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Pharmacology in Pain Management
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Pharmacology in Pain Management

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pharmacology".

Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 17629

Special Issue Editor

Prof. Dr. Sebastiano Mercadante

E-Mail Website
Guest Editor
Main Regional Center for Pain Relief & Supportive Care, La Maddalena Cancer Center, 90100 Palermo, Italy
Interests: cancer pain; supportive care; symptom management; palliative care
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Pain is described as a vital sign, but it is not fully recognized. Treating pain and exploring potential drug interactions and side effects are significant. They also factor in the patient’s anxieties, coping strategies, cultural background, and previous experiences of pain. This Special Issue will discuss pain management, involve papers related to pharmacological/action mechanisms in addition to assessment and therapeutics, thus involving both basic and clinical science. Furthermore, in this Special Issue, we wish to discuss the pharmacological action of the major groups of analgesic drugs, consider common pitfalls, and suggest appropriate drug dosing. We also want to study feasible approaches to target nociceptor pain pathways and to reduce the side effects caused by large doses of monotherapy; discuss the novel use of analgesic agents used for chronic pain; the acute-on-chronic pain, drug tolerance, drug addiction or complex pain management.

It is a pleasure to Guest Edit this Special Issue of IJMS dedicated to pain, which has long been my principal field of interest. I am strongly convinced that basic research provides ideas for clinical activity, which will have to confirm these observations. On the other hand, the clinic often provides questions that basic sciences can subsequently answer with appropriate methodologies. It is therefore evident that a continuous exchange of information can accelerate the knowledge and application processes to provide the best solutions to patients.

Prof. Dr. Sebastiano Mercadante
Guest Editor

Manuscript Submission Information

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Keywords

  • Chronic pain
  • Cancer pain
  • Pain assessment
  • Opioids
  • Adjuvants
  • Opioid-related adverse effects
  • Pharmacodynamics
  • Pain mechanisms
  • Addiction

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Published Papers (5 papers)

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Research

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18 pages, 5195 KiB  
Article
Modulation of Aryl Hydrocarbon Receptor Expression Alleviated Neuropathic Pain in a Chronic Constriction Nerve Injury Animal Model
by Meei-Ling Sheu, Liang-Yi Pan, Jason Sheehan, Meng-Yin Yang and Hung-Chuan Pan
Int. J. Mol. Sci. 2022, 23(19), 11255; https://doi.org/10.3390/ijms231911255 - 24 Sep 2022
Cited by 4 | Viewed by 1855
Abstract
Neuropathic pain is well known to occur after damage to the somatosensory system. Aryl hydrocarbon receptor (AhR) has neuroprotective effects when the central nervous system is subjected to internal and external stimulations. However, the exact mechanism by which AhR regulates neuropathic pain is [...] Read more.
Neuropathic pain is well known to occur after damage to the somatosensory system. Aryl hydrocarbon receptor (AhR) has neuroprotective effects when the central nervous system is subjected to internal and external stimulations. However, the exact mechanism by which AhR regulates neuropathic pain is poorly understood. Nerve explant culture and the chronic constrictive nerve injury (CCI) model in wild or AhR-knockout mice were used in this study. In the nerve explant culture, the ovoid number increased in the AhR−/− condition and was decreased by omeprazole (AhR agonist) in a dose-dependent manner. Increased nerve degeneration and the associated inflammation response appeared in the AhR−/− condition, and these changes were attenuated by omeprazole. High expression of AhR in the injured nerve was noted after CCI. Deletion of AhR aggravated nerve damages and this was restored by omeprazole. Deletion of AhR increased NGF expression and reduced axon number in the paw skin, but this was attenuated by omeprazole. A highly expressed inflammation reaction over the dorsal spinal cord, somatosensory cortex, and hippocampus was noted in the AhR-deleted animals. Administration of omeprazole attenuated not only the inflammatory response, but also the amplitude of somatosensory evoked potential. Deletion of AhR further aggravated the neurobehavior compared with the wild type, but such behavior was attenuated by omeprazole. Chronic constrictive nerve injury augmented AhR expression of the injured nerve, and AhR deletion worsened the damage, while AhR agonist omeprazole counteracted such changes. AhR agonists could be potential candidates for neuropathic pain treatment. Full article
(This article belongs to the Special Issue Pharmacology in Pain Management)
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26 pages, 4406 KiB  
Article
Concomitant Antihyperalgesic and Antitumor Effects of Gabapentin in a Murine Cancer Pain Model
by Beatriz Elena Brito, María Alejandra García, Yetsenia María De Gouveia, Pura Bolaños, Sindy Devis, Geraldinee Bernal, Víctor Alejandro Tortorici-Brito, Leslie Baute, Gabriel Díaz-Serrano and Víctor Tortorici
Int. J. Mol. Sci. 2021, 22(18), 9671; https://doi.org/10.3390/ijms22189671 - 7 Sep 2021
Cited by 9 | Viewed by 2971
Abstract
Cancer pain may be the consequence of physical nerve compression by a growing tumor. We employed a murine model to study whether gabapentin was able to regulate tumor growth, in addition to controlling hyperalgesic symptoms. A fluorescent melanoma cell line (B16–BL6/Zs green) was [...] Read more.
Cancer pain may be the consequence of physical nerve compression by a growing tumor. We employed a murine model to study whether gabapentin was able to regulate tumor growth, in addition to controlling hyperalgesic symptoms. A fluorescent melanoma cell line (B16–BL6/Zs green) was inoculated into the proximity of the sciatic nerve in male C57BL/6 mice. The tumor gradually compressed the nerve, causing hypersensitivity. Tumor growth was characterized via in vivo imaging techniques. Every other day, gabapentin (100 mg/Kg) or saline was IP administered to each animal. In the therapeutic protocol, gabapentin was administered once the tumor had induced increased nociception. In the preventive protocol, gabapentin was administered before the appearance of the positive signs. Additionally, in vitro experiments were performed to determine gabapentin’s effects on cell-line proliferation, the secretion of the chemokine CCL2, and calcium influx. In the therapeutically treated animals, baseline responses to noxious stimuli were recovered, and tumors were significantly reduced. Similarly, gabapentin reduced tumor growth during the preventive treatment, but a relapse was noticed when the administration stopped. Gabapentin also inhibited cell proliferation, the secretion of CCL2, and calcium influx. These results suggest that gabapentin might represent a multivalent strategy to control cancer-associated events in painful tumors. Full article
(This article belongs to the Special Issue Pharmacology in Pain Management)
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Review

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15 pages, 1832 KiB  
Review
Pharmacological Interventions Targeting Pain in Fibrous Dysplasia/McCune–Albright Syndrome
by Anthony Tucker-Bartley, Daryl J. Selen, Emma Golden, Raquel van Gool, David Ebb, Michael Mannstadt and Jaymin Upadhyay
Int. J. Mol. Sci. 2023, 24(3), 2550; https://doi.org/10.3390/ijms24032550 - 29 Jan 2023
Cited by 10 | Viewed by 3581
Abstract
Fibrous dysplasia (FD) is a rare, non-inherited bone disease occurring following a somatic gain-of-function R201 missense mutation of the guanine-nucleotide binding protein alpha subunit stimulating activity polypeptide 1 (GNAS) gene. The spectrum of the disease ranges from a single FD lesion to [...] Read more.
Fibrous dysplasia (FD) is a rare, non-inherited bone disease occurring following a somatic gain-of-function R201 missense mutation of the guanine-nucleotide binding protein alpha subunit stimulating activity polypeptide 1 (GNAS) gene. The spectrum of the disease ranges from a single FD lesion to a combination with extraskeletal features; an amalgamation with café-au-lait skin hyperpigmentation, precocious puberty, and other endocrinopathies defines McCune–Albright Syndrome (MAS). Pain in FD/MAS represents one of the most prominent aspects of the disease and one of the most challenging to treat—an outcome driven by (i) the heterogeneous nature of FD/MAS, (ii) the variable presentation of pain phenotypes (i.e., craniofacial vs. musculoskeletal pain), (iii) a lack of studies probing pain mechanisms, and (iv) a lack of rigorously validated analgesic strategies in FD/MAS. At present, a range of pharmacotherapies are prescribed to patients with FD/MAS to mitigate skeletal disease activity, as well as pain. We analyze evidence guiding the current use of bisphosphonates, denosumab, and other therapies in FD/MAS, and also discuss the potential underlying pharmacological mechanisms by which pain relief may be achieved. Furthermore, we highlight the range of presentation of pain in individual cases of FD/MAS to further describe the difficulties associated with employing effective pain treatment in FD/MAS. Potential next steps toward identifying and validating effective pain treatments in FD/MAS are discussed, such as employing randomized control trials and probing new pain pathways in this rare bone disease. Full article
(This article belongs to the Special Issue Pharmacology in Pain Management)
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21 pages, 721 KiB  
Review
The Impact of P-Glycoprotein on Opioid Analgesics: What’s the Real Meaning in Pain Management and Palliative Care?
by Flaminia Coluzzi, Maria Sole Scerpa, Monica Rocco and Diego Fornasari
Int. J. Mol. Sci. 2022, 23(22), 14125; https://doi.org/10.3390/ijms232214125 - 16 Nov 2022
Cited by 8 | Viewed by 4139
Abstract
Opioids are widely used in cancer and non-cancer pain management. However, many transporters at the blood–brain barrier (BBB), such as P-glycoprotein (P-gp, ABCB1/MDR1), may impair their delivery to the brain, thus leading to opioid tolerance. Nonetheless, opioids may regulate P-gp expression, thus altering [...] Read more.
Opioids are widely used in cancer and non-cancer pain management. However, many transporters at the blood–brain barrier (BBB), such as P-glycoprotein (P-gp, ABCB1/MDR1), may impair their delivery to the brain, thus leading to opioid tolerance. Nonetheless, opioids may regulate P-gp expression, thus altering the transport of other compounds, namely chemotherapeutic agents, resulting in pharmacoresistance. Other kinds of painkillers (e.g., acetaminophen, dexamethasone) and adjuvant drugs used for neuropathic pain may act as P-gp substrates and modulate its expression, thus making pain management challenging. Inflammatory conditions are also believed to upregulate P-gp. The role of P-gp in drug–drug interactions is currently under investigation, since many P-gp substrates may also act as substrates for the cytochrome P450 enzymes, which metabolize a wide range of xenobiotics and endobiotics. Genetic variability of the ABCB1/MDR1 gene may be accountable for inter-individual variation in opioid-induced analgesia. P-gp also plays a role in the management of opioid-induced adverse effects, such as constipation. Peripherally acting mu-opioid receptors antagonists (PAMORAs), such as naloxegol and naldemedine, are substrates of P-gp, which prevent their penetration in the central nervous system. In our review, we explore the interactions between P-gp and opioidergic drugs, with their implications in clinical practice. Full article
(This article belongs to the Special Issue Pharmacology in Pain Management)
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16 pages, 1645 KiB  
Review
Pharmacological Probes to Validate Biomarkers for Analgesic Drug Development
by Johannes van Niel, Petra Bloms-Funke, Ombretta Caspani, Jose Maria Cendros, Luis Garcia-Larrea, Andrea Truini, Irene Tracey, Sonya C. Chapman, Nicolás Marco-Ariño, Iñaki F. Troconiz, Keith Phillips, Nanna Brix Finnerup, André Mouraux and Rolf-Detlef Treede
Int. J. Mol. Sci. 2022, 23(15), 8295; https://doi.org/10.3390/ijms23158295 - 27 Jul 2022
Cited by 1 | Viewed by 4254
Abstract
There is an urgent need for analgesics with improved efficacy, especially in neuropathic and other chronic pain conditions. Unfortunately, in recent decades, many candidate analgesics have failed in clinical phase II or III trials despite promising preclinical results. Translational assessment tools to verify [...] Read more.
There is an urgent need for analgesics with improved efficacy, especially in neuropathic and other chronic pain conditions. Unfortunately, in recent decades, many candidate analgesics have failed in clinical phase II or III trials despite promising preclinical results. Translational assessment tools to verify engagement of pharmacological targets and actions on compartments of the nociceptive system are missing in both rodents and humans. Through the Innovative Medicines Initiative of the European Union and EFPIA, a consortium of researchers from academia and the pharmaceutical industry was established to identify and validate a set of functional biomarkers to assess drug-induced effects on nociceptive processing at peripheral, spinal and supraspinal levels using electrophysiological and functional neuroimaging techniques. Here, we report the results of a systematic literature search for pharmacological probes that allow for validation of these biomarkers. Of 26 candidate substances, only 7 met the inclusion criteria: evidence for nociceptive system modulation, tolerability, availability in oral form for human use and absence of active metabolites. Based on pharmacokinetic characteristics, three were selected for a set of crossover studies in rodents and healthy humans. All currently available probes act on more than one compartment of the nociceptive system. Once validated, biomarkers of nociceptive signal processing, combined with a pharmacometric modelling, will enable a more rational approach to selecting dose ranges and verifying target engagement. Combined with advances in classification of chronic pain conditions, these biomarkers are expected to accelerate analgesic drug development. Full article
(This article belongs to the Special Issue Pharmacology in Pain Management)
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