Depressive and anxiety disorders appear during the transplant process due to psychological stressors, medications and physiological disturbances Treatment is necessary to prevent impact on patient compliance, morbidity and mortality Psychotropic medications provide an effective option, although most are only available as oral formulations Because of this, they are more susceptible to alterations in pharmacokinetic behaviour arising from organ dysfunction in the pretransplant period Kinetics are also an issue when considering potential drug-drug interactions before and after transplantation Prior to transplant, organ dysfunction can change the pharmacokinetic behaviour of some psychotropic agents, requiring adjustment of dosage and schedules Thoracic or abdominal organ failure may reduce drug absorption through disturbances in intestinal motility, perfusion and function Cirrhotic patients experience increased drug bioavailability due to portosystemic shunting, and thus dosage is adjusted downward In contrast, dosage needs to be raised when peripheral oedema expands the drug distribution volume for hydrophilic and protein-bound agents Drug clearance for most psychotropic medications is dependent upon hepatic metabolism, which is often disrupted by endstage organ disease Selection of drugs or their dosage may need to be adjusted to lower the risk of drug accumulation Further adjustments in dosage may be called for when renal failure accompanies thoracic or abdominal organ failure, resulting in further impairment of clearance Studies regarding the treatment of anxiety and depressive disorders in the medically ill are limited in number, but recommendations are possible by review of clinical and pharmacokinetic data Selective serotonin reuptake inhibitors are well tolerated and efficacious for depression, panic disorder and post-traumatic stress disorder Adjustments in dosage are required when renal or hepatic impairment is present Among them, Citalopram and escitalopram appear to have the least risk of drug-drug interactions Paroxetine has demonstrated evidence supporting its use with generalised anxiety disorder Venlafaxine is an alternative option, beneficial in depression, post-traumatic stress and generalised anxiety disorders Nefazodone may also be considered, but there is some risk of hepatotoxicity and interactions with immunosuppressant drugs Mirtazapine still needs to be studied further in anxiety disorders, but can be helpful for depression accompanied by anorexia and insomnia Bupropion is effective in the treatment of depression, but data are sparse about its use in anxiety disorders Psychostimulants are a unique approach if rapid onset of antidepressant action is desired Acute or short-term anxiolysis is obtained with benzodiazepines, and selection of particular agents entails consideration of distribution rate, half-life and metabolic route

Treatment of anxiety and depression in transplant patients: Pharmacokinetic considerations

Prediction of drug clearance in liver cirrhosis patients is currently based on in vitro–in vivo extrapolation and physiologically-based pharmacokinetic models. No static model for this purpose has been described. The objectives of this study were to (1) derive a static model for predicting drug exposure in cirrhotic patients, and (2) to evaluate the model on a large set of published data. The impact of cirrhosis was characterized by the ratio of the total and unbound drug area under the concentration–time curve (AUC) in cirrhotic patients to the AUC measured in healthy subjects These ratios were predicted for Child–Pugh classes A, B, and C. The AUC ratios observed in published data were compared with AUC ratios predicted by the model. Among 171 drugs examined, 83 published AUC ratios for 45 drugs in cirrhotic patients were available for analysis. The mean ± standard deviation relative prediction error for the total and unbound AUC ratios was 0.22 ± 0.58 and 0.24 ± 0.56, respectively. There were four outliers among the 83 predicted values. Simulations showed that the prediction error was negligible provided that the hepatic extraction coefficient was less than 0.8. For mild and moderate cirrhosis (classes A and B), the predicted unbound AUC ratio is typically approximately 2 and 3.5, respectively, for most drugs. In the absence of data in cirrhotic patients, the drug dose might be empirically reduced by these factors. In severe cirrhosis (class C), our model may help clinicians to adjust their prescriptions.

A Prediction Model of Drug Exposure in Cirrhotic Patients According to Child-Pugh Classification.

Psychotropic drugs often need to be prescribed to patients who also have pre-existing gastrointestinal (GI) and/or hepatic disease. This paper addresses the effect of GI and hepatic disease on the pharmacokinetics of psychotropic drugs, the effect of psychotropic drugs on pre-existing GI and hepatic diseases, the adverse GI and hepatic effects of psychotropic medications, the effects of GI medications on mental status, and the potential drug interactions between commonly prescribed GI medications and psychotropic drugs. Drug selection and dosage modification based on these considerations should allow safe and effective psychotropic treatment for patients with pre-existing GI and/or hepatic disease.

Psychopharmacology in patients with hepatic and gastrointestinal disease.

Fiedler, K., and K. Simons (1992) Protein sorting and detergent-insoluble complexes in MDCK cells. American Society for Cell Biology, Denver, Colorado, U.S.A. November 1992. Mol. Biol. of the Cell 3, supplement p308. Fiedler, K., Kellner, R., Dupree, P., Etzold, T., and K. Simons (1993) VIP36, a novel component of TGN-derived exocytic carrier vesicles and glycolipid-enriched rafts in MDCK cells. American Society for Cell Biology, New Orleans, U.S.A. December 1993. Mol. Biol. of the Cell 4, supplement p209.

https://edoc.unibas.ch/28421/1/Dissertation_Yves_J__Gschwind_print_20130428.pdf

Inauguraldissertation zur Erlangung der Würde eines Doktors der Philosophie vorgelegt der

Buspirone in the Treatment of Anxiety Disorders

The pharmacokinetics of a single oral dose of buspirone (20 mg) were determined in 12 patients with cirrhosis and 12 normal subjects. The mean AUC of buspirone was 55 +/- 38 s.d. ng ml-1 h in cirrhotics and 3.5 +/- 2.4 s.d. ng ml-1 h in normals. The time until maximum concentration (tmax) attained was similar in the two groups (0.6 vs 0.7 h), but mean maximum concentration Cmax was higher in patients (18.8 +/- 16.3 s.d. ng ml-1) than in normals (1.2 +/- 0.8 s.d. ng ml-1). Mean elimination half-life of buspirone was greater in cirrhotics, but this difference was marginally significant statistically (cirrhotics, 6.1 +/- 3.5 s.d. h, normals 3.2 +/- 1.5 s.d. h, P = 0.05). Eight of 12 patients and seven of 12 normal subjects had a second peak in the plasma concentrations of buspirone. In patients this occurred at 10.8 +/- 7.4 s.d. h after the dose, and its mean concentration was 3.1 +/- 6.6 ng ml-1. In normal subjects the second peak occurred at 4.3 +/- 2.1 h after the dose and its mean concentration was 0.5 +/- 0.3 ng ml-1. On the kinetic evidence buspirone should be used with caution in liver disease.

/pdf/buspirone-pharmacokinetics-in-patients-with-cirrhosis-33xye3zitj.pdf

Buspirone pharmacokinetics in patients with cirrhosis.

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Buspirone pharmacokinetics in patients with cirrhosis.