scholarly journals Effects of long-term prolactin-raising antipsychotic medication on bone mineral density in patients with schizophrenia

2004 ◽  
Vol 184 (6) ◽  
pp. 503-508 ◽  
Author(s):  
Anna Maria Meaney ◽  
Shubulade Smith ◽  
O. D. Howes ◽  
Moira O'Brien ◽  
Robin M. Murray ◽  
...  

BackgroundHigh rates of osteoporosis in schizophrenia may result from the prolactin-raising effects of some antipsychotic medication.AimsTo examine bone mineral density in relation to relevant endocrine variables in patients with schizophrenia taking prolactin-raising antipsychotics.MethodFifty-five patients who had been receiving prolactin-raising antipsychotic medication for > 10 years underwent dual-energy X-ray absorptiometry of their lumbar and hip bones. Among the endocrine variables assessed were plasma prolactin and sex hormones.ResultsAge-related reduced bone mineral density measures were found in 17 (57%) of the male and 8 (32%) of the female patients. Higher doses of medication were associated with increased rates of both hyperprolactinaemia and bone mineral density loss. Bone loss for the whole group was correlated with medication dose, and for men was inversely correlated with testosterone values.ConclusionsThese results suggestthat patients with schizophrenia on long-term prolactin-raising antipsychotic medication are at high risk of developing reduced bone mineral density as a consequence of hyperprolactinaemia-induced hypogonadism.

2014 ◽  
Vol 30 (6) ◽  
pp. 553-559 ◽  
Author(s):  
Ei Kinai ◽  
Takeshi Nishijima ◽  
Daisuke Mizushima ◽  
Koji Watanabe ◽  
Takahiro Aoki ◽  
...  

2013 ◽  
Author(s):  
C Klap B ◽  
L te Winkel M ◽  
den Hoed M ◽  
van Waas M ◽  
J C M M Neggers S ◽  
...  

2014 ◽  
Author(s):  
Maria Rodriguez-Sanz ◽  
Natalia Garcia-Giralt ◽  
Pliego Elisa Torres-del ◽  
Daniel Prieto-Alhambra ◽  
Sonia Servitja ◽  
...  

2019 ◽  
Vol 19 (3) ◽  
pp. 259-273 ◽  
Author(s):  
Neelam Kaushal ◽  
Divya Vohora ◽  
Rajinder K Jalali ◽  
Sujeet Jha

Background And Objective:Osteoporosis is a common bone disorder that increases susceptibility to fragility bone fractures. The clinical and public health repercussions of osteoporosis are huge due to the morbidity, mortality, and cost of medical care linked with fragility fractures. Clinical assessment of osteoporotic risk factors can help to identify candidates at an early stage that will benefit from medical intervention and potentially lowering the morbidity and mortality seen with fractures and complications. Given this, research is ongoing to evaluate the association of osteoporosis with some novel or less well-studied risk factors/bio-markers such as uric acid (UA).Discussion:Uric acid’s antioxidant activity has been proposed to be one of the factors responsible for increasing longevity and lowering rates of age-related cancers during primate evolution, the level of which increased markedly due to loss of uricase enzyme activity (mutational silencing). Accumulated evidence shows that oxidative stress is the fundamental mechanism of age-related bone loss and acts via enhancing osteoclastic activity and increasing bone resorption. Antioxidant substances such as ascorbic acid scavenge free radicals are positively related to bone health. Thus, it is hypothesized that uric acid holds bone-protective potential owing to its potent antioxidative property. Several correlation studies have been conducted globally to investigate the relationship between serum uric acid with bone mineral density and osteoporosis. Few pre-clinical studies have tried to investigate the interaction between uric acid and bone mineral density and reported important role played via Runt-related transcription factor 2 (RUNX2)/core-binding factor subunit alpha-1 (CBF-alpha-1), Wingless-related integration site (Wnt)-3a/β-catenin signaling pathway and 11β Hydroxysteroid Dehydrogenase type 1.Conclusion:In this review, the authors provided a comprehensive summary of the literature related to association studies reported in humans as well work done until date to understand the potential cellular and molecular mechanisms that interplay between uric acid and bone metabolism.


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