The reversibility of exogenous corticosteroid-induced osteoporosis

265 SALMON CALCITONIN NASAL - INDUCED DSTEUPDRDSJS. L.Montemurro, G.Rizznto Sarcoldosis EO Niguardn,

SPRAY

P.Fraloli. Clinic;

“Dept

IX

CORTICDSTERO

ID

M.G.Rramhilla .of

TllE REVERSIBILITY OSTEOPOROSIS. Rxzzato Hospital.

OF EXOGENOUS CORTICOSTEROID-INDOCED

G., Montemurro Milan. Italy,

L.,

Sarcoid

Clinic,

Niguarda

Physics;

Milan.

We have already shor;n a good action of salmon (s.CT) nasal calcitonin spray in preventing prednlsone induced osteoporosis. The aim of this study was to evaluste the effect of sCT nasal preventing bone loss spray in induced by an bone-losing less other corticosteroid (deflazacort). We followed two groups of sarcoid patients steroid requiring long-term thtlrapy for one (n=l4, me.in year. The first group age 39.7 + given deflazacort II.? years) was at the mean daily dose of 14.7 ?: 5.8 mg for II.41 + 4.24 monI.hs and the second group (n=H, mean ag,r 37.5 7, ! ! 9.41 yea r 5 ) 14.26 _* me/day of + deflazacort with 200 IU of sCT nitsal spray for 4.54 mineral 14.12 ,c month. Bane corltelkt of vertebral spongiasa was measured by quant.itative computed tomography 1umb;kr spine of thr using calibration phnntom. ik1. thr b~einninc UP the a I,t e r 0 ,I 1? y d 9 r , We Utrs I! I v e 11 n 5 t ud y and bone mineral lrrss 11f -11.77 i 9.14 pl?rrenC ill the t i! .a c 0 r t whekeas irk onlyk. 1 he first group (def. second group (def lazncnxt wllh sCT nasal spray) wss significantly lower -.i.Sl -+ the minersI loss 4.23 (p c.001). sCT nasal spray appears useful We concludp that in reducing corti costeroid induced bone loss.

266 ELCATONIN NASAL SPRAY IN LONG-TERM TREATMENT OF POSTMENOPAUSAL OSTEOPOROSIS. COMPARISON OF THREE ADMINISTRATION SCHEDULES. 0. COST1 *, C 1s UUISETTQ @, /4. MUSSETTA +, $, 0RTOLiiiI.I. i?'",A&iI I TIZIAN @, F UL !I 21 Q TQ k' AND

J'&ERI * "NI\;ERSI::I:; "!iAN ir, &": @. PARMA TURIN +, ITALY. To compare three different treatment schedules Elcatonin and phosphate on BMO and bone metabolrsm markers, 113 postmenopausalwomen aged between 50 and 65 with menopauseonset (physiological or surgical)in previous lo-20years were enrolledIn a 4-centre study. BMD of lumbar spine (L2 -L4) and femur using X-ray absorptlometry(Hologlc QDR-lOOO> was less than 750 mglcm2. After a B-month wash-out period without any active treatment,patients were assigned randomly to one of the following treatments in a double-blind double-dummystudy: a) phosphate (1.5 g/day) for days 1-7, Elcatoninnasal Spray (80 I.U./day)for days B-14, free period until the 45th day, phosphate(1.5 g/day) for days 46-52, Elcatoninnasal Spray (80 I.U.lday)for days 53-59. free period until the 90th day. b) Elcatoninnasal Spray (80 I.U./day)for 60 days, free period until 90th day. c) phosphate (1.5 g/day) for days l-7. ElcatonOnnasal Spray (80 I.U./day)for days 8-28. free period until 90th day. These cycles,each of three months, are repeated four tlmeslyear for two years. Blood and urinary bone mineral markers are also evaluated at various times during the study. TO guarantee the omogenelty of results centralized evaluation of densitometric assessments and bone mineral markers is performed. Preliminaryresults on the wash-outperiod (t-6-t0) from 54 evaluablepatients (L2-L4) and 41 patients (femur) do not show, as expected,appreciablechanges: L2-L4 mean BMD from 650 2 64.8 to 650 + 69.4 mg/cm2, femur mean BMD from 696 + 95.6 to 691 + 91.1 mglcm2. Active treatmentsresultson BMD and bone metabolismmarkers will be available in the near future.

Usually osteoporosis is not reversible brcause its causes (ne1ng, POSUWnOPaUSal status) cannot be removed. However the reversibility of exogenous ccrticosteroid induced osteoporosis after discontinuation of steroid therapy is an open question: in. patients with Cushing disease the reversibility was demonstrated after surgical treatment, while the effect of discontinuing steroid treatment on the course of osleoporosis has never been studied. We present the first seven patients in the world literature where the study has been carried out. Material and methods. Using computed tomography of lumbar spine we have been able to follow up Bone Mineral Content irk seven patients (4 males, three females mean age 32.3 + 5.4 ys) with histologically proven sarcoidosis. needing long terz prednisone therapy. before and after discontinuatxon of prednisone. Due to declining activity of their chroolc sarcoidosis. in all prednisone (given long term for Z5.i +, 11.5 months at the mean daily dose of 14.7 i. 6.5 me) could be discontinued without rebounds. No drugs were taker1 during the frkrther follow up after prednisone withdrawal. Results. Prednisone therapy resulted in a Mineral Loss of 15.4 t 6.51:. However, 16.6 t 7.0 months after prednisone withdrawal. %neral CJ~TI averaged 17. 1 L 8.8”: (range 5.1 to 31,Ol. Conclusion. Prednisone induced bone loss may be reversible after drscont inuation oi corticosterold therapy, at least in young patients.

267

OSTEOPOROSIS ASSOCIATED WITH RHEUMATOID ARTHRITIS : A HISTOMORPHOMETRIC STUDY K.Nakano, H.Tsuji. K.Yoh, H.Tateishi. S.Mm Department of Orthopaedic

Medicine, Nishinomiya, In order

to study

associated

Surgery,

Japan. the disease

with rheumatoid

iliac bones, proximal

Hyogo College of

process of osteoporosis

arthritis

tibias

(RA), we examined

and femoral

necks by bone

histomorphometry. All patients (OA)

were women. Patients

with osteoarthrosis

were taken for the control. Specimens were taken

from patients

in operations

of total knee replacement

total hip replaceme It. Proximal

or

tibias were 32 cases with

RA and 17 cases with OA. Femoral

necks

were

10 cases

and

10 cases, and

iliac

thickness

(Tb.

bones were 15 cases and 10 cases. In tibias Th)

and femurs

was

decreased

of RA, trabecular

and eroded

surface (ES/E61

increased. In iliac bones we found in

any

places

osteoblast

increased. As similar we thought

that

patterns

osteoporosis

increasing of bone absorption

141

surface

similar

was

patterns.

And

( Ob . S / BS 1

was

were found in iliac bones,

in RA was caused by with activated

osteoblasts.