| Summary: | 博士 === 高雄醫學院 === 醫學研究所 === 86 === The epidemiological study of gout in Taiwan Aborigines(1998) The
Graduate Institute of MedicineThe Graduate student : Shun-Jen
Chang, Adviser: Ying-Chin KoStudent No: 8381005Abstract There
are three aboriginal tribes (Bunun, Paiwan and Atayal) and
twonon-aborigines (Fukien-Taiwanese and Hakka ) were included
as study''spopulation. This study was divided into three parts,
the first subject wasto explore the hyperuricemic prevalence and
related factors from the abovefive populations whose age were
between five and 14 years. The secondsubject focused the adult''s
gout and hyperuricemic prevalence and therelated factors. We
visited the persons whose age great than 40 years bydoor to
door, the gout disease was self-reported from the subject and
hadbeen identified by a practical doctor. The third was to
reveal the HPRT genefrom a severe gout patient who was with gout
pedigree, after finding themutation from the patient, then by
using PCR-RFLP method to screen hisfamilies and three tribes''
children. The results showed that (1) there were 1214
children had been includedin this study from the five tribes
between Jul 1993 and Mar 1994; Overall,the hyperuricemic ( uric
acid ≧ 7.5 mg/dl) prevalence was 27.3% (332/1214),the
hyperuricemic rate among male was 30.4%, and 24.2% among female
andthere was statistical difference among sex (186/611, 146/
603; p<0.05). TheAtayal tribe, no matter male or female, had the
highest prevalence ofhyperuricemia, the Paiwan tribe followed,
and the non-Aboriginal tribes thelowest. After the preliminary
and logistic regression model adjusted theconfounders, the
result showed that the factors related to hyperuricemia hadage,
sex, body mass index, tribes, the serum triglycerides and
cholesterolconcentration. Without the interference of the
living habits in adults such as tobaccosmoking, alcohol
consumption and betel nut chewing, the factor of Aborigineshad
major effect on serum uric acid was concluded. (2) The
prevalence of gout disease among aboriginal male and female
were9.3% (26/281) and 3.0% (11/371), which were significant
higher than thenon-aborigines (0.4% in both male and female).
The related factors of goutdisease were explored by logistic
regression model, and found that theaboriginal men with
hyperuricemia tended to get the gout disease. About thefactors
related to hyperuricemia showed that the aborigines
withtriglycerides over 170 mg/dl and the ratio of waist line
over hip linegreater than 0.9 were likely to have hyperuricemia.
The factor of tribe havethe major effect on the onset of gout
disease was included. (3) One new mutation locate at the HPRT
cDNA 152 nucleotide was foundfrom a severe gout patient
(proband) whose mother originated from Tsou tribe, thus the
mutation was named as HPRTTsou according to his mother''s tribe.
The mutation cause the nucleotide transition from G to A which
cause the 51amino acid transgression from argentine to
glutamate. After that, wescreened the proband''s families, the
children from Tsou''s tribes, Atayaltribe and Bunun tribe by
using the PCR-RFLP method. The results showed that85.7% (6/7) of
the proband''s siblings had HPRTTsou from their mother, andalso
there were 50% (4/8) of the children of proband''s siblings
inheritedthis mutation from their carried mother. Among the
children, only twofemales had this mutation which one from
Atayal tribe and one from Tsoutribe. In conclusion, no matter
the hyperuricemia or gout disease, theAborigines have the higher
prevalence than non-aborigines, thus the tribefactor may be
considered as a most important factor. In another hand,
theHPRTTsou distribute low prevalence among Atayal tribe and
Tsou tribe (1.4%;1/70, 4.5%; 1/22, respectively). This study
showed that both of the aboriginal children and adults havehigh
prevalence of hyperuricemia, and the gout disease also
predominated inthe Aborigines. Furthermore, there was a HPRT
point mutation would cause theuric acid accumulated existed in
the Tsou tribe''s offspring. Thus, afterexcluded the confounding
factors in environment, we believe the Aboriginesmay have
another gene mutation will cause the gout disease onset.
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