Publications by authors named "Valeria Frighi"

4 Publications

  • Page 1 of 1

Vitamin D deficiency in patients with intellectual disabilities: prevalence, risk factors and management strategies.

Br J Psychiatry 2014 Dec 25;205(6):458-64. Epub 2014 Sep 25.

Valeria Frighi, MD, Department of Psychiatry, University of Oxford and Oxfordshire Learning Disability NHS Trust (now Southern Health NHS Foundation Trust), Oxford; Alireza Morovat, PhD, FRCPath, Department of Clinical Biochemistry, Oxford University Hospitals NHS Trust, Oxford; Matthew T. Stephenson, FRCPsych, MSysPsych, Oxfordshire Learning Disability NHS Trust (now Southern Health NHS Foundation Trust), Oxford; Sarah J. White, RGN, Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford; Christina V. Hammond, BSc, Guy M. Goodwin, Dphil, FRCPsych, FMedSci, Department of Psychiatry, University of Oxford, Oxford, UK.

Background: People with intellectual disabilities have a high risk of osteoporosis and fractures, which could partly be as a result of vitamin D deficiency.

Aims: To compare the serum vitamin D (25(OH)D) levels of 155 patients with intellectual disabilities under psychiatric care and 192 controls, investigate potential risk factors for vitamin D deficiency in people with intellectual disabilities and assess available treatments.

Method: Cross-sectional observational study followed by treatment evaluation. Results Almost twice as many patients with intellectual disabilities had vitamin D deficiency (25(OH)D <50 nmol/l) compared with controls (77.3% v. 39.6%, P<0.0001). In the intellectual disabilities group, winter season (P<0.0001), dark skin pigmentation (P<0.0001), impaired mobility (P = 0.002) and obesity (P = 0.001) were independently associated with lower serum 25(OH)D. In most patients, 800 IU colecalciferol daily normalised 25(OH)D levels.

Conclusions: Vitamin D deficiency is highly prevalent in people with intellectual disabilities, partly because of insufficient exposure to sunlight. Screening and treatment strategies, aiming to reduce these patients' high fracture risk, should be introduced. Similar strategies may be required in other psychiatric populations at risk for fractures and with a tendency to spend excessive time indoors.
View Article and Find Full Text PDF

Download full-text PDF

Source Listing
December 2014

Safety of antipsychotics in people with intellectual disability.

Br J Psychiatry 2011 Oct;199(4):289-95

Department of Psychiatry, University of Oxford and Ridgeway Partnership (Oxfordshire Learning Disability NHS Trust), Oxford, UK.

Background: Despite frequent use, little is known about the metabolic and endocrine side-effects of antipsychotics in individuals with intellectual disability.

Aims: To compare indices of obesity, glucose, lipids and prolactin between antipsychotic-treated and antipsychotic-naive individuals with intellectual disability and also between participants with intellectual disability and controls from the general population.

Method: Observational study comparing 138 antipsychotic-treated and 64 antipsychotic-naive participants with intellectual disability in one National Health Service trust with general population controls.

Results: Antipsychotic treatment comprised: risperidone 48%,olanzapine 18%, thioxanthenes 10%, other 24%; monotherapy 95% of participants; mean treatment duration 8 years;median daily chlorpromazine equivalent dose 108 mg(range 16–667). Metabolic indices were the same or more favourable in the intellectual disability group than the general population control group but overweight/obesity and type 2 diabetes were more prevalent in the women in the intellectual disability group than the control group. Metabolic indices were similar, statistically or clinically, between the antipsychotic-treated and the antipsychotic-naive groups but there was a non-significant trend towards a higher rate of type 2 diabetes in the antipsychotic group. A total of 100%and 70% of participants on amisulpride/sulpiride and risperidone respectively had hyperprolactinaemia, with secondary hypogonadism in 77% and 4% of affected women and men.

Conclusions: Antipsychotics, on average, did not increase metabolic risk,although the existence of a susceptible subgroup at risk of diabetes cannot be excluded. Some antipsychotics induced hyperprolactinaemic hypogonadism, requiring active management. However, our findings suggest that antipsychotics at the low doses routinely prescribed for people with intellectual disability are generally safe in relation to metabolic adverse effects, even if efficacy remains poorly defined.
View Article and Find Full Text PDF

Download full-text PDF

Source Listing
October 2011

First United Kingdom Heart and Renal Protection (UK-HARP-I) study: biochemical efficacy and safety of simvastatin and safety of low-dose aspirin in chronic kidney disease.

Am J Kidney Dis 2005 Mar;45(3):473-84

Clinical Trial Service Unit, Oxford University, Oxford, UK.

Background: Patients with chronic kidney disease are at increased risk for cardiovascular disease, but the efficacy and safety of simvastatin and aspirin are unknown in this patient group.

Methods: Patients were randomly assigned in a 2 x 2 factorial design to the administration of: (1) 20 mg of simvastatin daily versus matching placebo, and (2) 100 mg of modified-release aspirin daily versus matching placebo.

Results: Overall, 448 patients with chronic kidney disease were randomly assigned (242 predialysis patients with a creatinine level > or = 1.7 mg/dL [> or =150 micromol/L], 73 patients on dialysis therapy, and 133 patients with a functioning transplant). Compliance with study treatments was 80% at 12 months. Allocation to treatment with 100 mg of aspirin daily was not associated with an excess of major bleeds (aspirin, 4 of 225 patients [2%] versus placebo, 6 of 223 patients [3%]; P = not significant [NS]), although there was a 3-fold excess of minor bleeds (34 of 225 [15%] versus 12 of 223 patients [5%]; P = 0.001). Among those with predialysis renal failure or a functioning transplant at baseline, aspirin did not increase the number of patients who progressed to dialysis therapy (7 of 187 [4%] versus 6 of 188 patients [3%]; P = NS) or experienced a greater than 20% increase in creatinine level (63 of 187 patients [34%] versus 56 of 188 patients [30%]; P = NS). After 12 months of follow-up, allocation to 20 mg of simvastatin daily reduced nonfasting total cholesterol levels by 18% (simvastatin, 163 mg/dL [4.22 mmol/L] versus placebo, 196 mg/dL [5.08 mmol/L]; P < 0.0001), directly measured low-density lipoprotein cholesterol levels by 24% (89 mg/dL [2.31 mmol/L] versus 114 mg/dL [2.96 mmol/L]; P < 0.0001), and triglyceride levels by 13% (166 mg/dL [1.87 mmol/L] versus 186 mg/dL [2.10 mmol/L]; P < 0.01), but there was no significant effect on high-density lipoprotein cholesterol levels (2% increase; P = NS). Allocation to simvastatin therapy was not associated with excess risk for abnormal liver function test results or elevated creatine kinase levels.

Conclusion: During a 1-year treatment period, simvastatin, 20 mg/d, produced a sustained reduction of approximately one quarter in low-density lipoprotein cholesterol levels, with no evidence of toxicity, and aspirin, 100 mg/d, did not substantially increase the risk for a major bleeding episode. Much larger trials are now needed to assess whether these treatments can prevent vascular events.
View Article and Find Full Text PDF

Download full-text PDF

Source Listing
March 2005