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References

Depression and anxiety disorders CHAPTER 3 References

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422 The Maudsley® Prescribing Guidelines in Psychiatry CHAPTER 3 42. Kukreti P, et  al. Rising trend of use of antidepressants induced non-­ puerperal lactation: a case report. J Clin Diagn Res 2016; 10:Vd01–Vd02. 43. Arslan FC, et al. Trazodone induced galactorrhea: a case report. Gen Hosp Psychiatry 2015; 37:373.e1–2. 44. Centner S, et al. Amitriptyline-­induced hyperprolactinemia in a pediatric patient. Cureus 2024; 16:e59604. 45. Mahableshwarkar AR, et al. A randomized, double-­blind, fixed-­dose study comparing the efficacy and tolerability of vortioxetine 2.5 and 10 mg in acute treatment of adults with generalized anxiety disorder. Hum Psychopharmacol 2014; 29:64–72. 46. Verma A, et al. Risks associated with vortioxetine in the established therapeutic indication. Curr Neuropharmacol 2020; 19:711–717.

Depression and anxiety disorders CHAPTER 3 Table 3.16  Effect of antidepressants on glucose homeostasis and weight. Antidepressant class Effect on glucose homeostasis SSRIs7–19 ■ ■Studies indicate that SSRIs have a favourable effect on diabetic parameters in patients with type II diabetes. Insulin requirements may be decreased. ■ ■Fluoxetine has been associated with improvement in HbA1c levels, reduced insulin requirements, weight loss and enhanced insulin sensitivity. Its effect on insulin sensitivity is independent of its effect on weight loss. Sertraline may also reduce HbA1c. ■ ■Escitalopram also seems to improve glycaemic control ■ ■Some evidence that long-term SSRIs may increase the risk of diabetes in general20 and gestational diabetes in particular21 but there is also evidence of no effect either way22 TCAs13,14,23–25 ■ ■TCAs are associated with increased appetite, weight gain and hyperglycaemia ■ ■Nortriptyline improved depression but worsened glycaemic control in diabetic patients in one study. Overall improvement in depression had a beneficial effect on HbA1c. Clomipramine reported to precipitate diabetes. ■ ■Long-term use of TCAs seems to increase risk of diabetes4 MAOIs26,27 ■ ■Irreversible MAOIs have a tendency to cause extreme hypoglycaemic episodes and weight gain ■ ■No known effects with moclobemide SNRIs24,28,29 ■ ■SNRIs do not appear to disrupt glycaemic control and have minimal impact on weight ■ ■Studies of duloxetine in the treatment of diabetic neuropathy show that it has little influence on glycaemic control. No data in depression and diabetes. ■ ■Limited data on venlafaxine but may slightly increase risk of incident diabetes20 ■ ■One report of hyperglycaemia with desvenlafaxine30 Mirtazapine31,32 ■ ■Mirtazapine does not appear to impair glucose tolerance in non-­diabetic depressed patients ■ ■Improvement in HbA1c was seen with short-term use but HbA1c worsened during a 1-­year follow-­up ■ ■Mirtazapine was associated with an increase in body mass index in patients with diabetes both in the short and long term Antidepressants and diabetes mellitus Depression and diabetes Prevalence rates of depression are high in both type I (22%) and type II (19%) diabetes.1 Comorbid depression in type II diabetes is associated with poorer glycaemic control, increased hospital admissions, increased diabetic complications and poorer compliance to diabetes treatments and dietary recommendations.1 The presence of depression has a negative impact on metabolic control and poor metabolic control may worsen depression.2 Considering all of this, the treatment of comorbid depression in patients with diabetes is of vital importance and drug choice should take into account likely effects on metabolic control (Table 3.16). In 2012, Cochrane3 concluded that antidepressants are effective in diabetes and moderately improve glycaemic control. In contrast, there is some evidence that the association between diabetes and depression is in part a reflection of the use of antidepressants. That is, antidepressants as a group may cause diabetes,4,5 although the association may not be present after adjusting for comorbidity.6 Evidence relating to individual drugs is described in Table 3.16. (Continued)

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