Use of escitalopram in a patient with secondary depression

Abstracts

As depressões secundárias freqüentemente remetem o psiquiatra a dificuldades maiores no tratamento do paciente, visto ser necessário uma abordagem mais ampla do caso para que a terapêutica alcance o efeito esperado sem piorar as doenças de base e sem interagir com outros medicamentos prescritos. Este artigo ilustra o caso de paciente com diabetes tipo II e hepatite C que, após fazer uso do interferon, apresentou sintomas depressivos. Estes só melhoraram, após diversas intervenções terapêuticas, com o uso do escitalopram. Também são discutidas as dificuldades no diagnóstico e tratamento da depressão e comorbidades psiquiátricas e clínicas de evolução crônica.

Depressão; diabetes; hepatite C; eletroconvulsoterapia; escitalopram; depressão secundária

CASE REPORT

Use of escitalopram in a patient with secondary depression

Uso de escitalopram en paciente con depresión secundaria

Fabiano Coelho Horimoto^I; Danusa Céspedes Guizzo Ayache^I; Juberty Antônio de Souza^II

^IProfessor of Psychiatry, Department of Medical Practice, UFMS, Campo Grande, MS, Brazil

^IIAssistant Professor of Psychiatry, Department of Medical Practice, UFMS, Campo Grande, MS, Brazil. Master's Degree in Community Health, UFMS, Campo Grande, MS, Brazil

^{Correspondence}

ABSTRACT

Treatment of secondary depression frequently involves a higher degree of difficulty. Such cases require a broader approach, so that the therapy may reach the expected effect without worsening the underlying diseases and without interacting with other prescribed drugs. This article describes the case of a patient with type II diabetes and hepatitis C who presented depressive symptoms after using interferon. Several drugs were tested, but symptoms only improved with the use of escitalopran. The authors also discuss the difficulty faced in the diagnosis and treatment of depression and psychiatric co-morbidities associated with the chronic illnesses presented by the patient.

Keywords: Depression, diabetes, hepatitis C, escitalopran, electroconvulsotherapy, secondary depression.

RESUMEN

Las depresiones secundarias frecuentemente remiten el psiquiatra a dificultades mayores en el tratamiento del paciente, una vez que es necesario un planteo más amplio del caso para que la terapéutica logre el efecto esperado sin empeorar las enfermedades de base y sin interactuar con otros medicamentos prescritos. Este artículo ilustra el caso de un paciente con diabetes de tipo II y hepatitis C que, después de utilizar el interferón, presentó síntomas depresivos. Éstos solo mejoraron después de diversas intervenciones terapéuticas, con el uso del escitalopram. También se discuten las dificultades en el diagnóstico y tratamiento de la depresión y comorbilidades psiquiátricas y clínicas de evolución crónica.

Palabras clave: Depresión, diabetes, hepatitis C, electroconvulsoterapia, escitalopram, depresión secundaria.

INTRODUCTION

Secondary depression is the result of a physical disease or the use of some type of drug, with a direct relationship of cause and effect between the event and the appearance of depression. According to Botega et al.,¹ associations with other clinical conditions, may take place through a variety of different modalities: adjustment disorder with depressed mood, secondary depression or drug-induced depressive disorder among others. Since many of the symptoms resulting from the clinical condition² are superimposed on the depressive symptoms, assessment of the depressive disorder is more complex.

In response to this, in 1983, Zigmond & Snaith³ developed the Hospital Anxiety and Depression Scale (HAD). A Portuguese version of this scale was validated by Botega et al.⁴ and, for each of its subscales a score of more than 7 suggests the presence of depressive and anxious states.⁵

Chronic diseases, such as diabetes⁶ and hepatitis C,⁷ are often associated with the psychiatric conditions, in particular with depression. There is a greater prevalence of depression among diabetics,⁸ for instance, when compared with the general population, and patients suffering from this comorbidity control their clinical disease less effectively and, consequently, have increased morbidity and mortality.

In hepatitis C, in addition to its chronic character and variable prognosis, treatment with interferon-alpha^1,9 has been described in the literature as capable of causing depression, in addition to other side effects such as fever, general feelings of unwellness and prostration, which greatly limit the patient's activities. Furthermore, according to Dwight et al.⁷ there are reports that document the presence of fatigue and depression with chronic hepatitis C virus (HCV) infections in addition to cognitive impairment.

The objective of this article is to illustrate the difficulties of depression diagnosis/treatment in the face of concomitant diseases such as diabetes and hepatitis C. These can trigger depressive disorders, which can equally be caused by the primary pathology or by its treatment, as is the case with interferon therapy.

CASE DESCRIPTION

A fifty-year old male patient, married, the manager of a transport business was first seen in December of 2001 when he was hospitalized due to diabetic decompensation, with glycemia at 486 mg/dl. The interdisciplinary referral had been made as a result of "depressive symptoms and apathy + mental confusion". The patient presented both diabetes type II and hepatitis C, diagnosed in 1996. He was using oral hypoglycemics and interferon-alpha (this last since November of 2000). At the initial evaluation the patient presented with impaired consciousness and found it difficult to supply information which had to be provided by his wife. She stated that 6 months before the patient had fallen back into an old habit of abusive alcohol use, drinking every day after work and arriving home inebriated, in addition to taking his medication irregularly, with the exception of the interferon. She also explained that the patient was dissatisfied with his own performance at work and was highly anxious.

Due to the presence of delirium we chose not to prescribe psychotropics. After 3 days the clinical status had improved. At the re-evaluation the patient complained of a depressed mood that had lasted for 1 year, since the start of interferon. Previously he used to be more motivated, could work normally and did not present depressive symptoms. Once on the medication he felt unmotivated, had problems working with loss of memory and concentration. Furthermore, on the days on which interferon was taken he had fever, fatigue and felt unwell. He had never had any previous hypomanic/maniac symptoms. He said that the only case of mental illness in his family was his brother, an alcoholic.

We started him on 25 mg of nortriptyline at night; the patient was discharged after 7 days on 75 mg of the tricyclic and 1 mg lorazepam at night. At the follow-up, 1 week later, the dose was increased to 125 mg. There was improved sleep, but the patient was still depressed.

On the day 24 of December 2001, three weeks after the beginning of the treatment, his family telephoned because the patient had left the house and returned inebriated and hostile (in Brazil the 24^th of December is "Christmas Day" and is more important than the 25^th). He was hospitalized and, on the next day, said he was feeling guilty for everything and that his depression was more intense. He described having first used alcohol at 20 years of age to reduce anxiety, particularly in social situations. When he was 45 years old, in 1996, he confirmed his diagnoses of hepatitis and diabetes, becoming depressed for a number of weeks. He did not seek treatment for the depression which resolved spontaneously. From 1996 to 2000 he did not exhibit further depressive symptoms — these had onset after the interferon was introduced.

We increased the nortriptyline to 175 mg/day and, after the tricyclic had been used for 66 days the medication was suspended due to little observed improvement. It was substituted by sertraline and the dose increased to 200 mg/day. After 2 months' treatment, due to the low level of response, the antidepressant was suspended. In May of 2002, the patient was evaluated by a neurologist, who requested a cranial tomography. This exam showed discrete frontotemporal atrophy and a functional test (scintigraphy) found frontal hypoperfusion.

We prescribed electroconvulsive therapy (ECT) and, after three sessions, the procedure was suspended due to increased arterial pressure (PA) during the 3^rd session (PA: 240 x 140 mmHg). Next we prescribed citalopram (July 2002) up to 60 mg/day, with little improvement in terms of mood volition or anxiety. The patient continued to suffer cognitive deficit that he had exhibited previous to the ECT.

In March 2003, we applied the Hospital Anxiety and Depression Scale (HAD),⁴ scoring 15 points for anxiety and 15 for depression, and changed the antidepressants for escitalopram at a dosage of 15 mg/day. After 1 week, amitriptyline was introduced at 25 mg/night, because the patient was experiencing insomniac problems. After 2 months' treatment, mood and general disposition had improved and the patient began again to perform activities such walking and controlling his diet, although the cognitive abnormalities persisted. When a HAD re-evaluation was made after 60 days, scores were 8 for anxiety and 9 for depression.

In March 2004, the test was once more applied, returning scores of 6 and 9, respectively. After this consultation, we chose to increase the escitalopram to 20 mg/day, due to the presence of residual symptoms of depression. Glycemia was controlled, and the interferon was being used for lesser periods.

Mood and general disposition reached a level that was considered acceptable by the patient and his relatives, something that "had not occurred for several years", as his wife described it.

DISCUSSION

In addition to the secondary depression, we would stress that an association with other psychiatric comorbidities, such as anxiety disorders and alcoholism,² is very common, complicating treatment and resulting in greater chances of relapses.

The cerebral abnormalities that the patient presented may have had a correlation with his reduced volition and cognitive dysfunction. The HCV infection itself, according to some authors,⁷ can cause cognitive deficit.

Goodnick & Hernandez⁹ suggest treatment with fluoxetine, sertraline and nortriptyline for patients with diabetes, although they emphasize the possibility that nortriptyline may exacerbate the glycemia, as a result of the noradrenergic specificity of the drug and the weight gain involved.

Nortriptyline was changed for sertraline monotherapy, which has been described as effective for patients with interferon-alpha induced depression.¹⁰ Cantrell et al.¹¹ postulate that higher doses are required to achieve a response, suggesting that efficacy increases to the extent that dosage is increased up to 150-200 mg per day. The patient in question, even taking sertraline for periods and at doses considered adequate did not improve. He was started on citalopram after ECT was discontinued, which is also very effective in such cases.¹²

Several authors^13,14 describe citalopram as offering a good level of efficacy in patients with interferon induce depression: Hauser et al.¹³ reported that 11 out of 13 patients that were treated with it improved. Gleason et al.,¹⁴ in an open study, observed improvements — reductions of 50% or more in HAM-D scores after 8 weeks — in 13 of the 15 patients in their study (average dose = 26.67 mg/day). Due to the lack of treatment success with citalopram, we changed the medication for its isomer, escitalopram, despite not finding any bibliographic references (Medline) to patients with diabetes and hepatitis C being treated with the drug. By objective testing (HAD scale)^3,4 and clinical evaluations, it was observed that depressive symptomatology was reduced, leading in turn to better compliance with other treatments and a consequent global improvement in the health of the patient.

By discussing the therapies employed, including a recently released drug (escitalopram), we hope to contribute to advances in studies of treatment options in cases of severe depression or depression associated with other pathologies. Nevertheless, as this is a report on a single case we will need further studies in the future with appropriate methodological design that are capable of confirming the findings here described in order that clinicians have new treatment options made available to them.

REFERENCES

Received on September 06, 2004.

Revised on September 21, 2004.

Approved on September 27, 2004.

The present study was carried out at the Department of Medical Practice, Universidade Federal de Mato Grosso do Sul (UFMS), Campo Grande, MS, Brazil.

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Publication Dates

• Publication in this collection
  14 Sept 2005
• Date of issue
  Dec 2004

History

• Received
  06 Sept 2004
• Reviewed
  21 Sept 2004
• Accepted
  27 Sept 2004