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Skeletal Radiological Findings in Thalassemia Major

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Skeletal Radiological Findings in Thalassemia Major Journal of Research and Practice on the Musculoskeletal System JOURNAL OF RESEARCH AND PRACTICE ON THE MUSCULOSKELETAL SYSTEM Review Article Skeletal radiological findings in thalassemia major Spyridon G. Adamopoulos1, Glykeria M. Petrocheilou2 1Radiology Department, General State Hospital of Athens “G. Gennimatas”, Athens, Greece; 2Radiology Department, Pathology Hospital of Athens Spiliopouleio - “Agia Eleni”, Athens, Greece Abstract Skeletal changes in beta-thalassemia major (βTM) create a wide spectrum of bone radiographic features. The main pathology is extensive marrow proliferation due to ineffective erythropoiesis but the relative skeletal findings are encountered with a progressively reduced frequency and severity nowadays due to the regular hypertransfusion programs. The resulting hemosiderosis and particularly iron chelation therapy have been associated with dysplastic features which are found more often. Skeletal radiological appearances in βTM relate to a complex multifactorial pathogenesis (i.e. marrow expansion, direct iron and chelation toxicity, endocrine complications) and depend on the severity and duration of the disease, the type and effectiveness of treatment and the toxic effects of chelation therapy. Awareness of these findings is very important since early recognition can be an indicator for therapy adaptation. Keywords: Bone, Chelation radiography, Skeletal, Thalassaemia major Introduction proliferation affects both cortical and cancellous bones causing widening of the medullary space - bone marrow Beta-thalassemia major (βTM) or Cooley’s anemia or can be expanded by a factor of up to 15 to 30 in untreated Mediterranean anemia was first described in 1925 by patients- cortical thinning and resorption of the secondary/ 1 Cooley and Lee . The disease has a high prevalence in tertiary bone trabeculae with subsequent prominent/coarse populations from the Mediterranean basin and refers to an primary trabeculae creating a “lace-like” appearance. A inherited hematologic disorder characterized by reduced generalized decrease in osseous density (osteopenia/ or absent synthesis of b-hemoglobin chains leading to osteoporosis) is resulting11. Focal marrow proliferation may ineffective erythropoiesis. If left untreated, βTM patients be also present causing small areas of lucency. Sometimes develop severe anemia, hepatosplenomegaly, several bone extra-medullary hemopoetic tissue extents to break through deformities, poor growth and usually die by heart failure in the bone cortex and grow beneath the periosteum forming 2,3 the first decade of life . Since 1965 long-term transfusion a scalloped cortical edge. A periosteal reactive response programs have been used from infancy to correct anemia may then initiate depending on the bone involved and and maintain acceptable levels of hemoglobin. From the late the proliferation extent7. In some cases, extramedullary 1970s chelation therapy has been also instituted to remove hemopoiesis creates large extraskeletal masses mimicking the resulting iron accumulation and prevent its serious soft tissue tumors. 2,4 complications within the heart, liver and endocrine glands . These skeletal findings are most often found in children The modern radiologist should be aware not only of the older than 1 year old. Not all bones are involved to the same classic well documented radiological findings caused by medullary expansion - although less common they may be seen in inadequately transfused patients - but of the skeletal deformities induced by therapeutic agents as well, since the The authors have no conflict of interest. latter are encountered more frequently nowadays and may Corresponding author: Spyridon G. Adamopoulos, indicate toxicity requiring dose adaptation5-7. Metamorfoseos 7, 152 34, Chalandri, Athens, Greece E-mail: [email protected] Pathophysiology and skeletal changes Edited by: Konstantinos Stathopoulos In untreated or poorly transfused βTM patients skeletal Accepted 6 September 2019 changes result primarily from marked erythroid hyperplasia 8-10 Published under Creative Common License CC BY-NC-SA 4.0 (Attribution-Non Commercial-ShareAlike) Common License CC BY-NC-SA 4.0 (Attribution-Non Creative Published under secondary to ineffective erythropoiesis . Marrow www.jrpms.eu 10.22540/JRPMS-04-076 JRPMS | September 2020 | Vol. 4, No. 3 | 76-85 76 Skeletal radiological findings in thalassemia major degree and at the same time. Intense skeletal changes are type and effectiveness of treatment and the toxic effects observed in the skull and hands, but are also found in the of chelation therapy. long bones, ribs and vertebral bodies. At first, both the This review is a location based radiological skeleton guide axial and the appendicular skeleton are affected. Towards covering the spectrum of bony appearances in βTM both in puberty, the findings in the appendicular skeleton diminish untreated and treated patients. following the normal regression of hematopoietic marrow12. In contrary, the deformities in the axial skeleton, e.g. skull, Radiological findings in axial skeleton ribs, clavicles, spine and pelvis, which are sites of active Skull persistent erythropoiesis remain throughout life or may even become more pronounced. Thus, according to Caffey13 ”the The attributed to marrow hyperplasia marked skull findings represent late skeletal manifestations and do not distal portions of the skeleton (hands and feet), which are always agree with the degree of anemia or the changes in the optimal sites for radiological identification of the disease the rest of the skeleton 8,18. Initially, radiography may show dur ing infancy and childhood, become the least diagnostic only a slight thickening of the vault and the bones look after puberty”. During the last decades these classic, well- “hazy” and “sandy” with increased porosity due to granular documented in the past, bone radiological findings appear osteoporosis. At a later stage, the skull bones have a more with a progressively reduced frequency and severity due spongy out line but well-circumscribed solitary or multiple to systematic hypertransfusion therapy. They have not lytic lesions may be also occasionally seen19. disappeared though, as bone marrow remains hyperactive As the disease pro gresses the hyper plastic marrow causes even with an optimal transfusion regimen10. widening of the diploë –reported to become as much as four In hypertransfused patients and before the institution of times wider than normal20. The residual diploic trabeculae chelation therapy a distinctive osteoarthropathy appeared. that don’t get destroyed become thickened. The earliest and Hemosiderosis has been related to synovial and cartilaginous most severe deformities occur in the frontal bones, whereas abnormalities which are probably caused by iron overload, the inferior part of the occiput is usually unaffected due to abnormal calcium metabolism, vitamin D function and its lower marrow content12,13. This asymmetry makes the hyperuricaemia. calvarium become hollow and assume a camelback shape After the introduction of iron-chelation therapy in the (helmeted aspect). The membranous skull bones do not late 1970s a new common pattern of skeletal changes expand adjacent to the sutures resulting in a “hot cross bun” 14 emerged over the next decade . Iron chelator agents may skull configuration. have a negative effect on bones and joints causing dysplastic The hyper plastic marrow makes the out er table so thin deformities in the spine and the metaphyses of long bones, as to be indistinguishable and perforates or destroys it. In growth retardation and arthropathy. Different mechanisms contrary, the inner table may become notably thinner but may be implicated including abnormal metaphyseal collagen remains intact8,12,13. Once the outer table is perforated, synthesis, inhibition of osteoblasts, a direct toxic effect and the expanding marrow may proliferate under the invisible loss of minerals other than iron (e.g., copper). Post chelation periosteum and cause reactive bone formation on the skull dysplastic bone features are found nowadays more often surface resulting in new bone spicules deposited vertically than those resulting from marrow expansion or extra- to the inner table21. These, along with the residual thickened, medullary hemopoiesis15. Thus the literature recommends perpendicular in orientation, trabeculae create with the close monitoring of the toxic effects of chelation therapy, radiolucent marrow hyperplasia the characteristic “hair-on- emphasising on the risks of chelation over-treatment and on end” sign or “crew cut” appearance, i.e. long, thin vertical the possible individual idiosyncrasy10. lines that cross the thickened calvarium beyond the outer To sum up, it is well known that in βTM many table looking like hair standing on end (Figure 1)22. The factors have an impact on skeleton including: marrow radiating spicules are easily seen in tangential radiographic proliferation; iron overload/toxicity with direct negative projections23. The hair-on-end pattern is a well documented effects on osteoblast and osteoclast activity; chelation but relatively uncommon finding that stops abruptly at the therapy toxicity; associated endocrine complications occipital bone due to lack of marrow activity within it. It is (hypogonadism due to pituitary failure and gonadal only evident in advanced stages in βTM and only sporadic dysfunction; growth hormone and insulin-like growth reports exist for thalassemia minor and thalassaemia factor-I abnormalities;
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