Transient osteoporosis of pregnancy

Share Embed


Descrição do Produto

Injury, Int. J. Care Injured 43 (2012) 1237–1241

Contents lists available at SciVerse ScienceDirect

Injury journal homepage: www.elsevier.com/locate/injury

Review

Transient osteoporosis of pregnancy George Maliha, Jordan Morgan *, Mark Vrahas Harvard Orthopaedic Trauma Service, Massachusetts General Hospital, 55 Fruit Street, Boston, MA 02114, USA

A R T I C L E I N F O

A B S T R A C T

Article history: Accepted 4 March 2012

Transient osteoporosis of pregnancy (TOP) is a rare yet perhaps under-reported condition that has affected otherwise healthy pregnancies throughout the world. The condition presents suddenly in the third trimester of a usually uneventful pregnancy and progressively immobilizes the mother. Radiographic studies detect drastic loss of bone mass, elevated rates of turnover in the bone, and oedema in the affected portion. Weakness of the bone can lead to fractures during delivery and other complications for the mother. Then, within weeks of labour, symptoms and radiological findings resolve. Aetiology is currently unknown, although neural, vascular, haematological, endocrine, nutrientdeficiency, and other etiologies have been proposed. Several treatments have also been explored, including simple bed rest, steroids, bisphosphonates, calcitonin, induced termination of pregnancy, and surgical intervention. The orthopedist plays an essential role in monitoring the condition (and potential complications) as well as ensuring satisfactory outcomes for both the mother and newborn. ß 2012 Elsevier Ltd. All rights reserved.

Keywords: Transient osteoporosis Pregnancy

Contents Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Pathophysiology and diagnosis . . . . . . . . . . . . . . . . . . . . . Effects on the unborn child and offspring . . . . . . . . . . . . Effects on future pregnancies . . . . . . . . . . . . . . . . . . . . . . Non-typical presentations . . . . . . . . . . . . . . . . . . . . . . . . . Aetiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Neurological . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Neurovascular . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Haematological . . . . . . . . . . . . . . . . . . . . . . . . . . . . Vascular. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Deficiencies in bone metabolism . . . . . . . . . . . . . . Similarity to Sudek’s atrophy conditions . . . . . . . . Treatment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Bed rest and restriction of mobility—conservative Steroids . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Bisphosphonates . . . . . . . . . . . . . . . . . . . . . . . . . . . Calcitonin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Termination of pregnancy . . . . . . . . . . . . . . . . . . . Surgical intervention . . . . . . . . . . . . . . . . . . . . . . . Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

......... ......... ......... ......... ......... ......... ......... ......... ......... ......... ......... ......... ......... treatment ......... ......... ......... ......... ......... ......... .........

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . .

1236 1237 1237 1238 1238 1238 1238 1238 1238 1238 1238 1238 1238 1239 1239 1239 1239 1239 1239 1239 1239

Introduction * Corresponding author at: Orthopaedic Trauma Service, Massachusetts General Hospital, Yawkey Center, Suite 3C, 55 Fruit Street, Boston, MA 02114, USA. Tel.: +1 617 643 3653; fax: +1 617 643 1094. E-mail addresses: [email protected] (G. Maliha), [email protected] (J. Morgan), [email protected] (M. Vrahas). 0020–1383/$ – see front matter ß 2012 Elsevier Ltd. All rights reserved. doi:10.1016/j.injury.2012.03.009

Transient osteoporosis of pregnancy (TOP) is a rare but perhaps under-reported condition that was first described by Curtiss and Kincaid in 1959 and has since been reported several times

1238

G. Maliha et al. / Injury, Int. J. Care Injured 43 (2012) 1237–1241

throughout the world.1 Although infrequent, it is likely that at least one case will present throughout an orthopedist’s career. The condition is usually unexpected as it tends to affect young, healthy females in an otherwise uneventful pregnancy. Nonetheless, TOP can affect the mother’s ability to deliver normally by causing excruciating pain in the hip and by promoting the formation of fractures in the femur before and during delivery.2,3 After the birth of the child, the mother may still suffer from unstable fractures that might require surgical intervention. The orthopedist, thus, is required at all stages of TOP to diagnose the condition, manage the pain, and potentially repair fractures. However, successful treatment and even diagnosis must consider the needs and risks to both the mother and child, which limit the number of options available to the orthopedist. Pathophysiology and diagnosis Lequesne first coined the term transient osteoporosis in 1968 to describe a sudden-onset, self-resolving degeneration of the femur.4 While the condition affects middle-aged men from 40 to 60 approximately twice as often as in pregnant women, the condition in pregnancy poses special challenges as it affects the mother at a sensitive time. Nonetheless, the similarity in the two forms of the condition provides essential data on the radiological progression of the disease as certain imaging studies are contraindicated in pregnant women. TOP usually presents in the final trimester of an otherwise healthy and normal pregnancy (although in one case, the mother had experienced transient osteoporosis while not pregnant).2,5 Typically, one hip is affected, although bilateral cases have been reported.6,7 The condition progresses through three stages4: Stage 1 Over several weeks, the patient reports progressive discomfort in walking or standing until she is nearly immobilized.4 Movement of the joint becomes extremely painful, especially at the extremes of the range of motion.4 The Trendelenburg sign presents when patients are allowed to stand upright, and most walk with an antalgic limp.4 At this stage, it is extremely important that other, more common conditions are eliminated from consideration. Thus, transient osteoporosis is a diagnosis of exclusion.8 Osteonecrosis (especially avascular necrosis9), infection, osteoarthritis, osteomyelitis, and nonosteoporotic stress fractures should be considered.10 Radiographic studies facilitate this distinction, for in the first few weeks of presentation, there are no radiographic changes associated with TOP.9 Theoretically, MRI scans should indicate oedema, and radioisotope studies should suggest elevated bone turnover as bone mass begins to decline and cause the initial presentation. Nonetheless, exposure to ionizing radiation is contraindicated except in extreme circumstances in pregnancy, and MRIs have been neither proven nor disproven to cause harm to the foetus.10 Institutional and regulatory policies on performing MRIs on pregnant women vary, and the decision on whether to prescribe the imaging study will be duly affected. Indeed, few definitive studies using MRI of the hip have been performed while the mother is carrying a foetus. However, MRI is a potential diagnostic tool for clinicians who wish to avoid exposing a pregnant patient to ionizing radiation. Most MRI studies, though, are ordered in the second stage of disease when other imaging techniques can also assist in diagnosing the condition. Moreover, ultrasonography can safely be used (at any stage of the disease) to assist in the diagnosis of joint effusion, but this sign can be associated with other conditions besides TOP.11 Nonetheless, during this stage of the disease, definitive diagnosis might be deferred for conservative bed rest until after

delivery. In general, the conditions that could be affecting the mother with these presenting symptoms can be managed noninvasively until after her child is born. Blood work is also typically not helpful and potentially conflicting across cases.5,12 Standard blood panels tend to be unremarkable for third trimester pregnancies. In particular, hydroxyproline, vitamin D, and alkaline phosphatase levels have been explored as possible markers of the condition. Hydroxyproline, a marker for collagen degradation that can be associated with bone remodelling, has been reported as elevated in a few patients. However, these results have not been universally replicated, and any potential use of hydroxyproline as an early marker must distinguish normal elevation in pregnancy from elevation from a pathological condition (which is not limited to TOP).13,14 Furthermore, alkaline phosphatase suffers from a similar problem. Levels are elevated in pregnancy,15 and further elevation during TOP has not been consistently reported.9,13,16,17 Vitamin D, while typically associated with calcium absorption in the gut and uptake, also does not provide a particularly accurate marker. Although case reports consisting of a few patients have reported vitamin D deficiency, these deficiencies can also be explained by population characteristics and have not been replicated in many cases.8 Stage 2 Several weeks after initial presentation, the condition enters its second stage. This phase of the condition does not present new clinical symptoms. However, radiographic and imaging studies do reveal significant calcium depletion. On X-ray, the proximal femur (especially the femoral neck and often the femoral head) appears to ‘‘fade out’’ with a phantom-like appearance.5 Importantly, the joint appears unaffected on plain films.16 Dual-energy X-ray scans (bony density scan) indicate a drop in bone density to levels consistent with osteoporosis.18 The signal intensity of the femoral head on MRI is diminished on the T1-weighted images but is increased on T2weighted scans, indicating oedema.5 Radioisotope studies provide evidence for increased turnover (over baseline).19 Examination of the synovial fluid tends to show non-specific inflammation,7 but these findings have been disputed.8 Bone biopsies—although usually unnecessary for a diagnosis at this stage—show bone under-calcification and display the diseased histology typical of osteoporosis.17,20 Stage 3 After the birth of the child, the patient’s symptoms typically disappear without clinical intervention within a few months. While recovery time is variable, in a typical case report, the patient was ordered to be non-weight-bearing for two weeks postpartum. Then, the mother was allowed to weight-bear as tolerated with a cane for eight additional weeks. After that period, the patient was relatively asymptomatic, and MRI studies at six months postpartum found no oedema.8 Another study found clinical improvement in mobility within two months postpartum with radiological improvement at three.18 While most patients do not require intervention besides a non-weight bearing regimen during the few weeks before and after labour, several treatments have been attempted (detailed in the ‘‘Treatment’’ section). Although there is some evidence that certain treatments can shorten the course of TOP, such evidence is weak and must consider the potential risks to the mother, foetus, and nursing newborn. Recovery can also be delayed if surgical intervention is required to repair a major (typically displaced) fracture, which is a rare complication of the condition.6,7,21,22 Effects on the unborn child and offspring Published data following the outcomes postpartum of pregnancies affected by this condition are isolated and sparse.

G. Maliha et al. / Injury, Int. J. Care Injured 43 (2012) 1237–1241

However, in the two studies evaluating the impact of TOP on the foetus noted bony changes in the offspring. One case report revealed growth arrest lines in the distal femur of the newborn at 2 months and multiple radiolucent lines at the ends of the long bones.19 Another revealed evidence of osteopenia as demonstrated through a bone density scan in two children of affected mothers approximately 10 years after birth.20 Importantly, in this second study, siblings of these children that were not born while the mother had transient osteoporosis did not show bone defects.20 While these are interesting findings, they have not been followed up in the literature. These are isolated case reports, and there has been no substantial evidence to establish a causal link between TOP and osteoporosis or other orthopaedic problems in the newborn. Effects on future pregnancies The condition does not appear to consistently recur across different pregnancies and does not appear to cluster in families.23 While many case studies describe the condition as occurring in the first pregnancy, transient osteoporosis has been documented during other pregnancies. Thus, the condition does not appear to present additional risk of recurrence in a future pregnancy. Non-typical presentations While the condition typically affects one or both femurs, transient osteoporosis has been documented to affect other bones, including those of the knee, ankle, wrist, and elbow.10,24,25 With or without other preexisting conditions, transient osteoporosis can evolve into transient migrating osteoporosis of pregnancy—a more painful and debilitating condition.21,22 Although recovery is delayed in the latter, patients typically regain normal bone mass and return to full mobility postpartum. It is important to note that case reports have not developed a link between underlying conditions and TOP. Aetiology Unfortunately, at present time, the literature has not yet reached a consensus as to the cause of transient osteoporosis of pregnancy. Several theories have been posited over the decades, but none has garnered substantial proof. Many of these theories have been developed to explain the occurrence of TOP in one or two particular studies. Thus, these theories lack wide applicability and often directly conflict with each other. Neurological Evidence of bone weakening and discomfort in cattle that had the obturator nerve severed or disrupted led Curtiss and Kincaid to theorize that the cause of the condition was a compression of the nerve by the foetus.1 However, when the nerve was cut in dogs, a decrease in bone mass during pregnancy was not seen. The authors continued to claim, however, that the cause of the disease is neurological.1

1239

Haematological Evidence also suggests that patients suffering from the condition have defects in fibrinolysis, which could cause ischemia in the bone.27 One study of a group of four avascular necrosis and one TOP patients found evidence of fibrinolytic abnormalities in all participants.27 Based on these results, the authors postulated that the two conditions were caused, then, by abnormalities in fibrinolysis. Nonetheless, this isolated study did not assay clotting markers in the transient osteoporosis patient (C-reactive protein, S protein, and antithrombin III), and other studies have not found abnormal C-reactive protein levels in TOP patients.13,27 Vascular Findings from angiographical and scintigraphical studies have concluded that there is vasodilation associated with oedema (presumably secondary to an increased rate of perfusion) in the vessels supplying the femoral head.18 This localized vascular change would provide insight into the localized nature of the disease. However, the mechanism for such vasodilation has not been posited, and there has not been work in this area to develop the theory.18 Deficiencies in bone metabolism Another theory suggests that an underlying vitamin D or preexisting calcium deficiency leads to bone depletion.10,17 The weight-bearing stresses of pregnancy and the needs of the foetus for new bone formation tend to trigger an increased production of 1,25-dihydroxycholecalciferol in order to facilitate increased calcium absorption from the gut.10 Finding that two patients were deficient in vitamin D, the authors of one study postulated that TOP was caused by a failure to upregulate vitamin D production in response to the weight-bearing stresses of pregnancy. Indeed, chronic vitamin D deficiency, failure to upregulate production at the skin, malabsorption, or interference by certain drugs (such as heparin) can lead to calcium depletion and bone weakness.10,28 However, the deficiency does not fully account for the relatively localized nature of the condition, and vitamin D and calcium deficiciency are not universal findings in TOP.10,17,20,28 In addition, an isolated case was reported with a failure to upregulate calcitonin in response to artificially induced hypercalcemia. The limited incidence of this type of response implies that, in this instance, the transient osteoporosis may have been caused by a different mechanism than in the majority of cases.28 However, no follow up study has been conducted to determine whether this calcitonin-response pathology represents a coincidental or causal factor in TOP. Similarity to Sudek’s atrophy conditions Arguing that the conditions possessed similar radiological findings, presented in a similar manner, and were resolved without clinical intervention, Lequesne4 proposed that the condition was a non-traumatic variant of Sudek’s Atrophy. However, the absence of trauma and swelling in the surrounding soft tissue makes this possibility unlikely.10

Neurovascular Treatment Isolated findings from Japan indicate that terminating the pregnancy will lead to a resolution of symptoms.26 It is plausible, then, that the foetus impinges upon or somehow blocks local vasculature or nerves. This theorized mechanism has been evoked to explain the relatively localized nature of the condition as often only one hip is affected.

Several treatments, beyond calcium/vitamin D supplementation and standard pain management techniques, have been proposed in the literature—many inspired by theorized etiologies. Any treatment proposed must consider the potential effects on the foetus as well as the breast-feeding newborn; data is not yet

1240

G. Maliha et al. / Injury, Int. J. Care Injured 43 (2012) 1237–1241

conclusive in this area. In addition, studies of clinical effectiveness are confounded by the self-resolving nature of the illness. Bed rest and restriction of mobility—conservative treatment In general, typical cases without complications from major fractures or pre-existing conditions resolve spontaneously and without intervention.4 Considering the risks to the mother, the foetus, or breast-feeding newborn of certain pharmacological agents, few such therapies significantly shorten recovery time to justify the risk. Thus, even in the case of major complications, most instances are treated by immobilization and weight-bearing restrictions on the affected joint.7 Steroids Steroids are sometimes prescribed to speed recovery, especially after a surgical intervention.29 However, in non-operative cases, steroids have been tried with limited effect. While prednisone 30– 40 mg per day orally for 4 months did not particularly affect recovery time, the bone-sparing steroid deflazacort (60 mg per day, orally, for 1 week with weaning over a month) did shorten recovery to 2–4 weeks.30 Considering the potential effects on the nursing newborn, each case will have to be considered individually to weight the risks and benefits to this apparently effective treatment. Bisphosphonates While bisphosphonates have long-term complications that are not the subject of the current review, they appear to help speed the recovery process in transient osteoporosis. Alendronate (10 mg per day orally) was prescribed in one case, and pain began to subside within days.31 Neridonate (25 mg per month intramuscularly for 6 months) has been used with some success.32 In addition, intravenous pamidronate (45 mg infused over 4 h per day for 3 days) also led to a reduction in pain and a statistically significant increase in bone density at 2 and 4 months after treatment.32,33 Another study explored the use of intravenous clodronate (300 mg infused over 3 h per day for 10 consecutive days) in men suffering from transient osteoporosis and found a reduction in recovery time; the same treatment has also reduced recovery time in one case in a pregnant patient (administered after the delivery of the child).34 The long half-life of these drugs and potential complications once again demand an individual consideration of the case and due review of the risks to the patient and to the nursing newborn. Calcitonin Salmon calcitonin has been used in several studies and appears to reduce recovery times and ease pain symptoms.33 However, much of study data is confounded by ambiguity in data reporting and results. For instance, in one case, calcitonin was used successfully to treat the initial incidence of the condition, but the transient osteoporosis returned after a year and was treated with a bisphosphonate, which may imply that calcitonin is not a curative long term treatment.33 The calcitonin dose used to treat various patients was also not uniform and in some cases not specified by study authors.10,33 Termination of pregnancy This treatment has only been reported in one case study from Japan. Symptoms of the condition resolved within three weeks of termination of the pregnancy.26

Surgical intervention Because of the contraindications to radiological studies in pregnant women, it is nearly impossible to determine the presence of the fracture or whether the fracture developed during pregnancy, although the stresses of the birthing process could be reasonably assumed to put sufficient stress on the hip to cause a fracture. Nonetheless, many pregnancies with TOP are carried full term and undergo normal vaginal delivery. In general, many TOPrelated fractures remain undiagnosed during pregnancy and heal without surgical intervention, especially if the mother is confined to bed rest. Evidence of subchondral trabecular healing has been found in TOP cases, but no further follow up was required.35 In other cases, however, complications arising from TOP have necessitated surgery to install hardware and perform fixation.6,21,22 For instance, one study described a mother who did not go through the typical spontaneous recovery of Stage 3 of bilateral TOP. She was found to have a consolidated subcapital fracture and was subsequently given a total hip athroplasty.36 In another case, the mother was found to have bilateral femoral neck fractures after delivery and underwent internal fixation.7 While most surgeries occur postpartum, in one case, a TOP patient underwent surgery while pregnant to correct an acute Garden grade III fracture caused by a fall.29 Although the procedure itself was relatively uneventful, the patient experienced contractions post operatively, but intravenous magnesium arrested labour, and the patient was discharged without any further complications.29 Appropriately, the literature on performing surgery to correct a fracture in TOP patients carrying a child is extremely sparse beyond one or two case reports.Nonetheless, looking at approximately 90 cases reported in the English language literature, about 15 required surgeries to correct fractures (excluding Caesarian sections, which were sometimes required due to excessive hip pain and limited range of motion). The cases requiring surgery were largely limited to unstable, displaced fractures, suggesting that surgical intervention for stress or occult fractures might not be necessary (a sampling of representative and atypical cases are cited).3,5,10,12,15,17,18,20,22,23,26,29,36–40 Summary Transient osteoporosis of pregnancy (TOP) is a rare, yet important potential complication to pregnancy. Its presentation in the third trimester of an otherwise uneventful pregnancy presents unique challenges to the orthopedist. Diagnosis is by exclusion, and several typically routine diagnostic methods are contraindicated by pregnancy. Aetiology is currently unknown, although several theories have been proposed. Likewise, several treatments have been proposed, but the effects on the mother and foetus and nursing newborn must be considered. The most common treatment, then, is currently bed rest. Surgery is required to repair severe fractures but is rarely necessary for full clinical and radiological recovery within a year. Conflict of interest Each author certifies that he has no commercial associations (e.g., consultancies, stock ownership, equity interest, patent/ licensing arrangements, etc.) that might pose a conflict of interest in connection with the submitted article. References 1. Curtiss Jr PH, Kincaid WE. Transitory demineralization of the hip in pregnancy. A report of three cases. J Bone Joint Surg Am 1959;41-A:1327–33. 2. Shifrin LZ, Reis ND, Zinman H, Besser MI. Idiopathic transient osteoporosis of the hip. J Bone Joint Surg Br 1987;69:769–73.

G. Maliha et al. / Injury, Int. J. Care Injured 43 (2012) 1237–1241 3. Thomas E, Cox C, Murphy D, Beddard K. Hip fracture during labour due to transient osteoporosis of the hip in pregnancy. J Obstet Gynaecol 2000;20: 197–8. 4. Lequesne M. Transient osteoporosis of the hip: a nontraumatic variety of sudeck’s atrophy. Ann Rheum Dis 1968;27:463–71. 5. Beaulieu JG, Razzano CD, Levine RB. Transient osteoporosis of the hip in pregnancy. Clin Orthop Relat Res 1976;115:165–8. 6. Wood ML, Larson CM, Dahners LE. Late presentation of a displaced subcapital fracture of the hip in transient osteoporosis of pregnancy. J Orthop Trauma 2003;17:582–4. 7. Willis-Owen CA, Daurka JS, Chen A, Lewis A. Bilateral femoral neck fractures due to transient osteoporosis of pregnancy: a case report. Cases J 2008;1:120. 8. Vernon LF, Dooley JC, Neidorf DL. Transient osteoporosis of the hip. J Clin Rheumatol 1997;3:176–80. 9. Guerra JJ, Steinberg ME. Distinguishing transient osteoporosis from avascular necrosis of the hip. J Bone Joint Surg Am 1995;77:616–24. 10. Arayssi TK, Tawbi HA, Usta IM, Hourani MH. Calcitonin in the treatment of transient osteoporosis of the hip. Semin Arthritis Rheum 2003;32: 388–97. 11. Koski JM, Mullykangas-Luosujarvi R. Transient osteoporosis of the hip with joint effusion detected by ultrasonography. Clin Rheumatol 1997;16:404–8. 12. Gruber HE, Gutteridge DH, Baylink DJ. Osteoporosis associated with pregnancy and lactation: bone biopsy and skeletal features in three patients. Metab Bone Dis Relat Res 1984;5:159–65. 13. Stevens RJ, Hall ML, Hughes RA. Imaging in transient regional osteoporosis. Br J Rheumatol 1997;36:705–6. 14. Longstreth PL, Malinak LR. Hydroxyproline and transient osteoporosis. Ann Intern Med 1972;76:833. 15. Funk JL, Shoback DM, Genant HK. Transient osteoporosis of the hip in pregnancy: natural history of changes in bone mineral density. Clin Endocrinol (Oxf) 1995;43:373–82. 16. Baker PN, Johnson IR, Harvey PR, Gowland PA, Mansfield P. A three-year followup of children imaged in utero with echo-planar magnetic resonance. Am J Obstet Gynecol 1994;170:32–3. 17. Ma FY, Falkenberg M. Case reports: transient osteoporosis of the hip: an atypical case. Clin Orthop Relat Res 2006;445:245–9. 18. Diwanji SR, Cho YJ, Xin ZF, Yoon TR. Conservative treatment for transient osteoporosis of the hip in middle-aged women. Singapore Med J 2008;49:e17–21. 19. Longstreth PL, Malinak LR, Hill Jr CS. Transient osteoporosis of the hip in pregnancy. Obstet Gynecol 1973;41:563–9. 20. Carbone LD, Palmieri GM, Graves SC, Smull K. Osteoporosis of pregnancy: long-term follow-up of patients and their offspring. Obstet Gynecol 1995;86: 664–6. 21. Kohlmeier LA, Federman M, Leboff MS. Osteomalacia and osteoporosis in a woman with ankylosing spondylitis. J Bone Miner Res 1996;11:697–703. 22. Fingeroth RJ. Successful operative treatment of a displaced subcapital fracture of the hip in transient osteoporosis of pregnancy: a case report and review of the literature. J Bone Joint Surg Am 1995;77:127–31.

1241

23. Bijl M, van Leeuwen MA, van Rijswijk MH. Transient osteoporosis of the hip: presentation of (a) typical cases and a review of the literature. Clin Exp Rheumatol 1999;17:601–4. 24. Stamp L, McLean L, Stewart N, Birdsall M. Bilateral transient osteoporosis of the knee in pregnancy. Ann Rheum Dis 2001;60:721–2. 25. Grey A, Dalbeth N, Doyle A. Clinical images: transient regional osteoporosis. Arthritis Rheum 2009;60:3145. 26. Chigira M, Watanabe H, Udagawa E. Transient osteoporosis of the hip in the first trimester of pregnancy: a case report and review of Japanese literature. Arch Orthop Trauma Surg 1988;107:178–80. 27. Van Veldhuizen PJ, Neff J, Murphey MD, Bodensteiner D, Skikne BS. Decreased fibrinolytic potential in patients with idiopathic avascular necrosis and transient osteoporosis of the hip. Am J Hematol 1993;44:243–8. 28. Smith R, Stevenson JC, Winearls CG, Woods CG, Wordsworth BP. Osteoporosis of pregnancy. Lancet 1985;1:1178–80. 29. Cohen I, Melamed E, Lipkin A, Robinson D. Transient osteoporosis of pregnancy complicated by a pathologic subcapital hip fracture. J Trauma 2007;62:1281–3. 30. Carmona-Ortells L, Carvajal-Mendez I, Garcia-Vadillo JA, Alvaro-Gracia JM, Gonzalez-Alvaro I. Transient osteoporosis of the hip: successful response to deflazacort. Clin Exp Rheumatol 1995;13:653–5. 31. Samdani A, Lachmann E, Nagler W. Transient osteoporosis of the hip during pregnancy: a case report. Am J Phys Med Rehabil 1998;77:153–6. 32. La Montagna G, Malesci D, Tirri R, Valentini G. Successful neridronate therapy in transient osteoporosis of the hip. Clin Rheumatol 2005;24:67–9. 33. Varenna M, Zucchi F, Binelli L, Failoni S, Gallazzi M, Sinigaglia L. Intravenous pamidronate in the treatment of transient osteoporosis of the hip. Bone 2002;31:96–101. 34. Schapira D, Braun Moscovici Y, Gutierrez G, Nahir AM. Severe transient osteoporosis of the hip during pregnancy: successful treatment with intravenous biphosphonates. Clin Exp Rheumatol 2003;21:107–10. 35. Kim YL, Nam KW, Yoo JJ, Hong SH, Kim HJ. CT evidence for subchondral trabecular injury of the femoral head in transient osteoporosis of the hip: a case report. J Korean Med Sci 2010;25:192–5. Epub 2009 Dec 26. 36. Chalouhi GE, Harb C, Atallah D, Mansour F, Ghanem I, Dagher F. Total hip replacement at thirty years: case report of crippling complications of a transient osteoporosis of the hip during pregnancy. Eur J Obstet Gynecol Reprod Biol 2010;149:226–7. Epub 2009 Dec 16. 37. Brodell JD,Burns Jr JE, Heiple KG. Transient osteoporosis of the hip of pregnancy: two cases complicated by pathological fracture. J Bone Joint Surg Am 1989;71:1252–7. 38. Lamarca M, Hernandez M, Campillos JM, Lapresta M, Tobajas JJ. Subcapital fracture of the hip in transient osteoporosis of pregnancy. Taiwan J Obstet Gynecol 2009;48:423–4. 39. Spinarelli A, Patella V, Speciale D, et al. Hip fracture in a patient affected by transient osteoporosis of the femoral head during the last trimester of pregnancy. Orthopedics 2009;32:365. 40. Kalender AM, Dogan A, Cakar A, Turkoz T. Neglected bilateral femoral neck fracture associated with pregnancy and primary hyperparathyroidism. Acta Orthop Belg 2010;76:559–63.

Lihat lebih banyak...

Comentários

Copyright © 2017 DADOSPDF Inc.