Osteoporosis in primary biliary cholangitis

Existing Reviews

Please note, new claims can take a short while to show up.

No claims yet.

Annotation Summary

Term Occurence Count Dictionary
hyperparathyroidism 1 endocrinologydiseases
hypogonadism 1 endocrinologydiseases
metabolic bone disease 2 endocrinologydiseases
osteoporosis 49 endocrinologydiseases
raloxifene 2 endocrinologydiseasesdrugs
secondary hyperparathyroidism 1 endocrinologydiseases
calcitriol 3 endocrinologydiseasesdrugs
cholic acid 4 endocrinologydiseasesdrugs

Graph of close proximity drug and disease terms (within 200 characters).

Note: If this graph is empty, then there are no terms that meet the proximity constraint.

Review

Having read the paper, please pick a pair of statements from the paper to indicate that a drug and disease are related.

Select Drug Character Offset Drug Term Instance
calcitriol 13756 fluoride8 (fluoride)N/A+2.9 (L)10Guañabens et al[[7]], 19928 (placebo)-6.6 (L)120Calcitriol0.5 mcg/d BID calcitriol 17 (calcitriol)+0.1 (L)1N/AN/AShiomi et al[[38]], 199917 (no treatment)3-3.1 (L)1Vitamin K45 mg/d vitamin
calcitriol 13770 (fluoride)N/A+2.9 (L)10Guañabens et al[[7]], 19928 (placebo)-6.6 (L)120Calcitriol0.5 mcg/d BID calcitriol17 ( calcitriol )+0.1 (L)1N/AN/AShiomi et al[[38]], 199917 (no treatment)3-3.1 (L)1Vitamin K45 mg/d vitamin K215 (vitamin
calcitriol 15943 supplementation is generally recommended[[14],[34],[35]]. The only randomized controlled trial (RCT) looking at calcitriol supplementation did not find a significant improvement in BMD from baseline at one year, though BMD
cholic acid 24665 been shown to improve bone disease. Patients enrolled in a randomized, controlled trial of ursodeoxy cholic acid (UDCA) were followed over a 3-year period with dual-photon densitometry annually. After 3 years, there
cholic acid 24892 significant difference in lumbar BMD between UDCA and placebo[[61]].In the initial phase 3 trial of obeti cholic acid , BMD was measured at baseline and 12 mo[[62]]. BMD continued to decline in the obeticholic acid groups
cholic acid 24988 obeticholic acid, BMD was measured at baseline and 12 mo[[62]]. BMD continued to decline in the obeti cholic acid groups (both 5-10 mg and 10 mg groups), however, this decline was significantly less at the femoral
cholic acid 25244 both groups at the lumbar spine as well and, while there was a trend toward less decline in the obeti cholic acid groups, there was no significant difference[[62]]. There was no difference in fracture rates[[62]].No
raloxifene 21889 with anti-estrogen effects in the uterus and breast. A single pilot study has examined the efficacy of raloxifene in PBC. In this study, 9 women with PBC treated with raloxifene were compared to 3 age-matched controls[[56]].
raloxifene 21953 study has examined the efficacy of raloxifene in PBC. In this study, 9 women with PBC treated with raloxifene were compared to 3 age-matched controls[[56]]. After 1 year, there was a small (0.02 g/cm2vs 0.00 g/cm2)
Select Disease Character Offset Disease Term Instance
hyperparathyroidism 8783 and vitamin D deficiencies may develop in those with cholestatic liver disease leading to secondary hyperparathyroidism and increased bone resorption. Data is conflicting, however. Some studies have found decreased calcium
hypogonadism 8183 play a role in osteoporosis in PBC in certain populations such as post-menopausal women and men with hypogonadism [[5],[14],[16]]. One study showed increased osteoblast numbers and increased eroded surface area indicative
metabolic bone disease 4932 therapies for osteoporosis in PBC.The term hepatic osteodystrophy is sometimes used to refer to all metabolic bone disease seen in chronic liver disease. It refers to both osteomalacia, or decreased bone mineralization, and
metabolic bone disease 5601 loose definition of osteomalacia[[14]]. It is now widely accepted that osteoporosis is the primary metabolic bone disease in PBC[[15]] and this review will focus on the management of osteoporosis in PBC.PathogenesisThe pathogenesis
osteoporosis 1277 effective therapy is lacking. We sought to summarize our current understanding of the pathophysiology of osteoporosis in PBC, as well as current and emerging therapies in order to guide future research directions. A complete
osteoporosis 1693 by decreased bone formation, which differs from the increased bone resorption seen in postmenopausal osteoporosis . Despite this fundamental difference, current treatment recommendations are based primarily on experience
osteoporosis 1832 difference, current treatment recommendations are based primarily on experience with postmenopausal osteoporosis . Trials specific to PBC-related osteoporosis are small and have not consistently demonstrated a benefit
osteoporosis 1877 are based primarily on experience with postmenopausal osteoporosis. Trials specific to PBC-related osteoporosis are small and have not consistently demonstrated a benefit in this population. As it stands, prevention
osteoporosis 1997 small and have not consistently demonstrated a benefit in this population. As it stands, prevention of osteoporosis in PBC relies on the mitigation of risk factors such as smoking and alcohol use, as well as encouraging
osteoporosis 2212 encouraging a healthy diet and weight-bearing exercise. The primary medical intervention for the treatment of osteoporosis in PBC remains bisphosphonates though a benefit in terms of fracture reduction has never been shown.
osteoporosis 2554 therapies.Core tip: This article reviews the available literature on the pathophysiology and management of osteoporosis in primary biliary cholangitis (PBC). PBC-related osteoporosis is driven mainly by decreased bone formation
osteoporosis 2617 the pathophysiology and management of osteoporosis in primary biliary cholangitis (PBC). PBC-related osteoporosis is driven mainly by decreased bone formation as opposed to the increased bone resorption seen in postmenopausal
osteoporosis 2742 mainly by decreased bone formation as opposed to the increased bone resorption seen in postmenopausal osteoporosis . Despite this and a lack of evidence of efficacy, bisphosphonates remain the cornerstone of treatment.
osteoporosis 2958 Future attention should be given to the use of anabolic bone agents in the treatment of PBC-related osteoporosis .INTRODUCTIONPrimary biliary cholangitis (PBC) is a chronic, progressive cholestatic liver disease associated
osteoporosis 3246 of decreased bone density and strength, is a common complication of PBC[[1]-[3]]. The prevalence of osteoporosis in patients with PBC is roughly 30%[[1]-[3]] and higher in advanced stages of liver disease, up to 44%
osteoporosis 4054 therefore benefit from a timely diagnosis, effective risk factor modification, and treatment of PBC-related osteoporosis .While effective treatments exist for postmenopausal osteoporosis, management of osteoporosis in PBC
osteoporosis 4119 modification, and treatment of PBC-related osteoporosis.While effective treatments exist for postmenopausal osteoporosis , management of osteoporosis in PBC is limited by an incomplete understanding of pathophysiology specific
osteoporosis 4147 PBC-related osteoporosis.While effective treatments exist for postmenopausal osteoporosis, management of osteoporosis in PBC is limited by an incomplete understanding of pathophysiology specific to this disease process
osteoporosis 4579 women as well as alendronate based on a single RCT in PBC[[11]]. An overreliance on postmenopausal osteoporosis data may lead to relatively ineffective treatment of PBC-related osteoporosis. To this end, we aim to
osteoporosis 4657 overreliance on postmenopausal osteoporosis data may lead to relatively ineffective treatment of PBC-related osteoporosis . To this end, we aim to summarize our current understanding of the pathophysiology behind bone disease
osteoporosis 4846 pathophysiology behind bone disease in PBC as well as the evidence behind current and emerging therapies for osteoporosis in PBC.The term hepatic osteodystrophy is sometimes used to refer to all metabolic bone disease seen
osteoporosis 5056 seen in chronic liver disease. It refers to both osteomalacia, or decreased bone mineralization, and osteoporosis , or decreased bone mass, which can both be seen in advanced liver disease. Osteomalacia was once thought
osteoporosis 5573 plagued by selection bias and a loose definition of osteomalacia[[14]]. It is now widely accepted that osteoporosis is the primary metabolic bone disease in PBC[[15]] and this review will focus on the management of osteoporosis
osteoporosis 5685 is the primary metabolic bone disease in PBC[[15]] and this review will focus on the management of osteoporosis in PBC.PathogenesisThe pathogenesis of osteoporosis in PBC appears to be largely driven by decreased
osteoporosis 5737 and this review will focus on the management of osteoporosis in PBC.PathogenesisThe pathogenesis of osteoporosis in PBC appears to be largely driven by decreased bone formation, though increased bone resorption may
osteoporosis 6228 towards osteoblast dysfunction and deficient bone formation as central to the pathogenesis of PBC-related osteoporosis [[5],[16]-[18]].Osteoblast dysfunction is a multifactorial process caused both by decreased osteoblast
osteoporosis 8097 osteoblast-mediated mineralization in humans and mice[[26]].Increased bone resorption may also play a role in osteoporosis in PBC in certain populations such as post-menopausal women and men with hypogonadism[[5],[14],[16]].
osteoporosis 9459 D[[32]].Diagnosis and monitoringNo data exists as to the optimal timing of screening and monitoring for osteoporosis in PBC, however, expert opinion recommends bone densitometry be performed in all PBC patients at diagnosis[[11]].
osteoporosis 9624 densitometry be performed in all PBC patients at diagnosis[[11]]. The World Health Organization defines osteoporosis as BMD at the spine or proximal femur less than 2.5 standard deviations (SDs) below the mean of a young
osteoporosis 10581 years[[36]].MANAGEMENTPreventionGeneral measures to prevent bone loss in PBC are extrapolated from osteoporosis risk factors in the general population. Epidemiologic data suggests lifestyle factors such as tobacco
osteoporosis 11601 compared to 4[[37]].TreatmentTiming of treatment is based on recommendations from the postmenopausal osteoporosis literature[[36]]. Treatment should be initiated in all PBC patients with osteoporosis (T score < -2.5).
osteoporosis 11687 postmenopausal osteoporosis literature[[36]]. Treatment should be initiated in all PBC patients with osteoporosis (T score < -2.5). The ideal time to start treatment in those with osteopenia (T score < -1 to -2.5)
osteoporosis 11977 treatment in individuals with a prior hip or vertebral fracture or 10-year hip fracture risk ≥ 3% or osteoporosis -related fracture risk ≥ 20% based on the World Health Organization Fracture Risk Assessment Tool in
osteoporosis 14294 P: Peripheral; BMD: Bone mineral density.Figure 1Summary of prevention and treatment strategies for osteoporosis in Primary biliary cholangitis. 1Prolonged steroid use (> 3 mo), BMI < 19 kg/m2, heavy alcohol or tobacco
osteoporosis 14524 2Summary of results in comparative randomized controlled trials of different agents for treatment of osteoporosis in primary biliary cholangitisAgentTreatmentNo. of patients (n)BMD changes at 1 yr (%)BMD changes at
osteoporosis 15660 density.THERAPEUTIC OPTIONSVitamin D and calcium supplementationIn PBC patients with osteopenia or osteoporosis , vitamin D and calcium supplementation has not been shown to improve BMD or reduce fracture risk, though
osteoporosis 16494 reduce bone resorption and are effective in increasing BMD while reducing fractures in postmenopausal osteoporosis [[41]]. Their effectiveness in PBC is not as clear due to the small number of studies with small study
osteoporosis 18514 group[[45]].Ibandronate was also compared to alendronate in a more recent study of 42 post-menopausal women with PBC and osteoporosis [[46]]. In this study, women were randomized to receive IV ibandronate monthly or weekly oral alendronate.
osteoporosis 19471 none demonstrating fracture risk reduction[[6],[43],[44]]. Similarly powered trials in postmenopausal osteoporosis have shown improvement benefit in terms of both fracture reduction and BMD improvement[[47]], and the
osteoporosis 19780 strong anti-resorptive effect on bones and for a period of time were widely used in postmenopausal osteoporosis [[48]]. Concerns over worsening of cholestasis initially limited their use in PBC. However, several observational
osteoporosis 21021 side effects limit their use.CalcitoninCalcitonin has been shown to have some effect in postmenopausal osteoporosis , however, data in PBC is lacking. A crossover study of IV calcitonin for 6 mo compared to oral calcium
osteoporosis 22323 fluorideSodium fluoride increases bone formation and has been shown to be effective in postmenopausal osteoporosis , but is not as effective as anti-resorptive agents. One randomized, controlled trial examined sodium
osteoporosis 23585 BMD[[57]].Parathyroid hormoneHuman parathyroid hormone (PTH) improves BMD and reduces fractures in postmenopausal osteoporosis through stimulating bone formation, the major driver of osteoporosis in PBC[[58],[59]]. The recombinant
osteoporosis 23654 reduces fractures in postmenopausal osteoporosis through stimulating bone formation, the major driver of osteoporosis in PBC[[58],[59]]. The recombinant form consisting of the bioactive portion of the hormone (teriparatide)
osteoporosis 23817 of the bioactive portion of the hormone (teriparatide) is approved for treatment of postmenopausal osteoporosis , but has not been studied in PBC. Recombinant human PTH 1-34 (rhPTH 1-34) has been studied in rats that
osteoporosis 25545 PBC.Future therapiesConcerns over long-term efficacy and safety of bisphosphonate use in postmenopausal osteoporosis have led to ongoing development of new medications. Abaloparatide, a parathyroid hormone-related peptide
osteoporosis 25761 peptide analog, was recently approved by the Food and Drug Administration for treatment of postmenopausal osteoporosis and may avoid the pro-resorptive and hypercalcemic effects of teriparatide[[63]]. Along with teriparatide,
osteoporosis 26059 the primary deficit in PBC, as opposed to decrease resorption, the driving issue in postmenopausal osteoporosis and the current target of most treatments. Based on our understanding of the pathogenesis of osteoporosis
osteoporosis 26165 osteoporosis and the current target of most treatments. Based on our understanding of the pathogenesis of osteoporosis in PBC, future studies should include therapies that promote bone formation and ample male and premenopausal
osteoporosis 26388 female PBC patients to decrease the likelihood that results reflect only treatment of postmenopausal osteoporosis .CONCLUSIONOsteoporosis is a common complication of PBC resulting in a significantly increased risk of
osteoporosis 26899 function. Increased bone resorption may also play a role in postmenopausal women.For prevention of osteoporosis , mitigation of risk factors is recommended through smoking and alcohol cessation as well as a balanced
osteoporosis 27133 weight-bearing exercise. Treatment is recommended in patients who have experienced fractures or have osteoporosis (T score < -2.5), though may also be considered in those with a T score < -1.5 in PBC. No treatment
osteoporosis 27723 required, with special attention to anabolic bone agents, to identify effective treatment in PBC-related osteoporosis
secondary hyperparathyroidism 8773 osteopenia[[16]].Theoretically, calcium and vitamin D deficiencies may develop in those with cholestatic liver disease leading to secondary hyperparathyroidism and increased bone resorption. Data is conflicting, however. Some studies have found decreased calcium

You must be authorized to submit a review.