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We studied the risk for hip fracture before and after total knee replacement (TKR) in the entire population in Sweden. Women and men had a low risk for hip fracture before TKR but an increased risk the first year after TKR. Purpose It is known that osteoarthritis is associated with high bone mass. We therefore studied the risk of hip fracture before and after total knee replacement (TKR), risk of different hip fracture types, and risk subdivided in genders and age groups. Methods We followed the total Swedish population born between 1902 and 1952 (n = 4,258,934) during the period 1987-2002 and identified all patients with TKR due to primary OA (n = 39,291), and all patients with hip fracture (n = 195,860) in the Swedish National Inpatient Register. The risk time analyses were based on Poisson regression models. Results The hazard ratio (HR) for hip fracture the last year before TKR was 0.86 (95% CI 0.74 to 1.00) and the first year after 1.26 (95% CI 1.11 to 1.42) compared to individuals without TKR. The HR for femoral neck fracture 0-10 years after TKR was 0.95 (95% CI 0.89 to 1.01) and for trochanteric fracture was 1.13 (95% CI 1.06 to 1.21). The HR for hip fracture in the age group 50-74 was 1.28 (95% CI 1.14 to 1.43) and in the age group 75-90 years was 0.99 (95% CI 0.94 to 1.04) 0-10 years after TKR, compared to individuals without TKR. Conclusion Individuals had a low risk for hip fracture before TKR but an increased risk the first year after TKR. The risk in individuals below age 75 years and for trochanteric fractures was increased after TKR. Possible explanations include changed knee kinematics after a TKR, physical activity level, fall risk, and other unknown factors.

We studied the risk for hip fracture before and after total knee replacement (TKR) in the entire population in Sweden. Women and men had a low risk for hip fracture before TKR but an increased risk the first year after TKR. Purpose It is known that osteoarthritis is associated with high bone mass. We therefore studied the risk of hip fracture before and after total knee replacement (TKR), risk of different hip fracture types, and risk subdivided in genders and age groups. Methods We followed the total Swedish population born between 1902 and 1952 (n = 4,258,934) during the period 1987-2002 and identified all patients with TKR due to primary OA (n = 39,291), and all patients with hip fracture (n = 195,860) in the Swedish National Inpatient Register. The risk time analyses were based on Poisson regression models. Results The hazard ratio (HR) for hip fracture the last year before TKR was 0.86 (95% CI 0.74 to 1.00) and the first year after 1.26 (95% CI 1.11 to 1.42) compared to individuals without TKR. The HR for femoral neck fracture 0-10 years after TKR was 0.95 (95% CI 0.89 to 1.01) and for trochanteric fracture was 1.13 (95% CI 1.06 to 1.21). The HR for hip fracture in the age group 50-74 was 1.28 (95% CI 1.14 to 1.43) and in the age group 75-90 years was 0.99 (95% CI 0.94 to 1.04) 0-10 years after TKR, compared to individuals without TKR. Conclusion Individuals had a low risk for hip fracture before TKR but an increased risk the first year after TKR. The risk in individuals below age 75 years and for trochanteric fractures was increased after TKR. Possible explanations include changed knee kinematics after a TKR, physical activity level, fall risk, and other unknown factors.

We studied the risk for hip fracture before and after total knee replacement (TKR) in the entire population in Sweden. Women and men had a low risk for hip fracture before TKR but an increased risk the first year after TKR. Purpose It is known that osteoarthritis is associated with high bone mass. We therefore studied the risk of hip fracture before and after total knee replacement (TKR), risk of different hip fracture types, and risk subdivided in genders and age groups. Methods We followed the total Swedish population born between 1902 and 1952 (n = 4,258,934) during the period 1987-2002 and identified all patients with TKR due to primary OA (n = 39,291), and all patients with hip fracture (n = 195,860) in the Swedish National Inpatient Register. The risk time analyses were based on Poisson regression models. Results The hazard ratio (HR) for hip fracture the last year before TKR was 0.86 (95% CI 0.74 to 1.00) and the first year after 1.26 (95% CI 1.11 to 1.42) compared to individuals without TKR. The HR for femoral neck fracture 0-10 years after TKR was 0.95 (95% CI 0.89 to 1.01) and for trochanteric fracture was 1.13 (95% CI 1.06 to 1.21). The HR for hip fracture in the age group 50-74 was 1.28 (95% CI 1.14 to 1.43) and in the age group 75-90 years was 0.99 (95% CI 0.94 to 1.04) 0-10 years after TKR, compared to individuals without TKR. Conclusion Individuals had a low risk for hip fracture before TKR but an increased risk the first year after TKR. The risk in individuals below age 75 years and for trochanteric fractures was increased after TKR. Possible explanations include changed knee kinematics after a TKR, physical activity level, fall risk, and other unknown factors.

We studied the risk for hip fracture before and after total knee replacement (TKR) in the entire population in Sweden. Women and men had a low risk for hip fracture before TKR but an increased risk the first year after TKR. Purpose It is known that osteoarthritis is associated with high bone mass. We therefore studied the risk of hip fracture before and after total knee replacement (TKR), risk of different hip fracture types, and risk subdivided in genders and age groups. Methods We followed the total Swedish population born between 1902 and 1952 (n = 4,258,934) during the period 1987-2002 and identified all patients with TKR due to primary OA (n = 39,291), and all patients with hip fracture (n = 195,860) in the Swedish National Inpatient Register. The risk time analyses were based on Poisson regression models. Results The hazard ratio (HR) for hip fracture the last year before TKR was 0.86 (95% CI 0.74 to 1.00) and the first year after 1.26 (95% CI 1.11 to 1.42) compared to individuals without TKR. The HR for femoral neck fracture 0-10 years after TKR was 0.95 (95% CI 0.89 to 1.01) and for trochanteric fracture was 1.13 (95% CI 1.06 to 1.21). The HR for hip fracture in the age group 50-74 was 1.28 (95% CI 1.14 to 1.43) and in the age group 75-90 years was 0.99 (95% CI 0.94 to 1.04) 0-10 years after TKR, compared to individuals without TKR. Conclusion Individuals had a low risk for hip fracture before TKR but an increased risk the first year after TKR. The risk in individuals below age 75 years and for trochanteric fractures was increased after TKR. Possible explanations include changed knee kinematics after a TKR, physical activity level, fall risk, and other unknown factors.

We studied the risk for hip fracture before and after total knee replacement (TKR) in the entire population in Sweden. Women and men had a low risk for hip fracture before TKR but an increased risk the first year after TKR. Purpose It is known that osteoarthritis is associated with high bone mass. We therefore studied the risk of hip fracture before and after total knee replacement (TKR), risk of different hip fracture types, and risk subdivided in genders and age groups. Methods We followed the total Swedish population born between 1902 and 1952 (n = 4,258,934) during the period 1987-2002 and identified all patients with TKR due to primary OA (n = 39,291), and all patients with hip fracture (n = 195,860) in the Swedish National Inpatient Register. The risk time analyses were based on Poisson regression models. Results The hazard ratio (HR) for hip fracture the last year before TKR was 0.86 (95% CI 0.74 to 1.00) and the first year after 1.26 (95% CI 1.11 to 1.42) compared to individuals without TKR. The HR for femoral neck fracture 0-10 years after TKR was 0.95 (95% CI 0.89 to 1.01) and for trochanteric fracture was 1.13 (95% CI 1.06 to 1.21). The HR for hip fracture in the age group 50-74 was 1.28 (95% CI 1.14 to 1.43) and in the age group 75-90 years was 0.99 (95% CI 0.94 to 1.04) 0-10 years after TKR, compared to individuals without TKR. Conclusion Individuals had a low risk for hip fracture before TKR but an increased risk the first year after TKR. The risk in individuals below age 75 years and for trochanteric fractures was increased after TKR. Possible explanations include changed knee kinematics after a TKR, physical activity level, fall risk, and other unknown factors.

Context: Cerebral palsy (CP) increases fracture risk through diminished ambulation, nutritional deficiencies, and anticonvulsant medication use. Studies examining bone mineral density (BMD) in adults with CP are limited. Objective(s): To examine the relationship between body composition, BMD, and fractures in adults with CP. The effect of functional, nutritional, and endocrine factors onBMDand body composition is also explored. Design(s): Retrospective cross-sectional study. Setting and Participants: Forty-five adults with CP (mean age, 28.3 +/- 11.0 years) who had dualenergy X-ray absorptiometry imaging at a single tertiary hospital between 2005 and 2015. Result(s): Seventeen (38%) had a past history of fragility fracture; 43% had a Z-score of +/--2.0 at the lumbar spine (LS) and 41% at the femoral neck (FN). In nonambulatory patients, every one unit decrease in FN Z-score increased the risk of fracture 3.2-fold (95% confidence interval, 1.07-9.70; P =.044). Stepwise linear regression revealed that the Gross Motor Function Classification System was the best predictor of LS Z-score (R2 = 0.550;-=-0.582; P =.002) and FN Z-score (R2 = 0.428;-=-0.494; P =.004); 35.7% of the variance in BMD was accounted for by lean tissue mass. Hypogonadism, present in 20% of patients, was associated with reduced lean tissue mass and reduced LS BMD. Lean tissue mass positively correlated with BMD in eugonadal patients, but not in hypogonadal patients. Conclusion(s): Low BMD and fractures are common in adults with CP. This is the first study to document hypogonadism in adults with CP with detrimental changes in body composition and BMD.Copyright © 2016 by the Endocrine Society.

Context: Cerebral palsy (CP) increases fracture risk through diminished ambulation, nutritional deficiencies, and anticonvulsant medication use. Studies examining bone mineral density (BMD) in adults with CP are limited. Objective(s): To examine the relationship between body composition, BMD, and fractures in adults with CP. The effect of functional, nutritional, and endocrine factors onBMDand body composition is also explored. Design(s): Retrospective cross-sectional study. Setting and Participants: Forty-five adults with CP (mean age, 28.3 +/- 11.0 years) who had dualenergy X-ray absorptiometry imaging at a single tertiary hospital between 2005 and 2015. Result(s): Seventeen (38%) had a past history of fragility fracture; 43% had a Z-score of +/--2.0 at the lumbar spine (LS) and 41% at the femoral neck (FN). In nonambulatory patients, every one unit decrease in FN Z-score increased the risk of fracture 3.2-fold (95% confidence interval, 1.07-9.70; P =.044). Stepwise linear regression revealed that the Gross Motor Function Classification System was the best predictor of LS Z-score (R2 = 0.550;-=-0.582; P =.002) and FN Z-score (R2 = 0.428;-=-0.494; P =.004); 35.7% of the variance in BMD was accounted for by lean tissue mass. Hypogonadism, present in 20% of patients, was associated with reduced lean tissue mass and reduced LS BMD. Lean tissue mass positively correlated with BMD in eugonadal patients, but not in hypogonadal patients. Conclusion(s): Low BMD and fractures are common in adults with CP. This is the first study to document hypogonadism in adults with CP with detrimental changes in body composition and BMD.Copyright © 2016 by the Endocrine Society.

A 16 year old fully ambulant boy born to consanguineous Indian parents, presented with a fragility femoral neck fracture, with autism and moderately severe intellectual disability. He had a thin body habitus with long fingers and a high arched palate. He had no speech and negligible social interaction. Serum creatinine was undetectable and a urinary metabolic screen showed elevated GUA:Phe of 160 (<36) and a decreased creatinine of 0.3 mmol/l (1.2-29.5) consistent with the diagnosis of guanidinoacetate methyltransferase (GAMT) deficiency. Following oral creatine 5 g three times daily for 3 years, physical activity, height and bone density improved, with no discernable improvement in his intellectual functioning. His serum creatinine increased from undetectable to 58 mmol/l (normal range 40-100). DXA BMD pre-treatment at the lumbar spine (L1-L4)was 0.673 g/cm2 (sds-4.7) and increased to 0.982 g/cm2 (sds-1.90); total body BMD increased from 0.846 g/cm2 (sds -3.43) to 1.016 982 g/cm2 (sds -2.10). Proton and phosphorus brain and leg magnetic resonance spectroscopy (MRS) at baseline showed an increased inorganic phosphorus peak and decreased phosphocreatine synthesis in brain and decreased creatine concentration in muscle. Following creatine treatment total brain creatine (1H-MRS) and phosphocreatine/ATP ratio (31P-MRS) content increased to 30% and 60% of control values, respectively. Brain GUA normalised. Creatine deficiency syndrome is a rare disorder first described in 1994 with intellectual disability, mutism, autism, dyskinesia and epilepsy as in our patient. Osteopenia observed by us in this condition is consistent with phosphocreatine being a substrate for alkaline phosphatase, and we have shown that creatine supplementation in our patient with GAMT deficiency resulted in improved BMD with no further fragility fractures.

Case report: A 16 y.o. fully ambulant boy born to consanguineous Indian parents, presented for assessment of a fragility femoral neck fracture sustained against a background of autism and moderately severe intellectual disability. He had a past history of infantile eczema, and epilepsy treated with anticonvulsants from 2 to 10 years of age, with no further seizures following cessation of anticonvulsants. He had a thin body habitus (see Table 1) with long fingers and a high arched palate. He had no speech and negligible social interaction, but physical examination was otherwise unremarkable. Positive investigations revealed an undetectable serum creatinine and a urinary metabolic screen which showed an elevated GUA:Phe of 160 (<36) and a decreased creatinine of 0.3 mmol/l (1.2-29.5) consistent with the diagnosis of guanidinoacetate methyltransferase (GAMT) deficiency. He was commenced on oral creatine 5 g three times daily. Despite improvement in physical activity, height and bone density, there was no discernable improvement in his intellectual functioning. Proton and phosphorous brain and leg magnetic resonance spectroscopy (MRS) was performed at baseline and showed an increased inorganic phosphorus peak and decreased phosphocreatine synthesis in brain and decreased creatine concentration in muscle. Following creatine treatment total brain creatine (1H-MRS) and phosphocreatine/ATP ratio (31P-MRS) content increased to 30% and 60% of control values, respectively. Brain GUA returned to normal levels. Table 1 Clinical features Baseline After treatment Age (years) 16.25 19.4 Height - cm (%) 169 (25th) 186 (90th-97th) Weight - kg (%) 41 (3rd) 57 (10th) Lumbar spine BMD L1 - L4 g/cm2 (z score) 0.673 (-4.7) 0.982 (-1.90) Total body BMD g/cm2 (z score) 0.846 (-3.43) 1.016 (-2.10) Serum creatinine (normal 40 - 100 mmol/l) <20 58 Discussion: Creatine deficiency syndrome is a rare disorder first described in 1994 characterised by intellectual disability, mutism, autism, dyskin

A 16 year old fully ambulant boy born to consanguineous Indian parents, presented with a fragility femoral neck fracture, with autism and moderately severe intellectual disability. He had a thin body habitus with long fingers and a high arched palate. He had no speech and negligible social interaction. Serum creatinine was undetectable and a urinary metabolic screen showed elevated GUA:Phe of 160 (<36) and a decreased creatinine of 0.3 mmol/l (1.2-29.5) consistent with the diagnosis of guanidinoacetate methyltransferase (GAMT) deficiency. Following oral creatine 5 g three times daily for 3 years, physical activity, height and bone density improved, with no discernable improvement in his intellectual functioning. His serum creatinine increased from undetectable to 58 mmol/l (normal range 40-100). DXA BMD pre-treatment at the lumbar spine (L1-L4)was 0.673 g/cm2 (sds-4.7) and increased to 0.982 g/cm2 (sds-1.90); total body BMD increased from 0.846 g/cm2 (sds -3.43) to 1.016 982 g/cm2 (sds -2.10). Proton and phosphorus brain and leg magnetic resonance spectroscopy (MRS) at baseline showed an increased inorganic phosphorus peak and decreased phosphocreatine synthesis in brain and decreased creatine concentration in muscle. Following creatine treatment total brain creatine (1H-MRS) and phosphocreatine/ATP ratio (31P-MRS) content increased to 30% and 60% of control values, respectively. Brain GUA normalised. Creatine deficiency syndrome is a rare disorder first described in 1994 with intellectual disability, mutism, autism, dyskinesia and epilepsy as in our patient. Osteopenia observed by us in this condition is consistent with phosphocreatine being a substrate for alkaline phosphatase, and we have shown that creatine supplementation in our patient with GAMT deficiency resulted in improved BMD with no further fragility fractures.

Case report: A 16 y.o. fully ambulant boy born to consanguineous Indian parents, presented for assessment of a fragility femoral neck fracture sustained against a background of autism and moderately severe intellectual disability. He had a past history of infantile eczema, and epilepsy treated with anticonvulsants from 2 to 10 years of age, with no further seizures following cessation of anticonvulsants. He had a thin body habitus (see Table 1) with long fingers and a high arched palate. He had no speech and negligible social interaction, but physical examination was otherwise unremarkable. Positive investigations revealed an undetectable serum creatinine and a urinary metabolic screen which showed an elevated GUA:Phe of 160 (<36) and a decreased creatinine of 0.3 mmol/l (1.2-29.5) consistent with the diagnosis of guanidinoacetate methyltransferase (GAMT) deficiency. He was commenced on oral creatine 5 g three times daily. Despite improvement in physical activity, height and bone density, there was no discernable improvement in his intellectual functioning. Proton and phosphorous brain and leg magnetic resonance spectroscopy (MRS) was performed at baseline and showed an increased inorganic phosphorus peak and decreased phosphocreatine synthesis in brain and decreased creatine concentration in muscle. Following creatine treatment total brain creatine (1H-MRS) and phosphocreatine/ATP ratio (31P-MRS) content increased to 30% and 60% of control values, respectively. Brain GUA returned to normal levels. Table 1 Clinical features Baseline After treatment Age (years) 16.25 19.4 Height - cm (%) 169 (25th) 186 (90th-97th) Weight - kg (%) 41 (3rd) 57 (10th) Lumbar spine BMD L1 - L4 g/cm2 (z score) 0.673 (-4.7) 0.982 (-1.90) Total body BMD g/cm2 (z score) 0.846 (-3.43) 1.016 (-2.10) Serum creatinine (normal 40 - 100 mmol/l) <20 58 Discussion: Creatine deficiency syndrome is a rare disorder first described in 1994 characterised by intellectual disability, mutism, autism, dyskin