June 09-41-2.indd - Kma.org.kw

More documents

Recommendations

Info

June 2009KUWAIT MEDICAL JOURNAL 153Fig. 1: X-ray showing fracture of the both femurs with signs ofhealingas her Ca was 7.4 mg% (N = 8 - 10.5 mg%) and PTH152 pg/ml (upper limit 62 pg/ml) with PO 42.3 mg%(N = 2.5 - 5 mg%), alkaline phosphatase 378 U/l (N =40 - 230 U/l) and normal albumin. Secondary adrenalinsufficiency was diagnosed as her cortisol was low,165.17 nmol/l (N ≥ 550 nmol/l) one hour after ACTHstimulation with normal electrolytes. Level of 25-hydroxy vitamin D and 1, 25-dihydroxy vitamin Dwere also normal. She had severe osteoporosis asrevealed by DEXA (T score = -3). Other investigationsshowed normal CBC, mild microcytic hypochromicanemia with normal ESR, renal and hepatic functions.Doppler sonography of the left leg was normal. Theultrasonography of thyroid showed right lobe 6 x 1.4x 3 mm and left lobe 6.9 x 1.7 x 2.2 mm with no focallesion. The plain X-ray of bilateral fibulae and femurrevealed multiple healing fractures. ECG showedsinus tachycardia.The patient was managed conservativelyby the orthopedic team. She was started onalendronate 70 mg weekly, alfacalcidol 1 µg dailyand calcium carbonate (CaCo 3) 600 mg thrice aday. Her fractures healed completely within fourmonths. Initially, her heart rate was controlled bypropranolol without compromising her asthmaticstate under the coverage of steroid which wasdiscontinued eventually. She was also subjectedto propylthiouracil therapy for hyperthyroidism.The follow up after six months revealed her to bein euthyroid state clinically and biochemically withcontrolled asthma.Fig. 2: X-ray showing fracture of the right fibula with signs ofhealingDISCUSSIONOsteoporosis represents a major and emergingpublic health problem with the aging population.Major clinical consequences and economic burdenof the disease pertain to the ensuing fractures.Many risk factors are associated with these fracturesincluding low bone mass, hormonal disorders namelyhyperparathyroidism and hyperthyroidism, thin built,use of certain drugs (e.g., glucocorticoids), cigarettesmoking, excessive intake of alchohol, low physicalactivity, vitamin D insufficiency and low intake ofcalcium [7] . Osteoporosis and thyroid dysfunction areboth common in older women. Eight to 13% of womenolder than 50 years of age have biochemical evidenceof thyroid dysfunction [8] and 30% are osteoporoticaccording to the bone density criteria [9] . The osteoporoticfractures have long been associated with floridhyperthyroidism [10] although the relationship betweenbiochemical evidence of excess thyroid hormone andfracture risk is not known [11] . The risk for hip fractureis more than threefold and that of nonspine fractureis twofold higher among women with low TSH levelsthan those with normal TSH levels [12] . Biochemicalmarkers of bone turnover are elevated in women withlow TSH levels supporting the view that low TSHlevels reflect excessive thyroid hormone, which inturn increases skeletal remodeling [12] . All patients withhyperparathyroid disease will eventually developosteoporosis regardless of their age or sex. Womentend to develop osteoporosis from parathyroid diseasefaster than men [13] . Osteoporosis is a well-recognized
154A Case of Severe Primary Hyperthyroidism, Secondary Hyperparathyroidism, Adrenal ...June 2009adverse effect of corticosteroid therapy. The bone lossis most marked during the first six to 12 months oftreatment. Corticosteroids affect both bone formationand bone resorption. A decrease in bone formationhas been attributed to a decrease in osteoblast activity,number and life span (apoptosis). Corticosteroids altergonadal sex steroid production through straight actionand inhibition of gonadotrophin secretion and suppressadrenal androgen production, resulting in decreasedbone formation [14] . They also increase the rate of boneresorption by stimulating the formation and actionof osteoclasts [15] . The increase in bone resorption alsomay be explained, in part, by increased parathyroidhormone (PTH) mediated activation of osteoblastshaving PTH receptors which osteoclasts are lacking.PTH-mediated stimulation of osteoclasts is believed tobe indirect, acting in part through cytokines releasedfrom osteoblasts to activate them [16] . The secondaryhyperparathyroidism results from reduced intestinal aswell as renal tubular calcium absorption by steroid [17] .Patient receiving glucocorticoids chronically mayhave depressed circulating level of 1, 25 dihydroxyvitamin D; the mechanism being unknown [18] .However, other studies show no consistentabnormalities in vitamin D, PTH, or calcitoninlevels in glucocorticoid-treated patients [19] . Commonosteoporotic fracture sites include the vertebrae, thehip, the distal radius of the forearm with an incidenceof 32, 16 and 15 percent respectively [20] . Osteoporoticbones are ten times more susceptible to fracture thannormal [13] which often does not become clinicallyapparent until a fracture occurs. The best screeningtest is dual energy X-ray absorptiometry (DEXA)which is quick, simple and precise. It measuresthe density of bones in the areas most likely to beaffected and accurately follows the changes inthese bones over time [21] . Recently, many studiesshowed the need to administer vitamin D 800 IU oralfacalcidol 1 µg or calcitriol 0.5 µg/day in treatmentof osteoporosis. Active vitamin D 3analogues, suchas calcitriol and alfacalcidol, stimulate the formationand action of osteoblasts [21] leading to increased boneformation [22] . Effects of vitamin D resulted in lowerrisk of fractures and falls, as well as improvementof neuromuscular performances. In more than tenyears of practice and several short and long termclinical studies, alendronate 70 mg/week loweredthe risk of vertebral and extra-vertebral fracturesand improved bone mineral density (BMD) of allmeasured sites in both sexes with osteoporosis. Thepositive results of alendronate were demonstratedin different entities like persons of various agesand grades of lower BMD or patients withglucocorticoid-induced osteoporosis. Combinationof vitamin D with efficacious antiresorptive drug likealendronate maintains all pharmacological featuresand demnstrates the clinical effects of weeklyalendronate [23] . PTH analogue seems superior inprevention of vertebral fractures although their longterm safety needs to be established.We report a case of severe primary hyperthyroidism,secondary hyperparathyroidism, adrenal insufficiency,and osteoporosis with multiple fractures, most likely dueto chronic steroid intake because of steroid dependentbronchial asthma. Secondary hyperparathyroidismin our patient may be explained by hypocalcemiaresulting from decreased intestinal absorption andincrease renal excretion of calcium due to decreasedtubular reabsorption by steroid. Adrenal insufficiencyresulted from chronic steroid administration.CONCLUSIONThe atypical presentation (uncommon early age -osteoporosis and unusual site of fracture) is probablymultifactorial. The treatment was directed towardsthe etiology and consequences of the diseases,leading to uneventful recovery. In such a patientpresenting with osteoporosis even with subtlesymptoms of thyrotoxicosis, thyroid hormonalevaluation is warranted. Furthermore, parathyroidhormone assay is indeed one of the most importantbiochemical markers in an osteoporotic subject.REFERENCES1. Adinoff AD, Hollister JR. Steroid-induced fracturesand bone loss in patients with asthma. N Engl J Med1983; 309:265-268.2. Recommendation for the prevention and treatmentof glucocorticoid-induced osteoporosis. AmericanCollege of Rheumatology Task Force on OsteoporosisGuidelines. Arthritis Rheum1996; 39:1791-1801.3. de Nijs RN, Jacobs JW, Lems WF, et al. Alendronate oralfacalcidol in glucocorticoid-induced osteoporosis. NEngl J Med 2006; 355:675-684.4. Ringe JD, Coster A, Meng T, Schacht E, Umbach R.Treatment of glucocorticoid-induced osteoporosis withalfacalcidol/calcium versus vitamin D/calcium. CalcifTissue Int 1999; 65:337-340.5. Recommendations for the prevention and treatmentof glucocorticoid-induced osteoporosis: 2001 update.American College of Rheumatology Ad Hoc Committeeon Glucocorticoid-induced Osteoporosis. ArthritisRheum 2001; 44:1496-1503.6. Saag KG, Shane E, Boonen S, et al. Teriparatide oralendronate in glucocorticoid-induced osteoporosis. NEngl J Med 2007; 357:2028-2039.7. Cummings SR, Melton LJ. Epidemiology and outcomesof osteoporotic fractures. Lancet 2002; 359:1761-1767.8. Sawin CT, Geller A, Hershman JM, Castelli W, BacharachP. The aging thyroid. The use of thyroid hormone inolder persons. JAMA 1989; 261:2653-2655.9. Melton LJ 3 rd , Chrischilles EA, Cooper C, Lane AW,Riggs BL. Perspective. How many women haveosteoporosis? J Bone Miner Res 1992; 7:1005-1010.
Page 2 and 3:
Vol. 41 No. 1KUWAIT MEDICAL JOURNAL
Page 4:
KUWAIT MEDICAL JOURNALKUWAIT MEDICA
Page 8 and 9:
June 2009KUWAIT MEDICAL JOURNAL 91E
Page 10 and 11:
June 2009KUWAIT MEDICAL JOURNAL 93R
Page 12 and 13:
June 2009KUWAIT MEDICAL JOURNAL 95O
Page 14 and 15:
June 2009KUWAIT MEDICAL JOURNAL 97c
Page 16:
June 2009KUWAIT MEDICAL JOURNAL 99p
Page 20 and 21: June 2009KUWAIT MEDICAL JOURNAL 103
Page 74 and 75: June 2009400 mg/kg/day for five day
Page 86 and 87: March 2009KUWAIT MEDICAL JOURNAL 16
show all

June 09-41-2.indd - Kma.org.kw

Create successful ePaper yourself

Delete template?

Save as template?