Nicotine Gum Causing Pancreatitis

Nicholson, James; Smith, Darren; Scott, Michael H.

doi:10.1097/mpa.0b013e3181b65577

Cited by 3 publications

(3 citation statements)

References 2 publications

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“…However, there is an increasing body of evidence that they have an effect similar to the one described for nicotine. Although there are lower doses of nicotine in plasma than average smokers, clinical and epidemiological studies indicate that pure nicotine usage may have severe effects on patients with cardiovascular disease and may cause some inflammatory reactions (24). This suggests our model may in part represent the potential changes, which can occur during nicotine replacement therapy and offer some new directions regarding dosage and time of exposure.…”

Section: Discussionmentioning

confidence: 93%

Nicotine aggravates the brain postischemic inflammatory response

Bradford¹,

Stamatovic²,

Dondeti³

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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A substantial body of evidence suggests that nicotine adversely affects cerebral blood flow and the blood-brain barrier and is a risk factor for stroke. The present study investigated the effect of nicotine on cerebrovascular endothelium under basal and ischemia/reperfusion injury under in vivo condition. Nicotine (2 mg/kg sc) was administered to mice over 14 days, which resulted in plasma nicotine levels of ∼100 ng/ml, reflecting plasma concentrations in average to heavy smokers. An analysis of the phenotype of isolated brain microvessels after nicotine exposure indicated higher expression of inflammatory mediators, cytokines (IL-1β, TNF-α, and IL-18), chemokines (CCL2 and CX(3)CL1), and adhesion molecules (ICAM-1, VCAM-1, and P-selectins), and this was accompanied by enhanced leukocyte infiltration into brain during ischemia/reperfusion (P < 0.01). Nicotine had a profound effect on ischemia/reperfusion injury; i.e., increased brain infarct size (P < 0.01), worse neurological deficits, and a higher mortality rate. These experiments illuminate, for the first time, how nicotine regulates brain endothelial cell phenotype and postischemic inflammatory response at the brain-vascular interface.

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Section: Discussionmentioning

confidence: 93%

Nicotine aggravates the brain postischemic inflammatory response

Bradford¹,

Stamatovic²,

Dondeti³

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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“… a Note that only one reason for rejection was applied to an abstract or paper, although, particularly for the abstracts, more than one reason may have applied b The 25 papers rejected were Anthonisen et al (2005), Benowitz and Gourlay (1997), Cordier (2014), Dempsey and Benowitz (2001), Ebbert et al (2007), Ford and Zlabek (2005), Forest (2010), Harrell et al (2014), Hughes (2000), Jacobson and Jaklitsch (2013), Joseph and Fu (2003), Kotz et al (2015), Lancaster (2014), Lavelle et al (2003), Marsh et al (2005), Myung et al (2007), Nicholson et al (2010), Osadchy et al (2009), Pauly and Slotkin (2008), Reuther and Brennan (2014), Shahab and Goniewicz (2014), Smith et al (2002), Steinberg et al (2009), Weinberger et al (2014), Zatoński and Zatoński (2015) c The 7 papers rejected were Aubin et al (2008), Eliasson et al (1996), Haustein et al (2002), Oncken et al (1996, 1997), Shiffman et al (2002), Tappin et al (2015) d The 2 papers rejected were Black et al (2014) and Adams et al (2013)…”

Section: Methodsmentioning

confidence: 99%

“…b The 25 papers rejected were Anthonisen et al (2005), Benowitz and Gourlay (1997), Cordier (2014), Dempsey and Benowitz (2001), Ebbert et al (2007), Ford and Zlabek (2005), Forest (2010), Harrell et al (2014), Hughes (2000), Jacobson and Jaklitsch (2013), Joseph and Fu (2003), Kotz et al (2015), Lancaster (2014), Lavelle et al (2003), Marsh et al (2005), Myung et al (2007), Nicholson et al (2010), Osadchy et al (2009), Pauly and Slotkin (2008), Reuther and Brennan (2014), Shahab and Goniewicz (2014), Smith et al (2002), Steinberg et al (2009), Weinberger et al (2014), Zatoński and Zatoński (2015)…”

Section: Methodsmentioning

confidence: 99%

A systematic review of possible serious adverse health effects of nicotine replacement therapy

Fariss

2016

Arch Toxicol

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We conducted a systematic literature review to identify and critically evaluate studies of serious adverse health effects (SAHEs) in humans using nicotine replacement therapy (NRT) products. Serious adverse health effects refer to adverse events, leading to substantial disruption of the ability to conduct normal life functions. Strength of evidence evaluations and conclusions were also determined for the identified SAHEs. We evaluated 34 epidemiological studies and clinical trials, relating NRT use to cancer, reproduction/development, CVD, stroke and/or other SAHEs in patients, and four meta-analyses on effects in healthy populations. The overall evidence suffers from many limitations, the most significant being the short-term exposure (≤12 weeks) and follow-up to NRT product use in most of the studies, the common failure to account for changes in smoking behaviour following NRT use, and the sparse information on SAHEs by type of NRT product used. The only SAHE from NRT exposure we identified was an increase in respiratory congenital abnormalities reported in one study. Limited evidence indicated a lack of effect between NRT exposure and SAHEs for CVD and various reproduction/developmental endpoints. For cancer, stroke and other SAHEs, the evidence was inadequate to demonstrate any association with NRT use. Our conclusions agree with recent statements from authoritative bodies.Electronic supplementary materialThe online version of this article (doi:10.1007/s00204-016-1856-y) contains supplementary material, which is available to authorized users.

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Drug Induced Acute Pancreatitis: An Evidence Based Classification (Revised)

Saini

Marino

Badalov

et al. 2023

Clin Transl Gastroenterol

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We previously published an “Evidence Based Classification System” on Drug-Induced Acute Pancreatitis widely used by clinicians. Unfortunately, this prior analysis based only on published case reports has been misunderstood. The prior review did not include studies with higher evidentiary value, such as randomized trials, case control studies and/or pharmacoepidemiologic studies. Despite the extensive list of drugs included in our prior classification and review, which defined classes by the case reports showing rechallenges and latency, the value to clinicians and applicability to patients with unexplained acute pancreatitis is profoundly limited. The use of the prior classification system has led to many patients inappropriately labeled as having a drug-induced acute pancreatitis. We now propose a “Revised” Evidence Based Classification System for the purpose of determining which drugs cause acute pancreatitis based on the GRADE Criteria.

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Nicotine Gum Causing Pancreatitis

Cited by 3 publications

References 2 publications

Nicotine aggravates the brain postischemic inflammatory response

Nicotine aggravates the brain postischemic inflammatory response

A systematic review of possible serious adverse health effects of nicotine replacement therapy

Drug Induced Acute Pancreatitis: An Evidence Based Classification (Revised)

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