Læknablaðið - 15.11.1988, Síða 11

LÆKNABLAÐIÐ
357
þó talið að fylgjast með lifrarprófum öðru
hverju. Vöðvaþrota (myositis) hefur verið lýst
samfara þessu lyfi (11) en enginn í
rannsóknarhópi okkar fékk slík einkenni.
Aðrar rannsóknir hafa sýnt að lóvastatín eykur
ekki mettun galls (24) né heldur hefur það áhrif á
myndun sterahormóna (25), þ.e. á
lóvastatínmeðferð er ennþá nægileg
kólesterólmyndun til að sinna nauðsynlegu
hlutverki kólesteróls sem forstigsstera.
Niðurstöður liggja ekki fyrir um meðferð
lóvastatíns meðal einstaklinga með skerta nýrna-
og lifrarstarfsemi en allir þátttakendur í rannsókn
okkar höfðu slík próf eðlileg fyrir sem og eftir
meðferð. Verkun lóvastatíns á fóstur hefur ekki
verið fullkönnuð ennþá og því var það gert að
skilyrði í okkar rannsókn að allir
kvenþátttakendur væru úr barneign. Reynsla
hefur heldur ekki fengist af notkun þessa lyfs
meðal barna og unglinga.
Reynist lóvastatín jafn fylgikvillalítið til lengdar
og það hefur reynst til þessa og staðfesti
rannsóknir virkni þess í að draga úr
kransæðasjúkdómi í réttu hlutfalli við
kólesteróllækkun þess (1 % lækkun kólesteróls
með kólestyramíni (Questran) minnkar áhættu á
kransæðasjúkdómi um 2%) (16) þá er lítill vafi á
þvi að lóvastatín og aðrir
HMG-CoA-redúktasa-blokkar verða eitt helsta
tækið til að draga úr tíðni kransæðasjúkdóms
meðal þeirra sem hafa verulega hækkun
kólesteróls í blóði og ekki hafa svarað nægilega
megrun og matarráðgjöf.
Þakkir:
Höfundar þakka rannsóknadeildum
Landspítalans í blóðmeinafræði og
meinefnafræði fyrir veitta aðstoð, svo og Eiriki
Bjarnasyni augnlækni fyrir augnskoðun
þátttakenda.
SUMMARY
Fifty-one individuals with hyperlipoproteinemias were
followed up for six months whilst receiving therapy with
lovastatin (Mevacor), HMG-CoA reductase inhibitor
(MSD). Nineteen had familial hypercholesterolemia
(FH), 19 had type Ila (non-FH) lipoprotein pattern, 12
had type Ilb pattern and one had type III
hyperlipoproteinemia. The group received lovastatin 40
mg/day (q.p.m.) for 6-12 weeks and 80 mg/day (40 mg
b.i.d.) up to 6 months. Mean total serum cholesterol fell
from 386 mg/dl (10 mmol/1) to 255 mg/dl (6.6 mmol/1)
or 34%, LDL-cholesterol feíl by 41%, HDL-cholesterol
did not change significantly except slightly (+ 4 mg/dl)
on 40 mg q.p.m. LDL/HDL ratio fell markedly by
42%. Total serum triglycerides fell significantly from
153 mg/dl (1.73 mrnol/1) to 111 mg/dl (1.26 mmol/1) or
by 27%. The cholesterol reduction observed was the
same in FH as in non-FH patients. In type Ilb patients
serum triglycerides fell significantly by 36% (p<0.01)
and cholesterol by 41%. The serum cholesterol of the
only patient with type III fell from 361 mg/dl to 177
mg/dl (51%) and triglycerides fell from 461 mg/dl to
315 mg/dl (32%). The mean weight change after 6
months on therapy was + 1.1 kg.
HB, white cell counts, creatinine, CPK, ASAT, LDH,
gamma-GT, alkaline phosphatase, bilirubin and urin
protein analysis were performed every 6 weeks. No
significant changes in these parameters were observed.
Slit-lamp examination was unchanged in all individuals
after 6 months therapy. One male patient developed hair
loss during therapy, which was discontinued. His case
was considered most likely to be androgenic alopecia
areata by a dermatopathologist.
Conclusions: Lovastatin (Mevacor) is a very effective
cholesterol lowering agent in all types of
hypercholesterolemia. 40 mg/day is effective enough for
most cases except FH-patients where additional therapy
may be needed. The drug lowers also triglycerides and
can therefore be used in type Ilb patients. Lovastatin is
well tolerated and seems to be relatively free of
complications, although one case of hair loss was
observed. Its relation to lovastatin therapy is unclear.
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