The proportion of UGIB cases attributed to different
prescribed drugs in the population were as follows: 6.3 %
for NSAIDs, 1.4 % for metamizol, 4.2 % for low-dose
aspirin, 2.1 % for other antiplatelet drugs, and 2.2 % for
oral anticoagulants.
Among individual NSAIDs, the greatest RRs were found
with lornoxicam (13.57; 4.61–29.93), piroxicam (4.49;
2.36–8.54) and desketoprofen/ketoprofen (3.79; 1.70–
8.46). The lowest values were obtained with aceclofenac
(1.02; 95 % CI: 0.51–2.02), diclofenac (1.32; 0.87–1.98),
and ibuprofen (1.33; 0.94–1.89) (Table 3). For coxibs we
had only 5 exposed cases and 50 exposed controls yielding
an adjusted RR of 0.76 (0.29–2.00).
Use of multiple NSAIDs was associated with a higher RR
(3.13; 1.98–4.97) than single use (1.58; 1.29–1.94). Among
single users the RR appeared higher during the first 30 days
of treatment, when used at high doses and with long-acting
agents. No difference was found according to indication
(Table 4). We detected a negative linear correlation between
the RR of UGIB associated with NSAIDs and calendar year
(R2
00.96; p00.004; coefficient0−0.18) (appendix 2 in supplementary
material). In a parallel manner, the estimated
proportion of UGIB cases in the population attributed to
NSAIDs also decreased over time from 8.3 % in 2001 to
3.2 % in 2005.
The concomitant use of NSAIDs with low-dose aspirin,
oral steroids, and metamizole showed an additive effect
(RERI around 0), while it was synergistic with oral anticoagulants
(RERI0+6.45). No additional increased risk was
found with the concomitant use of either paracetamol or
SSRIs (Table 5).
The proportion of UGIB cases attributed to differentprescribed drugs in the population were as follows: 6.3 %for NSAIDs, 1.4 % for metamizol, 4.2 % for low-doseaspirin, 2.1 % for other antiplatelet drugs, and 2.2 % fororal anticoagulants.Among individual NSAIDs, the greatest RRs were foundwith lornoxicam (13.57; 4.61–29.93), piroxicam (4.49;2.36–8.54) and desketoprofen/ketoprofen (3.79; 1.70–8.46). The lowest values were obtained with aceclofenac(1.02; 95 % CI: 0.51–2.02), diclofenac (1.32; 0.87–1.98),and ibuprofen (1.33; 0.94–1.89) (Table 3). For coxibs wehad only 5 exposed cases and 50 exposed controls yieldingan adjusted RR of 0.76 (0.29–2.00).Use of multiple NSAIDs was associated with a higher RR(3.13; 1.98–4.97) than single use (1.58; 1.29–1.94). Amongsingle users the RR appeared higher during the first 30 daysof treatment, when used at high doses and with long-actingagents. No difference was found according to indication(Table 4). We detected a negative linear correlation betweenthe RR of UGIB associated with NSAIDs and calendar year(R200.96; p00.004; coefficient0−0.18) (appendix 2 in supplementarymaterial). In a parallel manner, the estimatedproportion of UGIB cases in the population attributed toNSAIDs also decreased over time from 8.3 % in 2001 to3.2 % in 2005.The concomitant use of NSAIDs with low-dose aspirin,oral steroids, and metamizole showed an additive effect(RERI around 0), while it was synergistic with oral anticoagulants(RERI0+6.45). No additional increased risk wasfound with the concomitant use of either paracetamol orSSRIs (Table 5).
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