UNASSIGNED: Although abdominal pain is one of the major criteria to diagnose acute pancreatitis (AP), there are no standardized guidelines to treat this troublesome symptom in the hospital setting. The aims of the study are to conduct a meta-analysis and to assess the efficacy of nonopioids vs opioids for pain management in AP.
UNASSIGNED: We searched the medical literature through May 2021 to identify randomized controlled trials that examined the efficacy of opioids with nonopioids in AP pain management. Efficacy was reported as odds ratio (OR) with 95% confidence intervals (CIs) of each comparison tested.
UNASSIGNED: We identified 7 eligible randomized controlled trials, containing 389 patients. No significant difference in terms of pain intensity at day 1 (OR 0.82, 95% CI -2.55 to 4.19) was found between opioids and nonopioids. Nonopioids have a significantly high risk of supplementary analgesic use compared with opioids (OR 3.87, 95% CI 1.25-12.04). However, this significance is not seen when comparing nonsteroidal anti-inflammatory drugs and paracetamol with opioids (OR 1.67, 95% CI 0.73-3.82) after excluding trials with procaine. Opioids did not show a significant increase in the complications of pancreatitis, nausea and vomiting, sedation, and deaths when compared with nonopioids.
UNASSIGNED: We found nonopioids, especially nonsteroidal anti-inflammatory drugs and paracetamol, can provide adequate pain relief in patients with AP with no change in supplementary analgesic use and adverse events when compared with opioids. Further research is needed to optimize the use of nonopioids along or in combination with opioids for better pain control in patients with AP.

Osmoprotectant osmolyte and nonsteroidal anti-inflammatory drug (NSAID) coadministration can work synergistically in cancer chemotherapy since most tumors are inflammatory and cancer cells experience osmotic stress. NSAIDs have been shown to inhibit cyclooxygenase (COX) enzymes, which in turn reduces prostaglandin synthesis and prevents inflammation. They also encourage cell death to prevent tumor growth and its spread to other tissues and prevent the construction of new blood vessels, which contributes to the growth of cancer. Taurine belongs to the class of osmolytes since it has been shown to stabilize macromolecular structures and maintain cellular osmotic balance when combined with betaine and glycine. When these drugs are taken together, as opposed to separately, the effectiveness of cancer treatment is increased by increasing cancer cell death and suppressing tumor growth. Notable therapeutic benefits include the reduction of local inflammatory milieu by NSAIDs, which promotes tumor development, and the protection of surviving, normal cells and tissues from treatment-induced damage caused by cancer. By enhancing this synergy, side-effect risk can be decreased and treatment outcomes improved in terms of quality. Put another way, peptides can increase the therapeutic index of NSAIDs in cancer patients by preventing cell damage, which may lessen the gastrointestinal (GI), cardiovascular (CV), and renal side effects of the drug. However, there are drawbacks because using NSAIDs for an extended period of time is linked to serious side effects that call for strict supervision. More research is required because the usefulness and significance of osmolytes in cancer therapy are still very unclear, if not fragmented. In addition, people who live in places with limited resources may find it difficult to afford the possible expenditures associated with osmolytes and selective cyclooxygenase-2 (COX-2) inhibitors. Only the molecular mechanisms of the two drugs\' interactions, the appropriate dosages for combination therapy, and clinical trials to validate the efficacy and safety of this dosage should be the focus of future research. The request is inviting because it presents hope for an extremely successful antiviral strategy; nevertheless, in order to implement this approach successfully, it is likely to be necessary to create affordable formulations and scalable solutions that do not necessitate excessive treatment regimen individualization. Due to their complementary capacities to demonstrate anti-inflammatory and cytoprotective effects, Akta and 5-aminosalicylic acid (5-ASA) administration may thus represent a significant advancement in the treatment of cancer.

UNASSIGNED: The history of any allergy to the medications should be asked by physicians before administration of the medication. The coincidence of allergic and ACS symptoms after a short time of drug administration might be an indicator of Kounis syndrome. Allergic and coronary symptoms should be considered and treated.
UNASSIGNED: Ischemic heart disease is still the leading cause of death worldwide. Some medications, including NSAIDS and antibiotics, can cause allergic reactions with cardiac manifestations due to spasms of the coronary arteries. In this case, we present a patient with chest pain syndrome due to a hypersensitivity reaction caused by an intramuscular (IM) diclofenac injection. The patient was a 51-year-old male who presented to the emergency department complaining of retrosternal chest pain, breathlessness, and pruritis that started half an hour after an IM diclofenac injection he had because of low back pain. The allergic symptoms subsided with an antihistamine injection, but chest pain and dyspnea remained stable. He was admitted due to the presence of ST-segment depression in leads II, III, and AVF and underwent percutaneous coronary angiography, which was normal. The patient was discharged with the diagnosis of Kounis syndrome, and he had an uneventful follow-up 1 year later. Kounis hypersensitivity-associated acute coronary syndrome, especially type I variant coronary spasm due to endothelial dysfunction is a type of acute myocardial syndrome. The following report describes an uncommon case of anaphylaxis-associated Kounis type I syndrome manifesting ST-segment changes in a male patient following an intramuscular injection of diclofenac.

BACKGROUND: Alzheimer\'s disease (AD), the main cause of dementia, is characterized by synaptic loss and neurodegeneration. Amyloid-β (Aβ) accumulation, hyperphosphorylation of tau protein, and neurofibrillary tangles (NFTs) in the brain are considered to be the initiating factors of AD. However, this hypothesis falls short of explaining many aspects of AD pathogenesis. Recently, there has been mounting evidence that neuroinflammation plays a key role in the pathophysiology of AD and causes neurodegeneration by over-activating microglia and releasing inflammatory mediators.
METHODS: PubMed, Web of Science, EMBASE, and MEDLINE were used for searching and summarizing all the recent publications related to inflammation and its association with Alzheimer\'s disease.
RESULTS: Our review shows how inflammatory dysregulation influences AD pathology as well as the roles of microglia in neuroinflammation, the possible microglia-associated therapeutic targets, top neuroinflammatory biomarkers, and anti-inflammatory drugs that combat inflammation.
CONCLUSIONS: In conclusion, microglial inflammatory reactions are important factors in AD pathogenesis and need to be discussed in more detail for promising therapeutic strategies.

As the most common cause of dementia, Alzheimer\'s disease (AD) is characterized by neurodegeneration and synaptic loss with an increasing prevalence in the elderly. Increased inflammatory responses triggers brain cells to produce pro-inflammatory cytokines and accelerates the Aβ accumulation, tau protein hyper-phosphorylation leading to neurodegeneration. Therefore, in this paper, we discuss the current understanding of how inflammation affects brain activity to induce AD pathology, the inflammatory biomarkers and possible therapies that combat inflammation for AD.

UNASSIGNED: This study aims to describe the clinical characteristics, disease activity, and structural damage in patients with axial spondyloarthritis (axSpA) who receive chronic treatment with nonsteroideal anti-inflammatory drugs (NSAIDs) or advanced therapies in a clinical setting.
UNASSIGNED: Cross-sectional study on axSpA patients consecutively recruited from the outpatient clinic of a tertiary hospital. We collected data on clinical and demographic characteristics, as well as treatment patterns involving NSAIDs and advanced therapies. Structural damage was assessed using mSASSS.
UNASSIGNED: Overall, data from 193 axSpA patients (83% ankylosing spondylitis) were gathered, with a mean disease duration of 21.4 years. Of these, 85 patients (44%) were exclusively taking NSAIDs, while 108 (56%) were receiving advanced therapies, with TNF inhibitors being the predominant choice (93 out of 108, 86.1%). Among patients using NSAIDs, 64.7% followed an on-demand dosing regimen, while only 17.6% used full doses. Disease activity was low, with a mean BASDAI of 3.1 and a mean ASDAS-CRP of 1.8. In comparison to patients under chronic NSAID treatment, those taking advanced therapies were primarily male (69.4% versus 51.8%, p = 0.025) and significantly younger (mean age of 49 versus 53.9 years, p = 0.033). Additionally, patients on advanced therapies exhibited lower ASDAS-CRP (p = 0.046), although CRP serum levels and BASDAI scores did not differ between the two groups. In the multivariable analysis, therapy (NSAID versus biological treatment) was not independently associated with ASDAS-CRP, BASDAI or mSASSS.
UNASSIGNED: This cross-sectional analysis of a real-world cohort of axSpA patients shows positive clinical and radiological outcomes for both NSAIDs and advanced therapies.

Chronic inflammation plays a crucial role in carcinogenesis. High levels of serum prostaglandin E2 and tissue overexpression of cyclooxygenase-2 (COX-2) have been described in breast, urinary, colorectal, prostate, and lung cancers as being involved in tumor initiation, promotion, progression, angiogenesis, and immunosuppression. Non-steroidal anti-inflammatory drugs (NSAIDs) are prescribed for several medical conditions to not only decrease pain and fever but also reduce inflammation by inhibiting COX and its product synthesis. To date, significant efforts have been made to better understand and clarify the interplay between cancer development, inflammation, and NSAIDs with a view toward addressing their potential for cancer management. This review provides readers with an overview of the potential use of NSAIDs and selective COX-2 inhibitors for breast cancer treatment, highlighting pre-clinical in vitro and in vivo studies employed to evaluate the efficacy of NSAIDs and their use in combination with other antineoplastic drugs.

Surgical removal of the third molar often resulted in postoperative pain which affected the quality of life of the patients. Pharmacological management of pain includes NSAIDS or steroids. The present study compared four drugs, viz. Group 1 (4 mg dexamethasone injection); Group 2 (30 mg ketorolac); Group 3 (50 mg tramadol injection); and Group 4 (1 mg butorphanol injection) in the management of postoperative pain after third molar surgery. We observed that in comparison with the first and third postoperative pain between groups, it revealed the lowest mean pain score in the butorphanol group, followed by dexamethasone and tramadol group and the highest mean score in the ketorol group (P value <0.0001). We conclude that butorphanol with low dosage can be effectively used for reducing postoperative discomfort after surgery.

UNASSIGNED: Numerous epidemiological studies have elucidated the intricate connection between inflammation and cancer, highlighting how sustained inflammatory responses can fuel carcinogenesis by fostering proliferation, angiogenesis, and metastasis, while dampening immune responses and sensitivity to chemotherapy. Previous clinical investigations have underscored the potential of anti-inflammatory medications in either preventing or mitigating tumor formation. Here, the causal relationship between anti-inflammatory drugs and cancer was further explored through Mendelian randomization studies.
UNASSIGNED: Employing Mendelian randomization, we scrutinized the causal links between three anti-inflammatory drugs-NSAIDs, Aspirin, and Anilide-and 37 types of cancer. We primarily utilized inverse variance weighting (IVW) as the primary analytical approach to delineate the causal association between these drugs and cancer types. Concurrently, sensitivity analyses were conducted to ascertain the absence of horizontal pleiotropy and heterogeneity.
UNASSIGNED: Our investigation revealed a discernible causal relationship between certain anti-inflammatory drugs and a subset of cancers, albeit without a pervasive impact across all cancer types. Specifically, NSAIDs exhibited a risk-reducing effect on non-small cell lung cancer (OR: 0.76, 95% CI: 0.59-0.97, p-value: 0.03) and gastric cancer (OR: 0.57, 95% CI: 0.34-0.98, p-value: 0.04). Conversely, aspirin was associated with an increased risk of oral malignant tumors (OR: 2.18, 95% CI: 1.13-4.21, p-value: 0.02). Notably, no statistically significant findings were observed for anilide drugs (p < 0.05).
UNASSIGNED: We identified several cancers with potential causal links to NSAIDs, including non-small cell lung cancer and gastric cancer. Despite our extensive analysis, we did not identify a substantial causal relationship between the use of anti-inflammatory drugs and the development of various cancers.

UNASSIGNED: Radiographic axial spondyloarthritis (r-axSpA), formerly known as ankylosing spondylitis (AS), is a chronic, inflammatory rheumatic disease associated with symptoms such as inflammatory back pain, morning stiffness, and arthritis. First-line recommendations for patients with AS include treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) for reducing pain and stiffness.
UNASSIGNED: The objective of our study is to evaluate the efficacy and short-term NSAID-sparing effect of secukinumab in patients with AS currently treated with NSAIDs.
UNASSIGNED: We assessed the clinical Assessment of SpondyloArthritis International Society (ASAS20) response to secukinumab and evaluated the extent to which the use of concomitant NSAID can be reduced between weeks 4 and 12 in r-axSpA patients treated with secukinumab 150 mg compared with placebo.
UNASSIGNED: ASTRUM was a prospective 24-week randomized controlled trial of adult patients with active r-axSpA [Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) ⩾4] who had a documented inadequate response to ⩾2 NSAIDs. Patients were randomized (1:1:1) to initiate treatment with subcutaneous secukinumab 150 mg from either week 0 (group 1), week 4 (group 2), or week 16 (group 3). From week 4 onward, tapering of NSAIDs was allowed in all groups.
UNASSIGNED: This study included 211 patients (n = 71, 70, and 70 in groups 1, 2, and 3, respectively). ASAS20 response at week 12 for pooled groups 1 and 2 versus group 3 was 51.1% versus 44.3% (p = 0.35). A higher proportion of patients in groups 1 and 2 achieved ASAS40 and BASDAI50 and showed improvements in other secondary clinical outcomes as compared to group 3 at week 16. More patients in groups 1 and 2 versus group 3 stopped their NSAID intake from baseline through week 16.
UNASSIGNED: Treatment with secukinumab improved clinical outcomes and showed a short-term NSAID-sparing effect in patients with r-axSpA, even though the primary endpoint was not met.
UNASSIGNED: ClinicalTrials.gov; NCT02763046, EudraCT 2015-004575-74.