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1
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Future treatment of peptic ulcer: is there room for anti-infective drugs?

100%
Dajani E. Z.
Journal of Physiology and Pharmacology
|
1993
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tom 44
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nr 1
2
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Prevention and treatment of ulcers induced by nonsteroidal anti-inflammatory drugs: an update

63%
Dajani E. Z., Agrawal N. M.
Journal of Physiology and Pharmacology
|
1995
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tom 46
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nr 1
3
Content available remote

Cardiovascular and gastrointestinal toxicity of selective cyclo-oxygenase-2 inhibitors in man

63%
Dajani E. Z., Islam K.
Journal of Physiology and Pharmacology. Supplement
|
2008
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tom 59
|
nr 2
It is well established that the use of traditional nonsteroidal anti-inflammatory drugs (NSAIDs) increase the vulnerability of the gastrointestinal (GI) mucosa for the development of peptic lesions and serious ulcer complications. In addition, selective and traditional NSAIDs have also been associated with increased frequency of cardiovascular toxicity, especially in susceptible patients. The objective of this communication is to provide an overview of the salient GI and cardiovascular (CV) toxicity for these drugs. Traditional NSAIDs inhibit the constitutional cyclooxygenase-1 (COX-1) enzyme responsible for eicosanoids biosynthesis not only in joints, a beneficial effect, but also in the stomach, a detrimental effect. Selective NSAIDs were specifically designed to preferentially inhibit the cyclooxygenase-2 (COX-2), an inducible enzyme mediating the production of inflammatory eicosanoids in the joints but sparing the endogenous protective eicosanoids in the stomach. Selective COX-2 inhibitors (COXIBs) have been shown to possess much improved GI tolerability and reduced GI related adverse events when compared with nonselective COX-1inhibitors. An unexpected CV toxicity had emerged during the COXIBs post marketing outcome studies. Many subsequent studies were carried out to define the CV risks associated with COXIBs and NSAIDs. All COX inhibitors had shown this CV toxicity. In many clinical studies, rofecoxib use was associated with significantly more elevated CV risk when compared with celecoxib and non selective NSAIDs. The COX inhibitors associated CV toxicity has multiple manifestations, which include the induction of myocardial infarction (MI), edema, thrombosis, blood pressure destabilization and death. Patients at risk of CV disease or with a history of CV disease were the most significant determinants of CV events after receiving COX inhibitors. This CV toxicity not only led to the marketing withdrawal of rofecoxib and valdecoxib but also resulted in more restricted, but essentially identical, product labels in the United States for celecoxib and traditional NSAIDS. This CV toxicity is dose and treatment duration dependent and appears to be compound specific rather than COX specific. Additional comprehensive, long-term, prospective investigations comparing the CV and GI safety profile of marketed NSAIDs against each other and against selective inhibitors are needed to address the controversy of COX inhibitors.
4
Content available remote

Overview of the preclinical pharmacological properties of Nigella sativa (black seeds): a complementary drug with historical and clinical significance

51%
Dajani E. Z., Shahwan T. G., Dajani N. E.
Journal of Physiology and Pharmacology
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2016
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tom 67
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nr 6
5
Content available remote

Prostaglandins and brain-gut axis

51%
Dajani E. Z., Shahwan T. G., Dajani N. E.
Journal of Physiology and Pharmacology. Supplement
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2003
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tom 54
|
nr 4
155-164
Prostaglandins (PGs) have well documented physiological and pharmacological actions on the gastrointestinal (GI) tract. This communication reviews the evidence for peripheral and central nervous system (CNS) physiological actions of PGs in order to determine their role in the brain-gut axis, if any. PGs are widely distributed in nearly all cells peripherally and centrally. Laboratory and clinical evidence indicate that there is a direct relationship between altered GI physiological functions and peripheral PGs biosynthesis. Either local or parenteral administration of natural E-series PGs alters GI physiological functions particularly those relating to mucosal defense. Furthermore, the cyclooxygenase enzymes (COX), which are responsible for the PGs biosynthesis, have been localized in the brain as well as peripherally. However, increased levels of PGs in the brain have been associated with pathological processes such as inflammation, pain, fever and addiction. Although PGs have been shown to modulate CNS effects of catecholaminergic, serotoninergic and cholinergic neurons, there is no meaningful information concerning their direct central effect on GI function. The evidence for a clear physiological role of central PGs on the GI tract is not convincing. At this time, we conclude that PGs primarily manifest their activity on the GI tract by peripheral rather than by central mechanisms.
6
Content available remote

Brain-gut axis in gastrointestinal system: Introductory remarks

51%
Konturek S. J., Pawlik W. W., Dajani E. Z.
Journal of Physiology and Pharmacology. Supplement
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2003
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tom 54
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nr 4
3-7
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