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Adverse, drug reactions hepatic disease

Lack of access to medicines and inappropriate doses result in serious morbidity and mortality, particularly for childhood infections and chronic diseases, such as hypertension, diabetes, epilepsy and mental disorders. Inappropriate use and over-use of medicines waste resources - often out-of-pocket payments by patients - and result in significant patient harm in terms of poor patient outcomes and adverse drug reactions. Furthermore, over-use of antimicrobials is leading to increased antimicrobial resistance and non-sterile injections to the transmission of hepatitis, HIV/AIDS and other blood-borne diseases. Finally, irrational over-use of medicines can stimulate inappropriate patient demand, and lead to reduced access and attendance rates due to medicine stock-outs and loss of patient confidence in the health system. [Pg.85]

Hepatotoxicity is not a particularly common form of adverse drug reaction and a patient with pre-existing liver disease does not have increased susceptibility to hepatic injury when taking drugs known to cause liver damage [1]. Therefore, drugs that are known to be hepato-toxic should not be contraindicated in this group of patients. There are... [Pg.135]

Lawson JA, Farhood A, Hopper RD, Bajt ML, Jaeschke H (2000) The hepatic mflammatoTy response after acetaminophen overdose role of neutrophils. Toxicol Sci 54 509-516 Lazarou J, Pomeranz BH, Corey PN (1998) Incidence of adverse drug reactions in hospitalized patients a meta-analysis of prospective studies. JAMA 279 1200-1205 Lazerow SK, Abdi MS, Lewis JH (2005) Drug-induced liver disease 2004. Curr Opin Gastroenterol 21 283-292... [Pg.24]

Drug-drug iuteractious Allopurinol Treatment with allopurinol, a xanthine oxidase inhibitor, shifts metabolism towards higher thioguanine concentrations, reduces aminotransferase activities, and improves disease activity scores. In 41 patients with adverse reactions to full-dose thiopurines (25 with non-hepatic reactions and 16 with hepatic reactions), a combination of allopurinol with reduced-dose thiopurine bypassed many adverse drug reactions [173 ]. Remissions were achieved in 32 patients with a median follow-up of 41 (range 0.5-400) weeks. Patients who did not respond to combination therapy tended to fail early with the same adverse reaction. [Pg.636]

Friedmann PS, Strickland I, Pirmohamed M, Park BK (1994) Investigation of mechanisms in toxic epidermal necrolysis induced by carbamazepine. Arch Dermatol 130 598-604 Fujino S, Andoh A, Bamba S, Ogawa A, Hata K, Araki Y, Bamba T, Fujiyama Y (2003) Increased expression of interleukin 17 in inflammatory bowel disease. Gut 52 65-70 Ganey PE, Luyendyk JP, Maddox JF, Roth RA (2004) Adverse hepatic drug reactions inflammatory episodes as consequence and contributOT. Chem Biol Interact 150 35-51 Gao B (2005) Cytokines, STATs and liver disease. Cell Mol Immunol 2 92—100... [Pg.223]

Orally active agents used in the treatment of ED are more affected by aging and disease processes than are those injected intracavernosally. In addition, alterations in hepatic metabolism and/or renal clearance in the elderly man (see Chapter 6) influence the frequency of appearance of adverse reactions between several coadministered drugs in the treatment of ED. For example, the concomitant use of sildenafil and nitroglycerin is contraindicated by cardiovascular complications. Also, the use of testosterone in the presence of androgen-dependent tumors may promote tumor growth. [Pg.739]

Livedo reticularis sometimes occurs in patients taking amantadine and usually clears within 1 month after the drug is withdrawn. Other dermatologic reactions have also been described. Peripheral edema, another well-recognized complication, is not accompanied by signs of cardiac, hepatic, or renal disease and responds to diuretics. Other adverse reactions to amantadine include headache, heart failure, postural hypotension, urinary retention, and gastrointestinal disturbances (eg, anorexia, nausea, constipation, and dry mouth). [Pg.611]

By 1988 it was possible to summarize the adverse effects reported after the distribution of over 1.8 million doses of plasma-derived hepatitis B vaccine (Table 1) (2). From 1982 onwards, the Centers for Disease Control, the Food and Drug Administration, and the manufacturers, Merck Sharp Dohme, had supported a special surveillance system to monitor spontaneous reports of reactions to plasma-derived hepatitis vaccine. During the first 3 years, about 850 000 persons were immunized. In all, 41 reports were received for one of the following neurological adverse events convulsion (n = 5), Bell s palsy (n — 10), Guillain-Barre syndrome (n = 9), lumbar radiculopathy (n — 5), brachial plexus neuropathy (n = 3), optic neuritis (n — 5), and transverse myelitis (n = 4). Half of these events occurred after the first vaccine dose. However, no conclusive causal association could be made between any neurological adverse event and the vaccine (3). [Pg.1601]


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See also in sourсe #XX -- [ Pg.48 ]




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