for treating malignant tumors (Joshi et al., 2011).
Systemic anticancer therapy, comprising chemotherapy agents alongside targeted therapies and immunotherapy, is clinically indicated for late-stage lung cancer. It is delivered in regimens often containing multiple anticancer agents as well as supportive care medicines to reduce side effects, raising potential for polypharmacy and therefore the possibility of drug–drug interactions with medicines taken for comorbidities. A pharmacy-led process commonly performed to assist safe prescribing in secondary care is medicines reconciliation; its benefit in minimising interactions involving systemic anticancer therapy medicines has not been assessed previously.
Objectives
The objectives were to characterise the potential drug–drug interactions between systemic anticancer therapy medicines for lung cancer and other medicines and to evaluate the rate of medicines reconciliation being performed and the extent of documentation of potential interactions (clinical audit).
Methodology
This retrospective case series study involved recording the medicines being taken by lung cancer patients undergoing systemic anticancer therapy elicited in consultations at Chelsea and Westminster Hospital, United Kingdom. Potential interactions were identified and characterised in terms of severity using the British National Formulary and other sources. Patient consultation records were also searched for documentation of medicines reconciliation and acknowledgement of potential drug–drug interactions. Systemic Anti Cancer Drug Therapy Essay.
Results
Twenty-three patients were included in this study. Eighty-eight potential drug–drug interactions were identified across 21 patients, 39% (34/88) of which involved the supportive care medicine dexamethasone. 3.0% of consultations included a documented medicines reconciliation, and 15.9% of potential interactions were documented in the notes, with no correlation between the two. Potentially serious interactions were significantly more likely to be documented (p < 0.05).
Conclusions
Many potential drug–drug interactions involving anticancer agents and supportive care medicines exist; particular attention should be paid to dexamethasone. Documentation of interactions and medicines reconciliation occur much less often than expected, suggesting there is scope for implementing methods of safe prescribing to prevent adverse drug effects.
Introduction
Systemic anticancer therapy (SACT)
There are many different treatment options for lung cancer, and these are influenced by type, extent and progression of disease. These treatments can be categorised into surgery, radiotherapy and systemic anticancer therapy (SACT), combinations of which are also possible. While surgery and radiotherapy tend to be of use in local, early-stage disease, SACT is largely used as first-line treatment in advanced stage IIIb-IV non-small-cell lung cancer (NSCLC), with extensive nodal involvement and metastases, to ‘improve survival, disease control and quality of life’ and is the preferred treatment for both limited and extensive small-cell lung cancer (SCLC) [1]. It is planned in cycles, between which the patient is reviewed for response to therapy.
SACT can be divided into three categories, based on mechanism of action in treating cancer. The most extensive group, chemotherapy, involves the use of cytotoxic drugs to directly destroy tumour cells. It has multiple applications in NSCLC, due to the various intentions of use across most stages of lung cancer. As an adjunct or in combination with radiotherapy, it can be considered pre-operatively in early-disease (stage I–II) patients suitable for surgery; adjuvant chemotherapy aiming to kill cancer cells following radiotherapy is an option in stage II–III disease [2]. There are multiple classes of chemotherapy drug available, with a variety of intracellular targets such as DNA and microtubules. Systemic Anti Cancer Drug Therapy Essay. Biological therapies, the second group, are anticancer agents that prevent the spread of cancer by ‘interfering with specific molecules involved in tumour growth and progression’ [3], as opposed to killing tumour cells directly. These targeted therapies have further developed as a result of advancements in tumour analysis for protein mutations that cause uncontrolled proliferation, such as those in epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) [4]. The third mechanism of SACT is immunotherapy, where monoclonal antibodies recruit the immune system to recognise and attack malignant cells [5]. Table 1 details the SACT agents recommended for use in lung cancer.
Table 1.
| Anticancer agent | Indication(s) in lung cancer | Class of anticancer agent | Main mechanism |
|---|---|---|---|
| Cyclophosphamide | Extensive SCLC | Nitrogen mustard | Intrastrand cross linking of DNA |
| Carboplatin, cisplatin | Stage I–II NSCLC (adjuvant) | Platinum-based compound | |
| Stage IIIb–IV NSCLC (palliative) | |||
| All-stage SCLC (palliative) | |||
| Pemetrexed | Stage IIIb–IV non-squamous NSCLC (first line) |
Folate antagonist | Blocking the synthesis of DNA and/or RNA |
| Gemcitabine | Stage IIIb–IV squamous NSCLC (first-line) | Pyrimidine pathway antimetabolite | |
| Doxorubicin | Extensive SCLC | Anthracycline | Multiple effects on DNA/RNA synthesis and topoisomerase action |
| Docetaxel, paclitaxel | Stage IIIb–IV NSCLC (first line) | Taxane | Microtubule assembly; prevents spindle formation |
| Vincristine | Extensive SCLC | Vinca alkaloid | |
| Vinorelbine | Stage IIIb–IV squamous NSCLC (first line) | ||
| Topotecan | Relapsed SCLC | Campothecin | Inhibition of topoisomerase |
| Etoposide | All-stage SCLC (palliative) | Other plant derivative | |
| Afatinib, erlotinib, gefitinib | Stage IV–NSCLC + EGFR mutation (first line) |
Epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) |
Inhibition of kinases involved in growth factor receptor transduction |
| Stage IV NSCLC (second line if refractory) | |||
| Crizotinib | Stage IIIb–IV NSCLC + ALK translocation (second line) | Anaplastic lymphoma kinase (ALK) inhibitor | |
| Nintedanib | Stage IIIb–IV non-squamous NSCLC (second line, if progressive disease after first line) Systemic Anti Cancer Drug Therapy Essay. | Vascular endothelial growth factor receptor (VEGFR1-3), fibroblast growth factor receptor (FGFR1-3) and platelet-derived growth factor receptor (PDGFRα,β) inhibitor | |
| Nivolumab | Stage IV squamous and non-squamous NSCLC | Anti-programmed cell death-1 (PD-1) monoclonal antibody |
Recruitment of T cells |
Application of SACT involves the use of combination therapies. The most recent statistics of the commonest regimens for lung cancer are shown in Figure 1.
Supportive care medicines are often prescribed as part of the SACT regimen to prevent side effects from occurring. These include various antiemetics such as aprepitant, domperidone, and ondansetron, to combat nausea and vomiting, a common adverse effect of most anticancer agents [6]. Notably, some have higher potential for nausea than others, particularly cisplatin, and different regimens thus require varying doses of antiemetic [17]. Corticosteroids, such as dexamethasone, also counter nausea but additionally reduce the incidence and severity of skin rash, another frequent adverse reaction [6]. Systemic Anti Cancer Drug Therapy Essay. Other medicines include folic acid and vitamin B12 for the antifolate drug pemetrexed [18, 19] and hydration guidelines for the nephrotoxic platinum-based compounds [20], encompassing combinations of oral furosemide, intravenous saline, and magnesium or potassium salt solutions [21, 22].
Drug–drug interactions
As discussed, cancer patients for whom SACT is indicated take a multitude of medicines, either within a complex regimen or due to a range of supportive therapies [23]. This increases the likelihood of drug–drug interactions (DDIs), where concurrent administration of two drugs allows one to influence the activity of another [24]. Moreover, interlinking these factors, older patients are the typical demographic of cancer and thus are more likely to be taking multiple regular medicines due to increased comorbidities [25–27].
DDIs, including those involving SACT medicines, can be beneficial and lead to a synergistic (augmented) effect of both drugs, a concept utilised in combination anticancer therapy [28]. However, there is potential for negative outcomes; due to the large number and difference in mechanisms of action between anticancer agents, there are a multitude of adverse DDIs involving chemotherapy drugs [28, 29]. Importantly, several SACT agents, including cisplatin, crizotinib, and EGFR tyrosine kinase inhibitors (TKIs), are CYP450 substrates, meaning they can influence hepatic metabolism of many drugs [29, 30]. Other possible DDIs include platinum-based compounds with nephrotoxic agents such as NSAIDs, a synergistic interaction causing impaired renal function [31], and EGFR-TKIs with antacids, which raise stomach pH and thus prevent absorption of the anticancer agent [32].
The impact of DDIs directly on healthcare is poorly characterised. However, the broader group of adverse drug reactions (ADRs) place a significant strain on patients and hospitals, accounting for 6.5% of all hospital admissions, with a total cost per year of over £500,000 to the NHS [33, 34]. Systemic Anti Cancer Drug Therapy Essay. The proportion of this attributed to DDIs is debatable; some suggest an increased risk of readmission related to DDIs [35], particularly in the elderly [36], while other reviews propose the opposite [37, 38]. Nevertheless, as the potential for DDIs in SACT patients is high, methods to increase awareness are crucial to minimise risk of adverse events with which they are associated [39, 40].
Medicines reconciliation
With regard to safe medicine prescribing, it is important that healthcare professionals (HCPs) are conscientious in maintaining the efficacy of medicines, in order for patients to get the best out of their treatment [27, 41]. This concept is known as medicines optimisation and comprises four guiding principles to improve patient outcome, as outlined by the Royal Pharmaceutical Society [42]: aiming to understand the patient’s experience; evidence-based choice of medicines; ensuring medicines use is as safe as possible; and making medicines optimisation part of routine practice. A major aspect of medicines optimisation that contributes to these aims is medicines reconciliation (Med-Rec), the process of ensuring the medicines a patient is taking are correctly documented [43].
This involves ‘creating and maintaining the most accurate list possible’ of the patient’s medicines, and then ‘comparing… with the current list in use, recognising any discrepancies, and documenting any changes, thereby resulting in a complete list of medicines, accurately communicated’ [27, 44], as defined by the Institute of Healthcare Improvement (IHI).Systemic Anti Cancer Drug Therapy Essay. These tasks can be summarised into three elements to form ‘reliable’ reconciliation: verification of the list of current medicines; validation (a review of the current medicines by a trained and competent HCP, noting whether to continue or alter any doses); and clarification, where the current list is compared with the prescribed ‘medication order’ [41, 44].
Previous studies highlight the potential for problems in healthcare without a formal Med-Rec procedure; unintentional discrepancies were found in 70% of medicines prescribed on admission (covering 60% of patients) in a large systematic review by Garfield [41, 45]. Actively implementing the process is also found to be beneficial; it decreases the rate of ‘medication errors’ by 70% and ADRs by 15% [44, 46, 47] in one hospital setting, while another trial found that it reduced potential ADRs by 80% [48]. This suggests Med-Rec is an important part of preventing harm to patients.
Rationale for study
As clarified, there is a considerable risk of DDIs occurring between anticancer agents, plus various supportive care medicines as part of SACT regimens, and other medicines being taken by patients. The complexity of regimens in lung cancer specifically, utilising drugs with various mechanisms, adds to the potential risk of harm. It was therefore of interest to characterise the severity of these potential DDIs (PDDIs), and review whether established processes of Med-Rec, or simply documentation of PDDIs, could have a role in preventing harm. Numerous studies report aspects of these separately: DDIs involving general chemotherapy have been identified retrospectively in several studies [49–55]; while outcomes of pharmacy-led intervention with Med-Rec [39, 56–62] have also been analysed. However, combining severity of PDDIs and improvement of patient safety has not been carried out previously. Systemic Anti Cancer Drug Therapy Essay.
Aims, objectives and standards
Aims
The aim is to evaluate the potential for DDIs between medicines in SACT regimens and other medicines taken by lung cancer patients treated at Chelsea and Westminster Hospital (CWH).
Objectives
-
To identify and characterise PDDIs present between SACT medicines (comprising anticancer agents and supportive care medicines) and other medicines taken by the patients.
-
To assess the process of Med-Rec and evaluate documentation of PDDIs by prescribing HCPs (clinical audit).
Standards for clinical audit
-
100% of consultations with a prescribing HCP since the patient started their current SACT regimen include a documented Med-Rec.
-
100% of PDDIs between SACT medicines and other medicines had been acknowledged and documented by a prescribing HCP. Systemic Anti Cancer Drug Therapy Essay.
Methodology
Study design, inclusion, and exclusion criteria
This was a single-centre, retrospective case series study. Patients were selected for inclusion if diagnosed with lung cancer and undergoing a SACT regimen as of 31st March 2016 under the care of the Oncology team (led by Professor Mark Bower and Dr Tom Newsom-Davis) at CWH.
Data collection
For each patient, every instance of documented patient contact at CWH during their SACT regimen was compiled from the patient records. The chosen start point was the last consultation with a prescribing HCP before starting the current SACT regimen in which a full medicines history was taken. For patients on a maintenance SACT regimen, data were recorded from the last consultation in which a full medicines history was elicited before starting the SACT regimen. The endpoint was the cut-off date of 31st March 2016. Data recorded for each consultation include documentation of medicines being taken and changes to the medicine profile as a result of the consultation.
Identifying PDDIs
A ‘drug chart’ overviewing how the medicine profile changed for each patient during their SACT regimen was then created from the data collection spreadsheet (Appendix 1). PDDIs were identified using three primary sources: the British National Formulary (BNF); Summary of Product Characteristics (SPC) at ku.gro.senicidem.www; and the London Cancer Alliance (LCA) protocols for each SACT regimen. Systemic Anti Cancer Drug Therapy Essay.Only PDDIs involving a SACT medicine—either the anticancer agent, or any prescribed supportive care medicine—were noted, and not between any two non-SACT medicines taken concurrently. Component drugs within a preparation were studied individually.
Assessment of Med-Rec and documentation of PDDIs
The same patient consultation records were analysed for documentation both of Med-Rec being performed and of any DDIs by prescribing HCPs.
Definitions
‘PDDI’ (potential drug–drug interaction) is defined as a possible DDI between two medicines (as reported in the BNF, SPC, or LCA protocols) that may have occurred when the patient was taking both concurrently.
‘Anticipated DDI’ is defined as a possible DDI that was identified but did not occur due to intervention before both medicines were being taken simultaneously. There is therefore no possibility of an adverse event due to this DDI occurring.
A DDI is ‘identified’ if noted by the author during retrospective analysis of the collected data; ‘acknowledged’ or ‘documented’ DDIs are those identified and written down during a consultation by a prescribing HCP. Systemic Anti Cancer Drug Therapy Essay.
Results
Twenty-three patients met the criteria for inclusion in this study. SACT regimens being followed, listed by route of administration, are shown in Table 2.
Table 2.
| SACT regimen | Frequency (%) |
|---|---|
| Intravenous | 14 (60.9) |
| – Pemetrexed (maintenance) | – 7 (30.4) |
| – Post-pemetrexed + cisplatin | – 6 (26.1) |
| – Post-gemcitabine + carboplatin | – 1 (4.3) |
| – Nivolumab | – 3 (13.0) |
| – Gemcitabine + carboplatin | – 2 (8.7) |
| – Etoposide + carboplatin | – 1 (4.3) |
| – Pemetrexed + carboplatin | – 1 (4.3) |
| Oral | 7 (30.4) |
| – Gefitinib | – 4 (17.4) |
| – Erlotinib | – 2 (8.7) |
| – Crizotinib | – 1 (4.3) |
| Combined (intravenous and oral) | 2 (8.7) |
| – Carboplatin + vinorelbine | – 1 (4.3) |
| – Docetaxel + nintedanib | – 1 (4.3) |
Identified PDDIs
A total of 88 instances of PDDIs involving SACT medicines across 21 patients were identified. This total includes anticipated DDIs (n = 13). Figure 2 presents the SACT medicines with at least one identified PDDI.
In order to present these data qualitatively, PDDIs were grouped based on effect of interaction and mechanism of the interacting medicine. These 30 distinct DDIs are summarised in Table 3.
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Table 3.
| SACT medicine | Interacting (class of) drug | Possible outcome (effect of interaction) | Severity of interaction | n |
|---|---|---|---|---|
| Aprepitant | Ritonavir | Aprepitant toxicity (increased exposure) | Non-serious | 1 |
| Warfarin | Reduced anticoagulation (reduced exposure to warfarin) | Non-serious | 1 | |
| Crizotinib | UGT substrates (amoxicillin, colecalciferol, diazepam, levomepromazine, metoclo-pramide, mirtazapine) | Various (increased exposure to UGT substrates) | Unknown | 6 |
| Dexamethasone | Poor crizotinib efficacy (reduced exposure) | Unknown | 1 | |
| Dexamethasone | Antihypertensives (ACEIs, CCBs, ARBs, beta-blockers, nitrates) | Raised blood pressure (antagonised effect of antihypertensives) | Non-serious | 11 |
| Antidiabetics (metformin, gliclazide, linagliptin) | Raised blood glucose (antagonised effect of antidiabetics) | Non-serious | 6 | |
| Diuretics (furosemide, bendroflumethiazide) | Hypokalaemia and associated signs and symptoms | Non-serious | 5 | |
| Aspirin | Gastrointestinal bleeding and ulceration (reduced exposure to salicylate) | Non-serious | 5 | |
| Calcium carbonate | Hypocalcaemia and associated signs and symptoms (reduced exposure to calcium salts) | Non-serious | 4 | |
| Coumarins | Enhanced (high-dose corticosteroids) or reduced anticoagulation (increased or reduced exposure to coumarins) | Potentially serious | 1 | |
| Phenindione | Enhanced or reduced anticoagulation (increased or reduced exposure to phenindione) | Non-serious | 1 | |
| Ritonavir | Adrenal suppression (increased exposure to corticosteroids) | Potentially serious | 1 | |
| Docetaxel | CYP3A inhibitors (paracetamol, PPIs) | Docetaxel toxicity (increased exposure) | Unknown | 2 |
| Clarithromycin | Myelosuppression; docetaxel toxicity (increased exposure) Systemic Anti Cancer Drug Therapy Essay. | Potentially serious | 1 | |
| Domperidone | Opioid analgesics (codeine, morphine) | Gastroparesis (antagonised gastrointestinal effects of domperidone) | Non-serious | 5 |
| Clarithromycin | Domperidone toxicity (increased exposure to domperidone); ventricular arrhythmias | Potentially serious | 2 | |
| Tiotropium | Gastroparesis (antagonised gastrointestinal effects of domperidone) | Non-serious | 1 | |
| Erlotinib | PPIs/H2 antagonists/antacids (lansoprazole, ranitidine, sodium bicarbonate) | Poor efficacy (reduced exposure to erlotinib) | Unknown | 3 |
| Statins | Myopathy | Unknown | 1 | |
| Folic acid | Sodium bicarbonate | Folate deficiency and associated signs and symptoms (reduced exposure to folic acid) | Non-serious | 2 |
| Gefitinib | ||||
| CYP3A4 inhibitors (diclofenac, clindamycin) | Gefitinib toxicity (increased exposure) | Unknown | 2 | |
| PPIs (lansoprazole, omeprazole) | Poor gefitinib efficacy (reduced exposure) | Unknown | 2 | |
| CYP3A4 inducers (nevirapine, flucloxacillin) | Poor gefitinib efficacy (reduced exposure) | Unknown | 2 | |
| Warfarin | Enhanced anticoagulation (increased exposure to warfarin) | Potentially serious | 1 | |
| Nivolumab | Dexamethasone | Systemic immunosuppression | Unknown | 1 |
| Ondansetron | Sertraline | Enhanced serotonergic effects | Non-serious | 1 |
| Pemetrexed | Nephrotoxic drugs (ibuprofen, ACEIs, sulphamethoxazole) | Nephrotoxicity; pemetrexed toxicity (increased exposure) | Non-serious | 6 |
| Platinum-based compounds (cisplatin, carboplatin) | Nephrotoxic drugs (aspirin, ibuprofen, ACEIs, sulphamethoxazole) | Nephrotoxicity | Unknown | 7 |
| Diuretics (bendroflumethiazide, furosemide) | Nephrotoxicity; ototoxicity | Non-serious | 5 | |
| Potassium chloride | Irbesartan | Hyperkalaemia and associated signs and symptoms | Potentially serious | 1 |
The most common identified DDI was that of dexamethasone + antihypertensives (12.5%), followed by: platinum-based compounds + nephrotoxic drugs (8.0%); crizotinib + UGT substrates, dexamethasone + antidiabetics; pemetrexed + nephrotoxic drugs (each 6.8%). Systemic Anti Cancer Drug Therapy Essay. The remaining PDDIs had five or fewer instances. In terms of severity, there were six ‘potentially serious’ DDIs, equating to 8.0% of the total number.
Medicines reconciliation and documentation of PDDIs
Standard 1: 100% of consultations with a prescribing HCP since the patient started their current SACT regimen include a documented Med-Rec.
Outcome 1 (standard not met): 3.0% of consultations with a prescribing HCP since the patient started their current SACT regimen include a documented Med-Rec.
A total of 480 instances of documented patient contact were recorded across all 23 patients. Forty-eight of these were excluded from further analysis: eight were phone calls, three were radiology scan appointments, and 37 were consultations with non-prescribing HCPs.
Of the remaining 432 instances, 13 (3.0%, across 7 patients) included a documented Med-Rec. Additionally, 95.7% of patients had at least one full medicines history elicited by a prescribing HCP. This translates to a full medicines history being taken in 11.8% of consultations.
Standard 2: 100% of identified PDDIs between SACT medicines and other medicines had been acknowledged and documented by a prescribing HCP.
Outcome 2 (standard not met): 15.9% of identified PDDIs between SACT medicines and other medicines had been acknowledged and documented by a prescribing HCP.
Of the 88 instances of PDDIs, 14 (15.9%, across 8 patients) were acknowledged and documented.Systemic Anti Cancer Drug Therapy Essay.
