Læknablaðið - 15.10.1983, Page 4

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LÆKNABLADID
NÝR DOKTOR í LÆKNISFRÆÐI - HARALDUR TÓMASSON
Haraldur Ó. Tómasson læknir á Hvamms-
tanga lauk 21. júlí sl. matersprófi í heimilis-
lækningum (Master of Clinical Science in
Family Medicine) við University of Western
Ontario í Kanada.
Prófritgerð Haraldar, sem ber heitið, Tuber-
culosis and Non-Steriodal Anti-flammatory
Drugs, fjallaði um hugsanlegt samband milli
notkunar algengra gigtarlyfja og endurvirkni
berklaveiki. Studdi rannsókn Haraldar þá til-
gátu, að samband væri milli notkunar þessara
lyfja og berklaveiki. Fer útdráttur úr ritgerð-
inni hér á eftir:
This thesis was stimulated by case reports in
1980 and 1982 by Brennan where reactivation
of pulmonary tuberculosis was associated with
the use of non-steroidal anti-inflammatory
drugs (NSAIDs). A case control study was
designed to determine if the association exi-
sted in a wider sample. The following hypo-
theses were tested.
1. There is an association between the taking
of NSAIDs and the diagnosis of tuberculo-
sis in persons born before 1937.
2. The association between NSAIDs and tu-
berculosis will become stronger with in-
creasing duration of NSAID exposure.
3. In patients with tuberculosis there is an
association betweeen NSAID exposure and
a past history of tuberculosis.
While ASA is a NSAID it was considered
separately from the other thirteen NSAIDs
available in Canada in 1982 on the basis of its
historical, marketing and chemical properties.
Family physicians and their charts in the
office setting provided the sole source of data.
Cases were identified in an anonymous way
with the help of the agencies concerned with
tuberculosis control and treatment and from
three specialists in infectious diseases. A case
was defined as a person that had been
diagnosed as having active tuberculosis and
put on chemotherapy between 1975-1982,
born before 1937 and resident of Canada for 5
years prior to the diagnosis of TB. Controls
were drawn in a paired fashion from the same
practice as cases and were matched on age,
sex, race and minimum time in the practice.
Of 103 patients fulfilling the inclusion crite-
ria, data were collected on 38 cases. The cases
were found to be a specific group of patients
not representative of tuberculosis patients in
Ontario. The proportion of foreign born in the
sample were lower, because of the exclusion
criteria, thus there were no cases of Asian
extraction.
Cases and controls were similar with regard
to occupation, long-term medication, ASA and
steroid use. Cases were more likely to have
supplementary information in the chart, past
tuberculosis history and arthritic conditions.
The association between NSAID use and
tuberculosis was significant at the p<0.05
with a relative risk of 4. When only NSAIDs
taken for more than one month were conside-
red, the association was signficant at p = 0.008
with a relative risk between 8 and infinity.
Thus a dose relationship appears to exist. It was
not possible to untangle the association of
arthritis, NSAIDs and tuberculosis because all
long-term NSAIDs were used for arthritis.
Although in all cases the arthritis predated the
tuberculosis and was not considered to be
tuberculosis related. Case histories of the
long-term NSAID users illustrated a striking
temporal relationship between NSAID treat-
ment and tuberculosis. The third hypothesis
was not supported by the findings.
Support for a causal association was drawn
from 1) the strength of the association 2) dose
response 3) appropriate time relationship 4)
weak epidemiolgical data and 5) a rational
explanation based on the anti-inflammatory
qualities of NSAIDs. The results of this pilot
study thus lend weight to a causal association.
It is therefore imperative that this be followed
by further case-control studies in different
localities and by prospective studies. Physici-
ans are urged to be aware of these drugs’
potent anti-inflammatory properties and their
potentially deleterious effects on infection.
Family physicians because of their continui-
ty of care are in an excellent position to
contribute to the detection of adverse drug
reactions.