Research

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13 pages, 679 KiB

Open AccessArticle

Use of Cyclo-Oxygenase Inhibitors Is Not Associated with Clinical Relapse in Inflammatory Bowel Disease: A Case-Control Study

by

Abigail Hensley

and

Ian L. P. Beales

Pharmaceuticals 2015, 8(3), 512-524; https://doi.org/10.3390/ph8030512 - 07 Sep 2015

Cited by 11 | Viewed by 4805

Abstract

Patients with inflammatory bowel disease (IBD) often have associated conditions, for which anti-inflammatory medication with cyclo-oxygenase (COX) inhibitors may be helpful. The current evidence is conflicting regarding the role of COX-inhibitors in causing relapse in IBD. This case-control study examined the association between [...] Read more.

Patients with inflammatory bowel disease (IBD) often have associated conditions, for which anti-inflammatory medication with cyclo-oxygenase (COX) inhibitors may be helpful. The current evidence is conflicting regarding the role of COX-inhibitors in causing relapse in IBD. This case-control study examined the association between the use of COX inhibitors and relapse of IBD. Logistic regression was used to analyse the relationship between COX-inhibitors and IBD relapse. Overall COX inhibitor use (combined non-steroidal anti-inflammatory drugs (NSAIDs) and selective COX-2 agents) had a negative association with relapse of IBD (adjusted OR 0.26, 95% CI 0.09–0.80). This negative association was confined to ulcerative colitis (UC) (adjusted OR = 0.06, 95% CI 0.01–0.50) and no association was found in Crohn’s disease (CD) patients (adjusted OR 1.25, 95% CI 0.18–7.46). The significant negative association between UC relapse and medication use was also seen with non-specific NSAIDs. Selective COX-2 inhibitor use was rare but non-significantly more common in stable patients. There was no association between low-dose aspirin or paracetamol use and relapse of CD or UC. We conclude that COX-inhibitor use was not associated with an increased risk of relapse in UC or CD, and may be protective in UC. Where indicated, NSAIDs should not be withheld from IBD patients. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

16 pages, 123 KiB

Open AccessArticle

Non-Steroidal Anti-Inflammatory Drugs, Variation in Inflammatory Genes, and Aggressive Prostate Cancer

by

Adam C. Reese

,

Jill Hardin

, Iona Cheng, Graham Casey and

John S. Witte

Pharmaceuticals 2010, 3(10), 3127-3142; https://doi.org/10.3390/ph3103127 - 08 Oct 2010

Cited by 3 | Viewed by 7985

Abstract

Increasing evidence suggests that prostatic inflammation plays a key role in the development of prostate cancer. It remains controversial whether non-steroidal anti-inflammatory drugs (NSAIDs) reduce the risk of prostate cancer. Here, we investigate how a previously reported inverse association between NSAID use and [...] Read more.

Increasing evidence suggests that prostatic inflammation plays a key role in the development of prostate cancer. It remains controversial whether non-steroidal anti-inflammatory drugs (NSAIDs) reduce the risk of prostate cancer. Here, we investigate how a previously reported inverse association between NSAID use and the risk of aggressive prostate cancer is modulated by variants in several inflammatory genes. We found that NSAIDs may have differential effects on prostate cancer development, depending on one’s genetic makeup. Further study of these inflammatory pathways may clarify the mechanisms through which NSAIDs impact prostate cancer risk. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

23 pages, 783 KiB

Open AccessArticle

In Silico Screening of Nonsteroidal Anti-Inflammatory Drugs and Their Combined Action on Prostaglandin H Synthase-1

by

,

,

,

,

and

Pharmaceuticals 2010, 3(7), 2059-2081; https://doi.org/10.3390/ph3072059 - 02 Jul 2010

Cited by 8 | Viewed by 11366

Abstract

The detailed kinetic model of Prostaglandin H Synthase-1 (PGHS-1) was applied to in silico screening of dose-dependencies for the different types of nonsteroidal anti-inflammatory drugs (NSAIDs), such as: reversible/irreversible, nonselective/selective to PGHS-1/PGHS-2 and time dependent/independent inhibitors (aspirin, ibuprofen, celecoxib, etc.) The computational [...] Read more.

The detailed kinetic model of Prostaglandin H Synthase-1 (PGHS-1) was applied to in silico screening of dose-dependencies for the different types of nonsteroidal anti-inflammatory drugs (NSAIDs), such as: reversible/irreversible, nonselective/selective to PGHS-1/PGHS-2 and time dependent/independent inhibitors (aspirin, ibuprofen, celecoxib, etc.) The computational screening has shown a significant variability in the IC50s of the same drug, depending on different in vitro and in vivo experimental conditions. To study this high heterogeneity in the inhibitory effects of NSAIDs, we have developed an in silico approach to evaluate NSAID action on targets under different PGHS-1 microenvironmental conditions, such as arachidonic acid, reducing cofactor, and peroxide concentrations. The designed technique permits translating the drug IC₅₀, obtained in one experimental setting to another, and predicts in vivo inhibitory effects based on the relevant in vitro data. For the aspirin case, we elucidated the mechanism underlying the enhancement and reduction (aspirin resistance) of its efficacy, depending on PGHS-1 microenvironment in in vitro/in vivo experimental settings. We also present the results of the in silico screening of the combined action of sets of two NSAIDs (aspirin with ibuprofen, aspirin with celecoxib), and study the mechanism of the experimentally observed effect of the suppression of aspirin-mediated PGHS-1 inhibition by selective and nonselective NSAIDs. Furthermore, we discuss the applications of the obtained results to the problems of standardization of NSAID test assay, dependence of the NSAID efficacy on cellular environment of PGHS-1, drug resistance, and NSAID combination therapy. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

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7 pages, 42 KiB

Open AccessArticle

Significant Acute Kidney Injury Due to Non-steroidal Anti-inflammatory Drugs: Inpatient Setting

by

Mehul Dixit

, Thuy Doan, Rebecca Kirschner and Naznin Dixit

Pharmaceuticals 2010, 3(4), 1279-1285; https://doi.org/10.3390/ph3041279 - 26 Apr 2010

Cited by 54 | Viewed by 13660

Abstract

In the United States non-steroidal anti-inflammatory drugs (NSAID) are freely available over-the-counter. Because of the adverse effects on the kidneys and the popularity of these drugs, unregulated use of NSAIDs is an under recognized and potentially dangerous problem. Fifteen inpatients, mean age of [...] Read more.

In the United States non-steroidal anti-inflammatory drugs (NSAID) are freely available over-the-counter. Because of the adverse effects on the kidneys and the popularity of these drugs, unregulated use of NSAIDs is an under recognized and potentially dangerous problem. Fifteen inpatients, mean age of 15.2 ± 2.3 years (five males, 10 females), were referred to nephrology for acute kidney injury. All patients admitted to taking ibuprofen and six also consumed naproxen. None of the patients had underlying renal diseases at the time of admission. Nine patients had proteinuria and 12 had hematuria (including one with gross hematuria). One patient had nephrotic syndrome but the condition resolved spontaneously without steroids and has remained in remission for four years. Two patients required dialysis. Only one of the dialyzed patients required steroid therapy for recovery of renal function. The mean duration of hospitalization was 7.4 ± 5.5 days. The serum creatinine peaked at 4.09 ± 4.24 (range 1.2-15.3) mg/dL. All patients recovered renal function with normalization of serum creatinine to 0.71 ± 0.15 mg/dL. The estimated GFR (glomerular filtration rate) at peak of renal failure was 38.2 ± 20.5 mL/min but did improve to a baseline of 134 ± 26.2 mL/min (range 89-177, p < 0.01). However, the duration from onset to normalization of serum creatinine was 37 ± 42 days indicating that majority of patients had abnormal renal function for a prolonged period. In conclusion, NSAIDs pose a significant risk of renal failure for significant duration and as an entity may be under recognized. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

10 pages, 301 KiB

Open AccessArticle

Structural Examination of 6-Methylsulphonylphenanthro- [9,10-C]-furan-1(3H)-one—A Rofecoxib Degradation Product

by

Pamela M. Dean

Pharmaceuticals 2010, 3(2), 369-378; https://doi.org/10.3390/ph3020369 - 01 Feb 2010

Cited by 1 | Viewed by 10138

Abstract

In the attempt to discover a new polymorph of rofecoxib (Vioxx®), an unexpected product resulted. The product was characterised by chemical composition, thermal behaviour and structure and found to be 6-methylsulphonylphenanthro-[9,10-C] furan-1(3H)-one, a photo-cyclization degradation product of rofecoxib. This is a [...] Read more.

In the attempt to discover a new polymorph of rofecoxib (Vioxx®), an unexpected product resulted. The product was characterised by chemical composition, thermal behaviour and structure and found to be 6-methylsulphonylphenanthro-[9,10-C] furan-1(3H)-one, a photo-cyclization degradation product of rofecoxib. This is a significant finding because it indicates that without appropriate control of the recrystallisation procedures, the structural integrity of rofecoxib may be seriously compromised. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

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Review

Jump to: Research

22 pages, 191 KiB

Open AccessReview

Non-Steroidal Anti-Inflammatory Drugs in the Carcinogenesis of the Gastrointestinal Tract

by

Debora Compare

,

Olga Nardone

and

Gerardo Nardone

Pharmaceuticals 2010, 3(8), 2495-2516; https://doi.org/10.3390/ph3082495 - 09 Aug 2010

Cited by 6 | Viewed by 7942

Abstract

It is estimated that underlying infections and inflammatory responses are linked to 15–20% of all deaths from cancer worldwide. Inflammation is a physiologic process in response to tissue damage resulting from microbial pathogen infection, chemical irritation, and/or wounding. Tissues injured throughout the recruitment [...] Read more.

It is estimated that underlying infections and inflammatory responses are linked to 15–20% of all deaths from cancer worldwide. Inflammation is a physiologic process in response to tissue damage resulting from microbial pathogen infection, chemical irritation, and/or wounding. Tissues injured throughout the recruitment of inflammatory cells such as macrophages and neutrophils, generate a great amount of growth factors, cytokines, and reactive oxygen and nitrogen species that may cause DNA damage that in turn predisposes to the transformation from chronic inflammation to neoplasia. Cyclooxygenase (COX), playing a key role in cell homeostasis, angiogenesis and tumourigenesis, may represent the link between inflammation and cancer. Currently COX is becoming a pharmacological target for cancer prevention and treatment.It is estimated that underlying infections and inflammatory responses are linked to 15–20% of all deaths from cancer worldwide. Inflammation is a physiologic process in response to tissue damage resulting from microbial pathogen infection, chemical irritation, and/or wounding. Tissues injured throughout the recruitment of inflammatory cells such as macrophages and neutrophils, generate a great amount of growth factors, cytokines, and reactive oxygen and nitrogen species that may cause DNA damage that in turn predisposes to the transformation from chronic inflammation to neoplasia. Cyclooxygenase (COX), playing a key role in cell homeostasis, angiogenesis and tumourigenesis, may represent the link between inflammation and cancer. Currently COX is becoming a pharmacological target for cancer prevention and treatment. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

31 pages, 225 KiB

Open AccessReview

Nonsteroidal Anti-Inflammatory Drugs and the Kidney

by

Walter H. Hörl

Pharmaceuticals 2010, 3(7), 2291-2321; https://doi.org/10.3390/ph3072291 - 21 Jul 2010

Cited by 160 | Viewed by 19264

Abstract

Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit the isoenzymes COX-1 and COX-2 of cyclooxygenase (COX). Renal side effects (e.g., kidney function, fluid and urinary electrolyte excretion) vary with the extent of COX-2-COX-1 selectivity and the administered dose of these compounds. While young healthy subjects will [...] Read more.

Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit the isoenzymes COX-1 and COX-2 of cyclooxygenase (COX). Renal side effects (e.g., kidney function, fluid and urinary electrolyte excretion) vary with the extent of COX-2-COX-1 selectivity and the administered dose of these compounds. While young healthy subjects will rarely experience adverse renal effects with the use of NSAIDs, elderly patients and those with co-morbibity (e.g., congestive heart failure, liver cirrhosis or chronic kidney disease) and drug combinations (e.g., renin-angiotensin blockers, diuretics plus NSAIDs) may develop acute renal failure. This review summarizes our present knowledge how traditional NSAIDs and selective COX-2 inhibitors may affect the kidney under various experimental and clinical conditions, and how these drugs may influence renal inflammation, water transport, sodium and potassium balance and how renal dysfunction or hypertension
may result. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

13 pages, 253 KiB

Open AccessReview

Nonsteroidal Anti-Inflammatory Drug-Induced Gastroduodenal Bleeding: Risk Factors and Prevention Strategies

by

Marino Venerito

,

Thomas Wex

and

Peter Malfertheiner

Pharmaceuticals 2010, 3(7), 2225-2237; https://doi.org/10.3390/ph3072225 - 14 Jul 2010

Cited by 15 | Viewed by 9232

Abstract

Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most widely prescribed medications in the World. A frequent complication of NSAID use is gastroduodenal bleeding. Risk factors for gastroduodenal bleeding while on NSAID therapy are age, prior peptic ulcer and co-medication with anti-platelet agents, anticoagulants, glucocorticosteroids [...] Read more.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most widely prescribed medications in the World. A frequent complication of NSAID use is gastroduodenal bleeding. Risk factors for gastroduodenal bleeding while on NSAID therapy are age, prior peptic ulcer and co-medication with anti-platelet agents, anticoagulants, glucocorticosteroids and selective serotonin-reuptake inhibitors (SSRI). Prevention strategies for at-risk patients include the use of the lowest effective dose of NSAIDs, co-therapy with proton-pump inhibitors and/or the use of a COX-2 selective agent. Treatment of Helicobacter pylori infection is beneficial for primary prophylaxis of NSAID-induced gastroduodenal bleeding in NSAID-naive patients. For patients with cardiovascular risk factors requiring NSAIDs, naproxen should be selected. In very high risk patients for both gastrointestinal and cardiovascular complications NSAID therapy should be avoided altogether. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

12 pages, 123 KiB

Open AccessReview

High-Dose Ibuprofen in Cystic Fibrosis

by

Larry C. Lands

and

Nurlan Dauletbaev

Pharmaceuticals 2010, 3(7), 2213-2224; https://doi.org/10.3390/ph3072213 - 13 Jul 2010

Cited by 24 | Viewed by 10097

Abstract

Cystic Fibrosis (CF) is the most common lethal genetic disorder in North America and Europe. Most patients succumb to progressive lung disease characterized by an exaggerated neutrophilic inflammation. In animal models of chronic infection, high-dose ibuprofen was demonstrated to reduce inflammation without hindering [...] Read more.

Cystic Fibrosis (CF) is the most common lethal genetic disorder in North America and Europe. Most patients succumb to progressive lung disease characterized by an exaggerated neutrophilic inflammation. In animal models of chronic infection, high-dose ibuprofen was demonstrated to reduce inflammation without hindering bacterial clearance. This led to two clinical trials, which demonstrated a benefit in slowing the progression of lung disease in CF. However, concerns about potential adverse effects have limited the use of high-dose ibuprofen in CF patients. There are a variety of potential mechanisms to account for the observed clinical benefit. A better understanding of these mechanisms could potentially lead to more targeted and better-tolerated anti-inflammatory therapies. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

17 pages, 163 KiB

Open AccessReview

Non-Steroidal Anti-Inflammatory Drugs: An Overview of Cardiovascular Risks

by

Inger L. Meek

,

Mart A.F.J. Van de Laar

and

Harald E. Vonkeman

Pharmaceuticals 2010, 3(7), 2146-2162; https://doi.org/10.3390/ph3072146 - 07 Jul 2010

Cited by 168 | Viewed by 23472

Abstract

While aspirin may offer protection, other non-aspirin non-steroidal anti-inflammatory drugs (NSAIDs) can cause serious cardiovascular side effects and complications. This has led to a general "black box" warning for cardiovascular adverse events for NSAIDs. This review explores the different mechanisms underlying the protective [...] Read more.

While aspirin may offer protection, other non-aspirin non-steroidal anti-inflammatory drugs (NSAIDs) can cause serious cardiovascular side effects and complications. This has led to a general "black box" warning for cardiovascular adverse events for NSAIDs. This review explores the different mechanisms underlying the protective effects of aspirin, the NSAID associated renovascular effects causing hypertension, edema and heart failure, the cardiovascular effects causing myocardial infarction and stroke, and the possible deleterious interaction between NSAIDs and aspirin. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

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8 pages, 85 KiB

Open AccessReview

Role of Non-Steroidal Anti-Inflammatory Drugs in Gynecology

by

Anna Livshits

and

Daniel S. Seidman

Pharmaceuticals 2010, 3(7), 2082-2089; https://doi.org/10.3390/ph3072082 - 05 Jul 2010

Cited by 25 | Viewed by 10361

Abstract

This review summarizes the current use of non-steroidal anti-inflammatory drugs (NSAIDs) in obstetrics, gynecology and infertility. These medications are commonly used in different fields of reproductive medicine, for pain management after operative procedures and to relieve dysmenorrhea. In addition to their analgesic effect, [...] Read more.

This review summarizes the current use of non-steroidal anti-inflammatory drugs (NSAIDs) in obstetrics, gynecology and infertility. These medications are commonly used in different fields of reproductive medicine, for pain management after operative procedures and to relieve dysmenorrhea. In addition to their analgesic effect, NSAIDs are helpful in the management of menorrhagia by decreasing menstrual blood loss. NSAIDs alleviate pain associated with medical abortion, assist in undertaking natural cycle in-vitro fertilization by preventing follicular rupture and reducing premature ovulation, and serve as tocolytics in preterm labor. New NSAIDs may have a growing role in management of women's health. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

15 pages, 132 KiB

Open AccessReview

NSAIDs and Cell Proliferation in Colorectal Cancer

by

Raj Ettarh

,

Anthony Cullen

and

Alvise Calamai

Pharmaceuticals 2010, 3(7), 2007-2021; https://doi.org/10.3390/ph3072007 - 24 Jun 2010

Cited by 22 | Viewed by 7903

Abstract

Colon cancer is common worldwide and accounts for significant morbidity and mortality in patients. Fortunately, epidemiological studies have demonstrated that continuous therapy with NSAIDs offers real promise of chemoprevention and adjunct therapy for colon cancer patients. Tumour growth is the result of complex [...] Read more.

Colon cancer is common worldwide and accounts for significant morbidity and mortality in patients. Fortunately, epidemiological studies have demonstrated that continuous therapy with NSAIDs offers real promise of chemoprevention and adjunct therapy for colon cancer patients. Tumour growth is the result of complex regulation that determines the balance between cell proliferation and cell death. How NSAIDs affect this balance is important for understanding and improving treatment strategies and drug effectiveness. NSAIDs inhibit proliferation and impair the growth of colon cancer cell lines when tested in culture in vitro and many NSAIDs also prevent tumorigenesis and reduce tumour growth in animal models and in patients, but the relationship to inhibition of tumour cell proliferation is less convincing, principally due to gaps in the available data. High concentrations of NSAIDs are required in vitro to achieve cancer cell inhibition and growth retardation at varying time-points following treatment. However, the results from studies with colon cancer cell xenografts are promising and, together with better comparative data on anti-proliferative NSAID concentrations and doses (for in vitro and in vivo administration), could provide more information to improve our understanding of the relationships between these agents, dose and dosing regimen, and cellular environment. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

22 pages, 265 KiB

Open AccessReview

NSAIDs in the Acute Treatment of Migraine: A Review of Clinical and Experimental Data

by

Arpad Pardutz

and

Jean Schoenen

Pharmaceuticals 2010, 3(6), 1966-1987; https://doi.org/10.3390/ph3061966 - 17 Jun 2010

Cited by 46 | Viewed by 16342

Abstract

Migraine is a common disabling neurological disorder with a serious socio-economical burden. By blocking cyclooxygenase nonsteroidal anti-inflammatory drugs (NSAIDs) decrease the synthesis of prostaglandins, which are involved in the pathophysiology of migraine headaches. Despite the introduction more than a decade ago of a [...] Read more.

Migraine is a common disabling neurological disorder with a serious socio-economical burden. By blocking cyclooxygenase nonsteroidal anti-inflammatory drugs (NSAIDs) decrease the synthesis of prostaglandins, which are involved in the pathophysiology of migraine headaches. Despite the introduction more than a decade ago of a new class of migraine-specific drugs with superior efficacy, the triptans, NSAIDs remain the most commonly used therapies for the migraine attack. This is in part due to their wide availability as over-the-counter drugs and their pharmaco-economic advantages, but also to a favorable efficacy/side effect profile at least in attacks of mild and moderate intensity. We summarize here both the experimental data showing that NSAIDs are able to influence several pathophysiological facets of the migraine headache and the clinical studies providing evidence for the therapeutic efficacy of various subclasses of NSAIDs in migraine therapy. Taken together these data indicate that there are several targets for NSAIDs in migraine pathophysiology and that on the spectrum of clinical potency acetaminophen is at the lower end while ibuprofen is among the most effective drugs. Acetaminophen and aspirin excluded, comparative trials between the other NSAIDs are missing. Since evidence-based criteria are scarce, the selection of an NSAID should take into account proof and degree of efficacy, rapid GI absorption, gastric ulcer risk and previous experience of each individual patient. If selected and prescribed wisely, NSAIDs are precious, safe and cost-efficient drugs for the treatment of migraine attacks. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

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17 pages, 242 KiB

Open AccessReview

Non-Steroidal Anti-Inflammatory Drugs and Brain Inflammation: Effects on Microglial Functions

by

Maria Antonietta Ajmone-Cat

,

Antonietta Bernardo

,

Anita Greco

and

Luisa Minghetti

Pharmaceuticals 2010, 3(6), 1949-1965; https://doi.org/10.3390/ph3061949 - 14 Jun 2010

Cited by 93 | Viewed by 19869

Abstract

The term NSAID refers to structurally diverse chemical compounds that share the ability to inhibit the activity of the prostaglandin (PG) biosynthetic enzymes, the cyclooxygenase (COX) isoforms 1 and 2. The suppression of PG synthesis at sites of inflammation has been regarded as [...] Read more.

The term NSAID refers to structurally diverse chemical compounds that share the ability to inhibit the activity of the prostaglandin (PG) biosynthetic enzymes, the cyclooxygenase (COX) isoforms 1 and 2. The suppression of PG synthesis at sites of inflammation has been regarded as primarily responsible for the beneficial properties of NSAIDs, but several COX-independent effects have been described in recent years. Epidemiological studies indicate that NSAIDs are neuroprotective, although the mechanisms underlying their beneficial effect remain largely unknown. Microglial cells play a major role in brain inflammation and are often viewed as major contributors to the neurodegeneration. Therefore, microglia represent a likely target for NSAIDs within the brain. In the present review, we focused on the direct effects of NSAIDs and selective COX-2 inhibitors on microglial functions and discuss the potential efficacy in controlling brain inflammation. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

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17 pages, 134 KiB

Open AccessReview

A Review of Topical Diclofenac Use in Musculoskeletal Disease

by

Bindu Nair

and

Regina Taylor-Gjevre

Pharmaceuticals 2010, 3(6), 1892-1908; https://doi.org/10.3390/ph3061892 - 11 Jun 2010

Cited by 37 | Viewed by 14311

Abstract

Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly prescribed medications for the treatment of musculoskeletal disorders. Osteoarthritis is the most common form of arthritis in humans and its prevalence rises with age. Oral NSAIDs have potential associated toxicities that must be monitored for and can [...] Read more.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly prescribed medications for the treatment of musculoskeletal disorders. Osteoarthritis is the most common form of arthritis in humans and its prevalence rises with age. Oral NSAIDs have potential associated toxicities that must be monitored for and can limit the use of these drugs in certain populations including people of older age. Topical NSAIDs are now being recognized as an option for the treatment strategy of osteoarthritis. We review the efficacy and safety of one of the most common topical NSAIDS, topical diclofenac, for the treatment of osteoarthritis. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

30 pages, 867 KiB

Open AccessReview

Non-Steroidal Anti-Inflammatory Drugs in Alzheimer's Disease and Parkinson's Disease: Reconsidering the Role of Neuroinflammation

by

Amy H. Moore

, Matthew J. Bigbee, Grace E. Boynton, Colin M. Wakeham, Hilary M. Rosenheim, Christopher J. Staral, James L. Morrissey and Amanda K. Hund

Pharmaceuticals 2010, 3(6), 1812-1841; https://doi.org/10.3390/ph3061812 - 02 Jun 2010

Cited by 74 | Viewed by 16386

Abstract

Alzheimer's disease (AD) and Parkinson's disease (PD) are the most common neurodegenerative diseases with age as the greatest risk factor. As the general population experiences extended life span, preparation for the prevention and treatment of these and other age-associated neurological diseases are warranted. [...] Read more.

Alzheimer's disease (AD) and Parkinson's disease (PD) are the most common neurodegenerative diseases with age as the greatest risk factor. As the general population experiences extended life span, preparation for the prevention and treatment of these and other age-associated neurological diseases are warranted. Since epidemiological studies suggested that non-steroidal anti-inflammatory drug (NSAID) use decreased risk for AD and PD, increasing attention has been devoted to understanding the costs and benefits of the innate neuroinflammatory response to functional recovery following pathology onset. This review will provide a general overview on the role of neuroinflammation in these neurodegenerative diseases and an update on NSAID treatment in recent experimental animal models, epidemiological analyses, and clinical trials. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

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10 pages, 274 KiB

Open AccessReview

The Role of Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) in the Management of the Post-Embolization Symptoms after Uterine Artery Embolization

by

Tiago Bilhim

and

João Martins Pisco

Pharmaceuticals 2010, 3(6), 1729-1738; https://doi.org/10.3390/ph3061729 - 26 May 2010

Cited by 16 | Viewed by 9865

Abstract

Uterine artery embolization (UAE) is usually a very painful procedure. Although pain after the procedure can occur as a single symptom, it usually is associated with other symptoms such as nausea, vomiting, pelvic pain, general malaise, fever and leukocytosis that characterize the post-embolization [...] Read more.

Uterine artery embolization (UAE) is usually a very painful procedure. Although pain after the procedure can occur as a single symptom, it usually is associated with other symptoms such as nausea, vomiting, pelvic pain, general malaise, fever and leukocytosis that characterize the post-embolization syndrome. Management of the post-embolization symptoms and of pain in particular, is paramount if UAE is to be performed as an outpatient procedure. Different protocols have used analgesic and/or anti-inflammatory agents to control these symptoms. Nonsteroidal anti-inflammatory drugs (NSAIDs) are frequently used in association with analgesic drugs to control post-embolization symptoms. In our institution the patients start oral medication with NSAIDs the day before the procedure and continue it during and after UAE. We also mix NSAIDs with the embolizing particles. This enables a reduction in the inflammation present in the uterine fibroids and helps controlling the pain. The purpose of this paper is to review the importance of NSAIDs in the management of the post-embolization symptoms. We describe the protocol that we use in our institution that enables us to perform the procedure on an outpatient basis with same day discharge and good control of the post-embolization symptoms with oral NSAIDs and analgesics. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

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26 pages, 266 KiB

Open AccessReview

Effect of Non-Steroidal Anti-Inflammatory Drugs on Bone Healing

by Jessica Cottrell and J. Patrick O’Connor

Pharmaceuticals 2010, 3(5), 1668-1693; https://doi.org/10.3390/ph3051668 - 25 May 2010

Cited by 77 | Viewed by 15987

Abstract

Nonspecific and COX-2 selective nonsteroidal anti-inflammatory drugs (NSAIDs) function by inhibiting the cyclooxygenase isoenzymes and effectively reduce pain and inflammation attributed to acute or chronic musculoskeletal pathologies. However, use of NSAIDs as an analgesic is thought to negatively contribute to bone healing. This [...] Read more.

Nonspecific and COX-2 selective nonsteroidal anti-inflammatory drugs (NSAIDs) function by inhibiting the cyclooxygenase isoenzymes and effectively reduce pain and inflammation attributed to acute or chronic musculoskeletal pathologies. However, use of NSAIDs as an analgesic is thought to negatively contribute to bone healing. This review strived to provide a thorough unbiased analysis of the current research conducted on animals and humans regarding NSAIDs and their effect on bone healing. Specifically, this review discusses the role of animal models, dosing regiments, and outcome parameters when examining discrepancies about NSAIDS and their effects on bone regeneration. The role of COX-2 in bone regeneration needs to be better defined in order to further elucidate the impact of NSAIDs on bone healing. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

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16 pages, 443 KiB

Open AccessReview

NSAIDs: Old Drugs Reveal New Anticancer Targets

by

Gary A. Piazza

, Adam B. Keeton, Heather N. Tinsley, Jason D. Whitt, Bernard D. Gary, Bini Mathew, Raj Singh, William E. Grizzle and Robert C. Reynolds

Pharmaceuticals 2010, 3(5), 1652-1667; https://doi.org/10.3390/ph3051652 - 25 May 2010

Cited by 54 | Viewed by 18938

Abstract

There is compelling evidence that nonsteroidal anti-inflammatory drugs (NSAIDs) and cyclooxygenase-2 selective inhibitors have antineoplastic activity, but toxicity from cyclooxygenase (COX) inhibition and the suppression of physiologically important prostaglandins limits their use for cancer chemoprevention. Previous studies as reviewed here suggest that the [...] Read more.

There is compelling evidence that nonsteroidal anti-inflammatory drugs (NSAIDs) and cyclooxygenase-2 selective inhibitors have antineoplastic activity, but toxicity from cyclooxygenase (COX) inhibition and the suppression of physiologically important prostaglandins limits their use for cancer chemoprevention. Previous studies as reviewed here suggest that the mechanism for their anticancer properties does not require COX inhibition, but instead involves an off-target effect. In support of this possibility, recent molecular modeling studies have shown that the NSAID sulindac can be chemically modified to selectively design out its COX-1 and COX-2 inhibitory activity. Unexpectedly, certain derivatives that were synthesized based on in silico modeling displayed increased potency to inhibit tumor cell growth. Other experiments have shown that sulindac can inhibit phosphodiesterase to increase intracellular cyclic GMP levels and that this activity is closely associated with its ability to selectively induce apoptosis of tumor cells. Together, these studies suggest that COX-independent mechanisms can be targeted to develop safer and more efficacious drugs for cancer chemoprevention. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

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23 pages, 543 KiB

Open AccessReview

Molecular Mechanism for Various Pharmacological Activities of NSAIDS

by

Tohru Mizushima

Pharmaceuticals 2010, 3(5), 1614-1636; https://doi.org/10.3390/ph3051614 - 25 May 2010

Cited by 17 | Viewed by 11952

Abstract

The anti-inflammatory action of non-steroidal anti-inflammatory drugs (NSAIDs) is mediated through their inhibitory effects on cyclooxygenase (COX) activity. On the other hand, NSAID use is often associated with gastrointestinal complications. The inhibition of COX by NSAIDs is not the sole explanation for the [...] Read more.

The anti-inflammatory action of non-steroidal anti-inflammatory drugs (NSAIDs) is mediated through their inhibitory effects on cyclooxygenase (COX) activity. On the other hand, NSAID use is often associated with gastrointestinal complications. The inhibition of COX by NSAIDs is not the sole explanation for the gastrointestinal side effects of NSAIDs. Furthermore, recent epidemiological studies have revealed that prolonged NSAID use reduces the risk of cancer and Alzheimer’s disease (AD) and a COX-independent unknown mechanism is suggested to be involved in these activities of NSAIDs. In this article, I review our recent work on the COX-independent mechanism involved in NSAID-induced gastric lesions and anti-tumor and anti-AD activities of NSAIDs. Using DNA microarray analysis, we found that NSAIDs affect expression of various genes in a COX-independent manner. We found that membrane permeabilization activity of NSAIDs and resulting NSAID-induced apoptosis are involved in NSAID-induced gastric lesions. On the other hand, induction of expression of tight junction-related genes and endoplasmic reticulum chaperones were suggested to be involved in anti-tumor and anti-AD, respectively, activities of NSAIDs. These results suggest that NSAIDs affect expression of various genes in a COX-independent manner, which is involved in various pharmacological activities of NSAIDs. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

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20 pages, 739 KiB

Open AccessReview

NSAIDs, Mitochondria and Calcium Signaling: Special Focus on Aspirin/Salicylates

by

Yoshihiro Suzuki

, Toshio Inoue and Chisei Ra

Pharmaceuticals 2010, 3(5), 1594-1613; https://doi.org/10.3390/ph3051594 - 19 May 2010

Cited by 20 | Viewed by 13167

Abstract

Aspirin (acetylsalicylic acid) is a well-known nonsteroidal anti-inflammatory drug (NSAID) that has long been used as an anti-pyretic and analgesic drug. Recently, much attention has been paid to the chemopreventive and apoptosis-inducing effects of NSAIDs in cancer cells. These effects have been thought [...] Read more.

Aspirin (acetylsalicylic acid) is a well-known nonsteroidal anti-inflammatory drug (NSAID) that has long been used as an anti-pyretic and analgesic drug. Recently, much attention has been paid to the chemopreventive and apoptosis-inducing effects of NSAIDs in cancer cells. These effects have been thought to be primarily attributed to the inhibition of cyclooxygenase activity and prostaglandin synthesis. However, recent studies have demonstrated unequivocally that certain NSAIDs, including aspirin and its metabolite salicylic acid, exert their anti-inflammatory and chemopreventive effects independently of cyclooxygenase activity and prostaglandin synthesis inhibition. It is becoming increasingly evident that two potential common targets of NSAIDs are mitochondria and the Ca²⁺ signaling pathway. In this review, we provide an overview of the current knowledge regarding the roles of mitochondria and Ca²⁺in the apoptosis-inducing effects as well as some side effects of aspirin, salicylates and other NSAIDs, and introducing the emerging role of L-type Ca²⁺channels, a new Ca²⁺ entry pathway in non-excitable cells that is up-regulated in human cancer cells. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

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11 pages, 55 KiB

Open AccessReview

The Role of Non-Steroidal Anti-Inflammatory Drugs in the Chemoprevention of Breast Cancer

by

Sarah L. Horn

and

Ian S. Fentiman

Pharmaceuticals 2010, 3(5), 1550-1560; https://doi.org/10.3390/ph3051550 - 17 May 2010

Cited by 6 | Viewed by 7833

Abstract

Epidemiological evidence suggests that non-steroidal anti-inflammatory drugs (NSAIDs) which act as cyclooxygenase (COX-2) inhibitors may reduce breast cancer incidence by up to 20%. These agents are often taken for pain relief by older women with osteoarthritis. Age is the major risk factor for [...] Read more.

Epidemiological evidence suggests that non-steroidal anti-inflammatory drugs (NSAIDs) which act as cyclooxygenase (COX-2) inhibitors may reduce breast cancer incidence by up to 20%. These agents are often taken for pain relief by older women with osteoarthritis. Age is the major risk factor for breast cancer in women with 50% cases being diagnosed in those aged >65 years. NSAIDs reduce serum estradiol by 17% in post-menopausal women and since most of these who develop breast cancers have estrogen receptor positive tumours; this suggests a possible preventative role. Careful use of these agents could provide a strategy for both relief of symptoms of osteoarthritis and also breast cancer prevention. Instead of conducting a randomised trial, proof of efficacy could be from an adequately powered cohort study within the breast screening programme. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

20 pages, 395 KiB

Open AccessReview

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs): Progress in Small Molecule Drug Development

by

Praveen P. N. Rao

, Saad N. Kabir and Tarek Mohamed

Pharmaceuticals 2010, 3(5), 1530-1549; https://doi.org/10.3390/ph3051530 - 14 May 2010

Cited by 83 | Viewed by 20891

Abstract

Ever since the discovery of aspirin, small molecule therapeutics have been widely prescribed to treat inflammation and pain. Aspirin and several small molecule NSAIDs are known to inhibit the enzymes cyclooxygenase-1 (COX-1) and -2 (COX-2). Despite the success of NSAIDs to treat inflammatory [...] Read more.

Ever since the discovery of aspirin, small molecule therapeutics have been widely prescribed to treat inflammation and pain. Aspirin and several small molecule NSAIDs are known to inhibit the enzymes cyclooxygenase-1 (COX-1) and -2 (COX-2). Despite the success of NSAIDs to treat inflammatory disorders, the development of a clinically useful small molecule NSAIDs with decreased side effect profiles is an ongoing effort. The recent discovery and development of selective COX-2 inhibitors was a step toward this direction. Emerging trends are represented by the progress in the development of hybrid agents such as nitric oxide donor-NSAIDs (NO-NSAIDs) and dual COX/lipoxygenase (LOX) inhibitors. This review focuses on the recent advances in the rational design of small molecule NSAIDs in therapy. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

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16 pages, 79 KiB

Open AccessReview

Critical Overview on the Benefits and Harms of Aspirin

by

Chun Shing Kwok

and

Yoon K. Loke

Pharmaceuticals 2010, 3(5), 1491-1506; https://doi.org/10.3390/ph3051491 - 14 May 2010

Cited by 12 | Viewed by 9675

Abstract

Aspirin is widely used internationally for a variety of indications, with the most prominent one being that of cardiovascular disease. However, aspirin has also been proposed as a treatment option in a diverse range of conditions such as diabetes mellitus, cancer prevention, and [...] Read more.

Aspirin is widely used internationally for a variety of indications, with the most prominent one being that of cardiovascular disease. However, aspirin has also been proposed as a treatment option in a diverse range of conditions such as diabetes mellitus, cancer prevention, and obstetrics. In our overview, we critically appraise the current evidence from recent systematic reviews and meta-analyses covering the benefits of aspirin across these conditions. We also look at evidence that some patients may not derive benefit due to the concept of aspirin resistance. Aspirin is also associated with the potential for significant harm, principally from haemorrhagic adverse events. We critically appraise the threat of haemorrhagic complications, and weigh up these risks against that of any potential benefit. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

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17 pages, 1064 KiB

Open AccessReview

Effects of NSAIDs on Differentiation and Function of Human and Murine Osteoclasts – Crucial ‘Human Osteoclastology’

by

,

,

and

Pharmaceuticals 2010, 3(5), 1394-1410; https://doi.org/10.3390/ph3051394 - 11 May 2010

Cited by 17 | Viewed by 12296

Abstract

Osteoclasts play a critical role in both normal bone metabolism and bone resorption in the joints of patients with rheumatoid arthritis. It has been reported that non-steroidal anti-inflammatory drugs (NSAIDs) inhibit murine osteoclastogenesis in vitro and murine arthritis models in vivo, but [...] Read more.

Osteoclasts play a critical role in both normal bone metabolism and bone resorption in the joints of patients with rheumatoid arthritis. It has been reported that non-steroidal anti-inflammatory drugs (NSAIDs) inhibit murine osteoclastogenesis in vitro and murine arthritis models in vivo, but not the destruction of joints of patients with rheumatoid arthritis. In the current review article, we review the recent findings in the effect of NSAIDs on the formation and function of human and murine osteoclasts both in vitro and in vivo, underlining the importance of studies using human osteoclasts. Since 2009, we have suggested a novel term ‘human osteoclastology’. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

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13 pages, 69 KiB

Open AccessReview

NSAIDs, Opioids, Cannabinoids and the Control of Pain by the Central Nervous System

by

Horacio Vanegas

,

Enrique Vazquez

and

Victor Tortorici

Pharmaceuticals 2010, 3(5), 1335-1347; https://doi.org/10.3390/ph3051335 - 29 Apr 2010

Cited by 37 | Viewed by 16253

Abstract

Nonsteroidal anti-inflammatory drugs (NSAIDs) act upon peripheral tissues and upon the central nervous system to produce analgesia. A major central target of NSAIDs is the descending pain control system. The rostral structures of the descending pain control system send impulses towards the spinal [...] Read more.

Nonsteroidal anti-inflammatory drugs (NSAIDs) act upon peripheral tissues and upon the central nervous system to produce analgesia. A major central target of NSAIDs is the descending pain control system. The rostral structures of the descending pain control system send impulses towards the spinal cord and regulate the transmission of pain messages. Key structures of the descending pain control system are the periaqueductal gray matter (PAG) and the rostral ventromedial region of the medulla (RVM), both of which are critical targets for endogenous opioids and opiate pharmaceuticals. NSAIDs also act upon PAG and RVM to produce analgesia and, if repeatedly administered, induce tolerance to themselves and cross-tolerance to opioids. Experimental evidence shows that this is due to an interaction of NSAIDs with endogenous opioids along the descending pain control system. Analgesia by NSAIDs along the descending pain control system also requires an activation of the CB1 endocannabinoid receptor. Several experimental approaches suggest that opioids, NSAIDs and cannabinoids in PAG and RVM cooperate to decrease GABAergic inhibition and thus enhance the descending flow of impulses that inhibit pain. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

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7 pages, 42 KiB

Open AccessReview

The Role of Non-Steroidal Anti-Inflammatory Drugs in Renal Colic

by

Kim Davenport

and

Elizabeth Waine

Pharmaceuticals 2010, 3(5), 1304-1310; https://doi.org/10.3390/ph3051304 - 28 Apr 2010

Cited by 25 | Viewed by 16797

Abstract

NSAIDs provide optimal analgesia in renal colic due to the reduction in glomerular filtration and renal pelvic pressure, ureteric peristalsis and ureteric oedema. Prevention of glomerular afferent arteriolar vasodilatation renders these patients at risk of renal impairment. NSAIDs have the additional benefit of [...] Read more.

NSAIDs provide optimal analgesia in renal colic due to the reduction in glomerular filtration and renal pelvic pressure, ureteric peristalsis and ureteric oedema. Prevention of glomerular afferent arteriolar vasodilatation renders these patients at risk of renal impairment. NSAIDs have the additional benefit of reducing the number of new colic episodes and preventing subsequent readmission to hospital. Despite recent work promoting the use of pharmacological agents to improve stone passage rates, NSAIDs do not appear to reduce the time to stone passage or increase the likelihood of stone passage in renal colic. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

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10 pages, 108 KiB

Open AccessReview

Effects of NSAIDs on the Inner Ear: Possible Involvement in Cochlear Protection

by

Tomofumi Hoshino

,

Keiji Tabuchi

and

Akira Hara

Pharmaceuticals 2010, 3(5), 1286-1295; https://doi.org/10.3390/ph3051286 - 27 Apr 2010

Cited by 16 | Viewed by 10492

Abstract

Cyclooxygenase and lipoxygenase, two important enzymes involved in arachidonic acid metabolism, are major targets of non-steroidal anti-inflammatory drugs (NSAIDs). Recent investigations suggest that arachidonic cascades and their metabolites may be involved in maintaining inner ear functions. The excessive use of aspirin may cause [...] Read more.

Cyclooxygenase and lipoxygenase, two important enzymes involved in arachidonic acid metabolism, are major targets of non-steroidal anti-inflammatory drugs (NSAIDs). Recent investigations suggest that arachidonic cascades and their metabolites may be involved in maintaining inner ear functions. The excessive use of aspirin may cause tinnitus in humans and impairment of the outer hair cell functions in experimental animals. On the other hand, NSAIDs reportedly exhibit protective effects against various kinds of inner ear disorder. The present review summarizes the effects of NSAIDs on cochlear pathophysiology. NSAIDs are a useful ameliorative adjunct in the management of inner ear disorders. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

15 pages, 3648 KiB

Open AccessReview

A Review of Anti-Inflammatory Drug-Induced Gastrointestinal Injury: Focus on Prevention of Small Intestinal Injury

by

Shunji Fujimori

, Katya Gudis and Choitsu Sakamoto

Pharmaceuticals 2010, 3(4), 1187-1201; https://doi.org/10.3390/ph3041187 - 20 Apr 2010

Cited by 15 | Viewed by 10933

Abstract

Capsule endoscopy and balloon endoscopy, advanced modalities that allow full investigation of the entire small intestine, have revealed that nonsteroidal anti-inflammatory drugs (NSAIDs) can cause a variety of abnormalities in the small intestine. Recently, several reports show that traditional NSAIDs (tNSAIDs) and acetylsalicylic [...] Read more.

Capsule endoscopy and balloon endoscopy, advanced modalities that allow full investigation of the entire small intestine, have revealed that nonsteroidal anti-inflammatory drugs (NSAIDs) can cause a variety of abnormalities in the small intestine. Recently, several reports show that traditional NSAIDs (tNSAIDs) and acetylsalicylic acid (ASA) can induce small intestinal injuries. These reports have shown that the preventive effect of proton pump inhibitors (PPIs) does not extend to the small intestine, suggesting that concomitant therapy may be required to prevent small intestinal side effects associated with tNSAID/ASA use. Recently, several randomized controlled trials used capsule endoscopy to evaluate the preventive effect of mucoprotective drugs against tNSAID/ASA-induced small intestinal injury. These studies show that misoprostol and rebamipide reduce the number and types of tNSAID-induced small intestinal mucosal injuries. However, those studies were limited to a small number of subjects and tested short-term tNSAID/ ASA treatment. Therefore, further extensive studies are clearly required to ascertain the beneficial effect of these drugs. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

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9 pages, 155 KiB

Open AccessReview

Non Steroidal Anti-Inflammatory Drugs and Inflammatory Bowel Disease

by Amir Klein and

Rami Eliakim

Pharmaceuticals 2010, 3(4), 1084-1092; https://doi.org/10.3390/ph3041084 - 12 Apr 2010

Cited by 63 | Viewed by 14590

Abstract

Inflammatory Bowel Diseases (IBD) are an immune mediated chronic or relapsing disorders of the gastrointestinal (GI) tract. IBD is characterized by a chronic intestinal inflammatory process with various components contributing to the pathogenesis of the disease including environmental factors such as smoking or [...] Read more.

Inflammatory Bowel Diseases (IBD) are an immune mediated chronic or relapsing disorders of the gastrointestinal (GI) tract. IBD is characterized by a chronic intestinal inflammatory process with various components contributing to the pathogenesis of the disease including environmental factors such as smoking or use of Non Steroidal Anti-Inflammatory Drugs (NSAIDS). NSAIDS are among the most commonly used medications for the treatment of various inflammatory conditions. The main factor limiting NSAIDS use is the concern for the development of gastrointestinal toxicity including mucosal injury. A possible association between the use of NSAIDS and the onset or relapse of IBD has been repeatedly suggested. This article will review the current concepts and evidence of the relationship between IBD and NSAIDS. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

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14 pages, 200 KiB

Open AccessReview

NSAIDs and Acute Pancreatitis: A Systematic Review

by

Raffaele Pezzilli

,

Antonio Maria Morselli-Labate

and

Roberto Corinaldesi

Pharmaceuticals 2010, 3(3), 558-571; https://doi.org/10.3390/ph3030558 - 10 Mar 2010

Cited by 32 | Viewed by 20231

Abstract

The resulting pain is the main symptom of acute pancreatitis and it should be alleviated as soon as possible. NSAIDs are the first line therapy for pain and they are generally administered to acute pancreatitis patients upon admission to the hospital. In addition, [...] Read more.

The resulting pain is the main symptom of acute pancreatitis and it should be alleviated as soon as possible. NSAIDs are the first line therapy for pain and they are generally administered to acute pancreatitis patients upon admission to the hospital. In addition, these drugs have also been used to prevent post-endoscopic cholangiopancreatography (ERCP) acute pancreatitis. On the other hand, there are several reports indicating that NSAIDs may be the actual cause of acute pancreatitis. We carried out a literature search on PubMed/MEDLINE; all full text papers published in from January 1966 to November 2009 on the use of NSAIDs in acute pancreatitis were collected; the literature search was also supplemented by a review of the bibliographies of the papers evaluated. Thus, in this article, we will systematically review the current literature in order to better illustrate the role of NSAIDs in acute pancreatitis, in particular: i) NSAIDs as a cause of acute pancreatitis; ii) their use to prevent post-retrograde ERCP pancreatitis and iii) their efficacy for pain relief in the acute illness of the pancreas. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

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13 pages, 57 KiB

Open AccessReview

Renal Side Effects of Non-Steroidal Anti-Inflammatory Drugs in Neonates

by

,

,

and

Pharmaceuticals 2010, 3(2), 393-405; https://doi.org/10.3390/ph3020393 - 03 Feb 2010

Cited by 10 | Viewed by 9792

Abstract

Non-steroidal anti-inflammatory drugs like ibuprofen or indomethacin are commonly prescribed drugs to induce pharmacologic closure of a patent ductus arteriosus in preterm neonates. Based on a recently published Cochrane meta-analysis, both drugs are equally effective to induce closure. Drug choice can therefore be [...] Read more.

Non-steroidal anti-inflammatory drugs like ibuprofen or indomethacin are commonly prescribed drugs to induce pharmacologic closure of a patent ductus arteriosus in preterm neonates. Based on a recently published Cochrane meta-analysis, both drugs are equally effective to induce closure. Drug choice can therefore be based on differences in side effects or pharmaco-economic arguments. The current review quantifies the negative impact of either ibuprofen or indomethacin on renal function, including diuresis, glomerular filtration rate and renal tubular function. Both ibuprofen and indomethacin have a quantifiable impact on renal function. However, compared to ibuprofen, the negative impact of indomethacin is more pronounced. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

9 pages, 177 KiB

Open AccessReview

Hypersensitivity Reactions to Nonsteroidal Anti-Inflammatory Drugs: An Update

by

Mario Sánchez-Borges

,

Fernan Caballero-Fonseca

,

Arnaldo Capriles-Hulett

and

Luis González-Aveledo

Pharmaceuticals 2010, 3(1), 10-18; https://doi.org/10.3390/ph3010010 - 05 Jan 2010

Cited by 35 | Viewed by 13660

Abstract

After beta lactam antibiotics, hypersensitivity reactions to nonsteroidal antiinflammatory drugs are the second cause of hypersensitivity to drugs. Acute manifestations affect the respiratory tract (aspirin exacerbated respiratory disease), the skin (urticaria and angioedema), or are generalized (anaphylaxis). Correct diagnosis and treatment in order [...] Read more.

After beta lactam antibiotics, hypersensitivity reactions to nonsteroidal antiinflammatory drugs are the second cause of hypersensitivity to drugs. Acute manifestations affect the respiratory tract (aspirin exacerbated respiratory disease), the skin (urticaria and angioedema), or are generalized (anaphylaxis). Correct diagnosis and treatment in order to prevent unnecessary morbidity and the potential risk of death from these severe reactions, and to provide proper medical advice on future drug use frequently requires the participation of allergology specialists familiar with these clinical conditions. Full article

(This article belongs to the Special Issue Non-Steroidal Anti-Inflammatory Drugs)

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