Discontinuation Of Alendronate Research Articles

Alendronate-Induced Nephropathy

Background: Alendronate is considered a safe drug with respect to kidney function when used per manufacturer recommendations. Objective: To describe reported cases of nephrotoxicity associated with alendronate. Methods: Pubmed search of English literature up to January 14, 2022. Search terms include alendronate, bisphosphonates, proteinuria, renal failure, adverse effects. Pertinent case reports, reviews, and guidelines of professional organizations are included. Results: Review of literature revealed 7 patients who developed nephrotoxicity likely due to alendronate therapy for osteoporosis. In 5 patients, kidney function was normal before starting alendronate. Five patients presented with nephrotic syndrome and had focal segmental glomerulosclerosis (FSGS) on renal biopsy. Collapsing FSGS was specifically demonstrated in 2 patients. Nephrotoxicity was diagnosed as early as 2 weeks and up to 3 years after starting alendronate. No clear predisposing factors or patient demographic characteristics could be outlined in association with this adverse effect. In addition to discontinuation of alendronate, treatment consisted of glucocorticoids followed by angiotensin-converting enzyme inhibitors and diuretics. In 4 of the 7 patients, renal function did not return to normal and 3 subjects required hemodialysis. Conclusions: Physicians should be aware that alendronate may be uncommonly associated with nephrotoxicity. Checking protein in urine 2 weeks after starting alendronate and periodically thereafter may help early diagnosis of this serious adverse effect.

Vitamin D Boosts Alendronate Tail Effect on Bone Mineral Density in Postmenopausal Women with Osteoporosis.

Vitamin D modulates bisphosphonate (BP) efficacy, but its contribution to bone mineral density (BMD) after BP discontinuation is not known. To address this topic, we performed a retrospective analysis of postmenopausal women exposed to alendronate (ALN) to treat osteoporosis who regularly continued the supplementation of cholecalciferol or calcifediol at recommended doses. In the ninety-six recruited women (age 61.1 ± 6.9 years), ALN was administered for 31.2 ± 20.6 months and then discontinued for 33.3 ± 18.9 months. The modification of 25(OH)D serum levels over time was associated with a change of alkaline phosphatase (r = −0.22, p = 0.018) and C-terminal collagen type 1 telopeptide (r = −0.3, p = 0.06). Women in the tertile of the highest increase in 25(OH)D level showed a 5.7% BMD gain at lumbar spine, that was twice as great in comparison with participants with a lower 25(OH)D variation. At a multiple regression analysis, BMD change was associated with time since menopause (ß = 2.28, SE 0.44, p < 0.0001), FRAX score for major fracture (ß = −0.65, SE 0.29, p = 0.03), drug holiday duration (ß = −2.17, SE 0.27, p < 0.0001) and change of 25(OH)D levels (ß = 0.15, SE 0.03, p = 0.0007). After ALN discontinuation, improving the vitamin D status boosts the ALN tail effect on BMD.

The predictive value of bone turnover markers during discontinuation of alendronate: the PROSA study.

It is unknown how to monitor patients discontinuing alendronate (ALN) after more than 5 years. We investigated if BTM measured before or during treatment discontinuation with ALN predict bone loss after 1 or 2 years. PROSA was a cohort study conducted at Aarhus University Hospital including postmenopausal women and men above 50 years treated with ALN ≥ 5 years who had osteopenia at the hip and BMD T-score at the lumbar spine > - 4. ALN was discontinued and BTMs were measured at baseline, months (M) 1, 3, 6, and 12, and DXA was performed at baseline, M6, and M12. We extended the study and measured BTMs and performed DXA at M24. The primary endpoint was if changes in p-CTX at M3 or M6 predict changes in THBMD after 1 year ( Clinicaltrials.gov : NCT03051620). We enrolled 136 participants discontinuing ALN after a median of 7.0 years (range 5.0-20.0 years) in PROSA and 124 participants in PROSA Extension. There was a significant decrease in LSBMD - 0.74% ± 0.27, THBMD - 2.65% ± 0.39, FNBMD - 2.35% ± 0.33, and trabecular bone score - 0.97% ± 0.35 and an increase in p-CTX by 61.1% ± 4.7 (p < 0.05 for all) after 24 months. Increase in p-CTX at M3 was associated with bone loss at the hip sites at M12 and M24. In patients discontinuing ALN, BMD decreased significantly and BTMs increased within the reference range over 2 years. An increase in p-CTX after 3 months was associated with greater bone loss at the hip confirming that maintenance of BMD during treatment discontinuation is dependent on continued suppression of bone turnover.

Atypical Femoral Fracture in McCune-Albright Syndrome

McCune-Albright Syndrome (MAS) is characterized by endocrinopathies, café-au-lait spots, and fibrous dysplasia. Bisphosphonates are the most prescribed treatment for reducing the pain but their long-term use has been associated with atypical fractures of cortical bones like femur in patients. We present a 23-year-old girl diagnosed with MAS. She had an atypical mid-shaft left femoral fracture that happened during simple walking. She also had a history of long-term use of alendronate. Because of the narrow medullary canal, we used 14 holes hybrid locking plate for the lateral aspect of the thigh to fix the fracture and 5 holes dynamic compression plate (instead of the intramedullary nail) in the anterior surface to double fix it, reducing the probability of device failure. With double plate fixation and discontinuation of alendronate, the complete union was achieved five months after surgery

Temporal Trends and Factors Associated with Bisphosphonate Discontinuation and Restart.

Adverse events related to long-term use of bisphosphonates have raised interest in temporary drug discontinuation. Trends in bisphosphonate discontinuation and restart, as well factors associated with these decisions, are not fully understood at a population level. We investigated temporal trends of bisphosphonate discontinuation from 2010 to 2015 and identified factors associated with discontinuation and restart of osteoporosis therapy. Our cohort consisted of long-term bisphosphonate users identified from 2010 to 2015 Medicare data. We defined discontinuation as ≥12 months without bisphosphonate prescription claims. We used conditional logistic regression to compare factors associated with alendronate discontinuation or osteoporosis therapy restart in the 120-day period preceding discontinuation or restart referent to the 120-day preceding control periods. Among 73,800 long-term bisphosphonate users, 59,251 (80.3%) used alendronate, 6806 (9.2%) risedronate, and 7743 (10.5%) zoledronic acid, exclusively. Overall, 26,281 (35.6%) discontinued bisphosphonates for at least 12 months. Discontinuation of bisphosphonates increased from 1.7% in 2010, reaching a peak of 14% in 2012 with levels plateauing through 2015. The factors most strongly associated with discontinuation of alendronate were: benzodiazepine prescription (adjusted odds ratio [aOR] = 2.5; 95% confidence interval [CI] 2.1, 3.0), having a dual-energy X-ray absorptiometry (DXA) scan (aOR = 1.8; 95% CI 1.7, 2.0), and skilled nursing facility care utilization (aOR = 1.8; 95% CI 1.6, 2.1). The factors most strongly associated with restart of osteoporosis therapy were: having a DXA scan (aOR = 9.9; 95% CI 7.7, 12.6), sustaining a fragility fracture (aOR = 2.8; 95% CI 1.8, 4.5), and an osteoporosis or osteopenia diagnosis (aOR = 2.5; 95% CI 2.0, 3.1). Our national evaluation of bisphosphonate discontinuation showed that an increasing proportion of patients on long-term bisphosphonate therapy discontinue medications. The factors associated with discontinuation of alendronate were primarily related to worsening of overall health status, whereas traditional factors associated with worsening bone health were associated with restarting osteoporosis medication. © 2019 American Society for Bone and Mineral Research.

Annals for Educators - 2 July 2019.

Annals for Educators - 2 July 2019.

An elderly woman with progressive odynophagia, epigastralgia and nausea

An 84-year-old woman presented to the author's hospital with a 5-day history of progressive odynophagia, epigastralgia and nausea. These symptoms developed 3 days after taking an alendronate oral tablet (35 mg once-weekly) for the treatment of postmenopausal osteoporosis. The patient's other medication consisted of 10 mg/day of rivaroxaban for atrial fibrillation; 200 mg/day of cilostazol for lacunar infarction; 20 mg/day of esomeprazole and 300 mg/day of rebamipide for the prevention of peptic ulcer. Esophagogastroduodenoscopy (EGD) revealed severe erosion and ulceration with sloughing mucosal casts in the mid and lower esophagus (Fig. 1, Panels A and B). What is the diagnosis? The abovementioned endoscopic findings are compatible with drug-induced esophagitis. Alendronate can cause chemical esophagitis including severe ulcerations [[1]de Groen P.C. Lubbe D.F. Hirsch L.J. et al.Esophagitis associated with the use of alendronate.N Engl J Med. 1996; 335: 1016-1021Crossref PubMed Scopus (700) Google Scholar]; therefore, alendronate-induced esophagitis was diagnosed. Alendronate therapy was discontinued, and the patient was hospitalized; thus, parenteral nutrition and intravenous administration of a proton pump inhibitor (PPI) (lansoprazole 30 mg twice-daily) were performed. The symptoms were disappeared within a few days, and 6 days later, EGD confirmed remarkable improvement of the esophagitis (Fig. 1, Panel C). The patient was discharged on the 8th day after admission, and monthly intravenous ibandronate 1 mg was prescribed as an alternative to weekly oral alendronate 35 mg. Alendronate, an aminobisphosphonate, is a selective inhibitor of osteoclast-mediated bone resorption and has been widely used to treat osteoporosis. A large review of worldwide post-marketing surveillance data for alendronate in 1996 showed that 0.04% (199/475,000) of patients had adverse effects related to the esophagus [[1]de Groen P.C. Lubbe D.F. Hirsch L.J. et al.Esophagitis associated with the use of alendronate.N Engl J Med. 1996; 335: 1016-1021Crossref PubMed Scopus (700) Google Scholar]. Recovery of the esophagitis can be solved by stopping alendronate, with additional treatment such as acid-suppressing agent and parenteral nutrition when necessary. Furthermore, drug-induced acid suppression is not a substitute for the discontinuation of alendronate [[1]de Groen P.C. Lubbe D.F. Hirsch L.J. et al.Esophagitis associated with the use of alendronate.N Engl J Med. 1996; 335: 1016-1021Crossref PubMed Scopus (700) Google Scholar]. Physicians need to be cautious of esophagitis induced by alendronate, even though the patient has taken an oral PPI. None declared.

Insights into the bisphosphonate holiday: a preliminary FTIRI study.

Bisphosphonates (BP) are the most commonly used and effective drugs to prevent fragility fractures; however, concerns exist that prolonged use may lead to adverse events. Recent recommendations suggest consideration of a BP "holiday" in individuals taking long-term BP therapy not at high risk of fracture. Data supporting or refuting this recommendation based on bone quality are limited. We hypothesized that a "holiday" of 5years would cause no major bone compositional changes. We analyzed the 31 available biopsies from the FLEX-Long-term Extension of FIT (Fracture Intervention Trial) using Fourier transform infrared imaging (FTIRI). Biopsies from two groups of post-menopausal women, a "Continuously treated group" (N = 16) receiving alendronate for ~ 10years and a "Discontinued group" (N = 15), alendronate treated for 5years taking no antiresorptive medication during the following 5years. Iliac crest bone biopsies were provided at 10years. Key FTIRI parameters, mineral-to-matrix ratio, carbonate-to-phosphate ratio, acid phosphate substitution, and collagen cross-link ratio as well as heterogeneity of these parameters were similar for Continuously treated and Discontinued groups in age-adjusted models. The Discontinued group had 2% greater cortical crystallinity (p = 0.01), 31% greater cortical acid phosphate heterogeneity (p = 0.02), and 24% lower trabecular crystallinity heterogeneity (p = 0.02). Discontinuation of alendronate for 5years did not affect key FTIRI parameters, supporting the hypothesis that discontinuation would have little impact on bone composition. Modest differences were observed in three parameters that are not likely to affect bone mechanical properties. These preliminary data suggest that a 5-year BP holiday is not harmful to bone composition.

Assessing the feasibility of the Effectiveness of Discontinuing Bisphosphonates trial: a pilot study.

The comparative effectiveness of continuing or discontinuing long-term alendronate (ALN) on fractures is unknown. A large pragmatic ALN discontinuation study has potential to answer this question. We conducted a 6-month pilot study of the planned the EDGE study among current long-term ALN users (women aged ≥65 with ≥3years of ALN use) to determine study work flow and feasibility including evaluating the administrative aspects of trial conduct (e.g., time to contract, institutional review board (IRB) approval), assessing rates of site and participant recruitment, and evaluating post-randomization outcomes, including adherence, bisphosphonate-associated adverse events, and participant and site satisfaction. We assessed outcomes 1 and 6months after randomization. Nine sites participated, including seven community-based medical practices and two academic medical centers. On average (SD), contract execution took 3.4 (2.3) months and IRB approval took 13.9 (4.1) days. Sites recruited 27 participants (13 to continue ALN and 14 to discontinue ALN). Over follow-up, 22% of participants did not adhere to their randomization assignment: 30.8% in the continuation arm and 14.3% in the discontinuation arm. No fractures or adverse events were reported. Sites reported no issues regarding work flow, and participants were highly satisfied with the study. Administrative procedures of the EDGE study were generally feasible, with minimal disruption to clinic flow. In this convenience sample, participant recruitment was suboptimal across most practice sites. Accounting for low treatment arm adherence, a comprehensive recruitment approach will be needed to effectively achieve the scientific goals of the EDGE study.

Bisphosphonate Withdrawal: Effects on Bone Formation and Bone Resorption in Maturing Male Mice.

Bisphosphonates are being increasingly used to treat pediatric patients with skeletal disorders. However, the effects of long-term bisphosphonate therapy and cessation of therapy during growth are unclear. Thus, studies were undertaken to determine the effects of alendronate discontinuation after treatment of C57Bl/6 mice during the period of rapid skeletal growth. Compared with vehicle-treated mice, 16 weeks of alendronate treatment starting at age 18 days resulted in a 3.7-fold increase in trabecular bone in the setting of suppressed bone formation. Alendronate therapy for 8 weeks followed by 8 weeks of vehicle treatment resulted in a more pronounced increase in trabecular bone compared with mice treated with alendronate for 16 weeks (1.7-fold) and to vehicle-treated controls (6.5-fold). Mice that received alendronate for 8 weeks followed by 8 weeks of vehicle exhibited increased osteoblast surface (2.5-fold), mineralizing surface (5.7-fold), and bone formation rate (5.1-fold) compared with mice treated continuously with alendronate. However, these parameters were not restored to the levels observed in the vehicle-treated mice. Thus, partial resumption of bone formation upon cessation of bisphosphonate therapy leads to a greater increase in trabecular bone than that found when bisphosphonates are administered continuously to growing mice. These data suggest that intermittent administration of bisphosphonates may optimize their beneficial effects on the growing skeleton. © 2017 American Society for Bone and Mineral Research.

Effects of drug discontinuation after short-term daily alendronate administration on osteoblasts and osteocytes in mice.

In order to determine whether osteoclastic bone resorption is restarted after withdrawn of bisphosphonates, we conducted histological examinations on murine osteoclasts, osteoblasts and osteocytes after discontinuation of a daily regimen of alendronate (ALN) with a dosage of 1mg/kg/day for 10days. After drug discontinuation, metaphyseal trabecular number and bone volume remained unaltered for the first 4days. Osteoclast number did not increase, while the number of apoptotic osteoclasts was elevated. On the other hand, tissue non-specific alkaline phosphatase-immunoreactive area was markedly reduced after ALN discontinuation. In addition, osteocytes showed an atrophic profile with empty lacunar areas during and after ALN treatment. Interestingly, as early as 36h after a single ALN injection, osteocytes show signs of atrophy despite the presence of active osteoblasts. Structured illumination microscopy system showed shortening of osteocytic cytoplasmic processes after drug cessation, suggesting a possible morphological and functional disconnection between osteocytes and osteoblasts. Taken together, it appears that osteoclastic bone resorption is not resumed after ALN discontinuation; also, osteoblasts and osteocytes hardly seem to recover once they are inactivated and atrophied by ALN. In summary, it seems that one must pay more attention to the responses of osteoblasts and osteocytes, rather focusing on the resuming of osteoclastic bone resorption after the ALN discontinuation.

A model of BMD changes after alendronate discontinuation to guide postalendronate BMD monitoring.

Women stopping alendronate are commonly monitored with serial bone mineral density (BMD) measurements, yet no information exists on how frequently or for whom these measurements should be performed. The objective of the study was to develop a tool to guide post-alendronate BMD monitoring. A predictive model was constructed to estimate the time until a given percentage of women's BMD T-scores drop below a given threshold that indicates a management change (such as retreatment) would be considered. This model was then used to estimate the time it would take for groups of women defined by their baseline BMDs to drop below the given threshold. Data were derived from the Fracture Intervention Trial Long Term Extension (FLEX), the largest multicenter clinical trial of its type to date. Four hundred four women who had received an average of 5.1 years of alendronate during the Fracture Intervention Trial and were subsequently observed for 5 treatment-free years (on placebo) during the FLEX trial were used to estimate the change in BMD over time. If a management change such as alendronate reinitiation would be considered when BMD T-score drops below -2.5, the model shows that women with total hip BMD greater than -1.9 T-scores at the time of alendronate discontinuation have less than a 20% probability that at follow-up, monitoring BMD will be below the threshold within 5 years. The model performed similarly, and results are provided over a range of management change thresholds from -1.75 to -3 T-scores. Using the tool developed in this analysis, it is possible to estimate when BMD repeat measurement after alendronate discontinuation could potentially be useful. Measuring BMD within 5 years after alendronate discontinuation is unlikely to change management for women with total hip BMD 0.6 T-scores above a prespecified retreatment threshold within the range of -1.75 to -3 T-scores.

Comment on Tadrous et al.: Comparative gastrointestinal safety of bisphosphonates in primary osteoporosis: a network meta-analysis

Dear Editor, The study by Tadrous et al. [1] identified zoledronic acid as the bisphosphonate with the “highest probability gastrointestinal (GI) adverse events (91 %) and nausea (70 %).” Many clinicians will have been surprised at this finding. First, in contrast to the established mechanisms of upper GI AE following oral preparation of bisphosphonates, there are no known mechanisms explaining GI AEs including nausea when bisphosphonates are administered in IV regimens. Of course, an acute face reaction is not uncommon after zoledronic acid infusion, especially after the first administration and more rarely after the next infusion and this could be accompanied in some cases by stomach upset and nausea. This could have been explored, had the authors included the acute face reaction in their analysis. Second, the frequency of events reported in Table 2 does not seem internally coherent. For alendronate, 54 % reportedly experienced esophageal AEs and 29 % nausea, yet there was no discontinuation of alendronate due to GI adverse events and the total probability of any GI events was stated as 1 %. For zoledronic acid, the authors state that there was no reporting of specific outcomes such as upper GI events or esophageal events, yet cite a probability of any GI event of more than 90 % with discontinuation in 14 %. At any rate, we are left with the impression that the included studies had extreme heterogeneity in their reporting of adverse events and that this may have led to a biased estimate favouring older studies. As a test of this, the authors could have compared the total AE event rate between the placebo groups in the trials. An unforeseen consequence of the conclusions of the study could be a shift away from zoledronic acid, which is now available as a cheaper generic preparation in many countries, to denosumab which remains on patent. Pending a more transparent and robust analysis, we are not persuaded that GI adverse events are more likely with zoledronic acid than with oral bisphosphonates. In reference to adherence, it is surprising the way the authors interpreted their findings when they concluded that annual administration of zoledronic acid may not improve adherence.

Inhibition of bone resorption by the cathepsin K inhibitor odanacatib is fully reversible

The cathepsin K (CatK) inhibitor odanacatib (ODN) is currently being developed for the treatment of osteoporosis. In clinical trials, efficacy and resolution of effect of ODN treatment on bone turnover biomarkers and accrued bone mass have been demonstrated. Here, we examine the effects of continuing treatment and discontinuation of ODN versus alendronate (ALN) on osteoclast (OC) function. First, accessibility and reversible engagement of active CatK in intracellular vesicles and resorption lacunae of actively resorbing OCs were demonstrated by the selective and reversible CatK inhibitors, BODIPY-L-226 (IC50=39nM) and L-873,724 (IC50=0.5nM). Next, mature human OCs on bone slices were treated with vehicle, ODN, or ALN for 2days, followed by either continuing with the same treatment, or replacement of the inhibitors by vehicle for additional times as specified per experimental conditions. Maintaining OCs on ODN or ALN significantly reduced CTx-I release compared to vehicle controls. However, only the treatment of OCs with ODN resulted in the formation of small shallow discrete resorption pits, retention of intracellular vesicles enriched with CatK and other lysosomal enzymes, increase in 1-CTP release and number of TRAP(+) OCs. Upon discontinuation of ODN treatment, OCs rapidly resumed bone resorption activity, as demonstrated by a return of OC functional markers (CTx-I, 1-CTP), cell number and size, morphology and number of resorption pits, and vesicular secretion of CatK toward the respective vehicle levels. As expected, discontinuation of ALN did not reverse the treatment-related inhibition of OC activity in the time frame of the experiment. In summary, this study demonstrated rapid kinetics of inhibition and reversibility of the effects of ODN on OC bone resorption, that differentiated the cellular mechanism of CatK inhibition from that of the bisphosphate antiresorptive ALN.

Predicting Fracture Risk After Alendronate Discontinuation

Because the balance between potential benefits and risks of bisphosphonates becomes less clear after extended use, some authorities recommend interrupting bisphosphonate therapy after about 5 years. However, the best way to follow patients who discontinue these drugs is unknown. In this post hoc analysis, investigators examined fracture data from the Fracture Intervention Trial Long-Term Extension Trial in which …

Do atypical femoral fractures in patients with prolonged alendronate treatment heal?

Osteoporosis, which is a major health problem, may have an adverse impact on the economic status of the society and the quality of the life of the patients. Long-term alendronate use may cause an increased susceptibility to fractures with an increased risk of delayed union. In this article, we describe two patients on long-term alendronate therapy which were treated for atypical femoral fractures healed with surgical treatment plus calcium, vitamin D support, and alendronate discontinuation.

Osteonecrose mandibular associada ao uso de bisfosfonato de sódio em paciente com mieloma múltiplo

Bisphosphonates reduce skeletal complications, thus improving the quality of life in patients who suffer from multiple myeloma. Bisphosphonate‐related osteonecrosis of the jaw (BRONJ) has become one of the most prominent enigmas in the medical community since 2003. This work reports a case of jaw osteonecrosis resulting from long‐term use of alendronate with a history of inadvertent dental extractions. Facial bone computed tomography of the patient showed an osteolytic area and changes in soft tissue adjacent to the mandible bone. After surgical debridement, antibiotic treatment, and discontinuation of alendronate, the patient has successfully recovered. In conclusion, the authors recommend these patients should be instructed as to prevent this disease prior to bisphosphonates treatment, and they should also do a dental check‐up, since osteonecrosis prevention is the best way to manage this complication.

199. Alendronate Discontinuation in Postmenopausal Women Treated for Osteoporosis

199. Alendronate Discontinuation in Postmenopausal Women Treated for Osteoporosis

Discontinuation of alendronate and administration of bone-forming agents after surgical nailing may promote union of atypical femoral fractures in patients on long-term alendronate therapy

BackgroundLong-term alendronate therapy may lead to atypical femoral fractures in a very few patients. However, the management protocol to optimize fracture healing remains undetermined. The purpose of this study was to describe the time to union of atypical femoral fractures after surgical nailing in patients on long-term alendronate therapy, with continuation of alendronate or discontinuation of alendronate, and administration of bone-forming agents.FindingsFrom January 2004 to December 2011, the records of patients at our institution on long-term alendronate therapy for more than 36 months and sustaining atypical femoral fractures that had undergone surgical nailing, with continuation of alendronate or discontinuation of alendronate and administration of bone-forming agents were reviewed.During the 8-year study period, we treated 10 atypical femoral fractures with surgical nailing in 7 consecutive osteopenic or osteoporotic patients on long-term alendronate therapy for more than 36 months. There were no post-operative complications or needs for revision surgery. All fractures achieved union during follow-up. Mean union time was 23.5 months (range, 18–31 months) for 6 fractures with continuation of alendronate after surgery, and 4.5 months (range, 4–5 months) for 4 fractures with discontinuation of alendronate and administration of bone-forming agents after surgery.ConclusionsDiscontinuation of alendronate and administration of bone-forming agents after surgical nailing may promote union of atypical femoral fractures in patients on long-term alendronate therapy.

Successful teriparatide treatment of atypical fracture after long-term use of alendronate without surgical procedure in a postmenopausal woman

Bisphosphonates are used as first-line therapy for postmenopausal osteoporosis owing to their potent inhibition of bone resorption. Long-term use of bisphosphonates may lead to low-energy femoral subtrochanteric or shaft fractures in a very few patients. The aim of this study was to describe the clinical course of a patient treated with alendronate for 3 years who developed an atypical femoral fracture and to hypothesize the beneficial effects of teriparatide on the healing of the patient's atypical femoral fracture. A 63-year-old Asian woman had a lumbar osteoporotic fracture and received 70 mg of alendronate for 3 years. Pain and soreness in the thigh presented initially and exacerbated thereafter. X-ray revealed a right femoral diaphysis stress fracture. She then received teriparatide for the treatment of osteoporosis and the femoral atypical fracture. Pain and tenderness improved remarkably after teriparatide treatment for 1 month, and these symptoms disappeared after teriparatide treatment for 9 months. The patient also received raloxifen as further therapy, and the fracture line had completely disappeared by 15 months after treatment. Even though a previous study has reported that teriparatide healed stress fractures in a rat model and even with the time course of fracture healing in our patient, we are still not certain that teriparatide played a primary role in the positive response to therapy. Vitamin D therapy, calcium, and alendronate discontinuation may have played secondary roles. This case report may serve to introduce a direction for future research into the pharmacological treatment of atypical femoral fractures. Surgical treatment of incomplete atypical femoral fractures may be a safer method.