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Unlike pharmacological approaches for treating hypochondria-sis that is secondary to another condition (e.g., depression, panic disorder), pharmacological approaches for treating primary hypo-chondriasis were considered generally unsuccessful until the 1990s, when reports emerged suggesting that serotonin reuptake inhibitors (SRIs) were particularly effective (see Table 2-2).

Ms. Q, a 19-year-old college student, had experienced hypo-chondriacal symptoms since age 8, when her frequent bouts of head pain precipitated a fear that she had cancer. She made fre-

Table 2-2. Pharmacologic trials for treatment of hypochondriasis

Study

N Design

Evaluation tools Type of patient Type(s) of therapy Results

Comments

Pilowsky 66 Retrospective Clinical interview Inpatients with pri-1968 mary hypochon driasis

50% received ECT, 50% received antidepressants

50% of all patients experienced improvement at 2-year follow-up

Good outcome associated with short duration of illness and absence of personality disorder

50% of all patients experienced improvement at 2-year follow-up

Good outcome associated with short duration of illness and absence of personality disorder

Wesner and Noyes 1991

10 8-week prospective

Outpatients with DSM-III-R hypochondriasis with good insight

Imipramine (150 mg/day)

100% experienced moderate improvement

Patients with illness phobia had good insight, possibly indicating a distinct subgroup

Fallon et al.

1993

16 12-week prospective

CGI Scale, SCID, Whiteley Index

Nondepressed outpatients with DSM-III-R hypochondriasis

Fluoxetine (20-80 mg/day)

71% responded after 12 weeks

Greater response at 12 weeks than at 6 weeks suggests higher dose or longer treatment is needed

Fallon et al. 1996

12-week pro- CGI Scale, IAS, Outpatients with spective, SCID, Whiteley DSM-IV hypo-

Fluoxetine (20-80 mg/day) or placebo

Fallon et al. 1996

12-week pro- CGI Scale, IAS, Outpatients with spective, SCID, Whiteley DSM-IV hypo-

controlled

Index chondriasis

Fluoxetine (20-80 mg/day) or placebo

80% response rate for fluoxetine group after 6 and 12 weeks, 50%-60% response rate for placebo group

50% of patients treated with fluoxetine were symptom free compared with 20% of patients receiving placebo, suggesting greater efficacy for fluoxetine, but placebo effect cannot be minimized

Fallon 2001 18 10-week pro- CGI Scale, IAS, Outpatients with Fluvoxamine spective, SCID, Whiteley DSM-IV hypo- (300 mg/day)

open label Index chondriasis after a 2- week placebo run-in

73% of 11 patients who Fluvoxamine may be an ef-

completed 6 weeks fective SSRI for treatment of treatment re- of hypochondriasis sponded

Note. CGI = Clinical Global Improvement; IAS = Illness Attitude Scale; SCID = Structured Clinical Interview for DSM-IV.

quent visits to the pediatrician for evaluation, magnetic resonance imaging (MRI), computed tomography (CT), and reassurance. Ms. Q's symptoms became particularly distressing at age 18, when she developed stomach aches, which led to the fear that she had appendicitis; a skin rash, which led to the fear that she had cancer; and head pain, which led to the conviction that her death was imminent. She experienced a rapidly escalating sense of terror. No identifiable stressor was evident before Ms. Q's condition worsened. Brief psychotherapy was of little help, and her illness fears were accompanied later by depressed mood. Ms. Q was treated with an SRI, citalopram (20 mg/day). After the first few weeks of treatment, her somatic sensations and fears worsened until, one morning, she awakened to find almost complete resolution of these symptoms. This resolution was sustained during the following 6 months as Ms. Q continued to take medication. Ms. Q had no history of OCD, primary major depression, or panic disorder. She reported no childhood history of trauma, interpersonal loss, or significant illnesses in those close to her.

Therapeutic options for this young woman could have included more intensive psychodynamic psychotherapy to explore unrecognized conflicts, cognitive-behavioral therapy to address her irrational appraisal of threat from bodily symptoms, and/or phar-macotherapy to address her immediate symptoms of profound anxiety and depression. The pharmacotherapy led to a rapid improvement that was sustained over time. Further evaluation of this woman revealed a childhood characterized by considerable emotional neglect. Exploratory psychodynamic psychotherapy was recommended. Based on pharmacologic studies of depression, this woman was advised to continue taking the SRI for at least a full year.

Pharmacotherapy for Secondary Hypochondriasis

Major depression. Kellner et al. (1986a) reported that 4 weeks of treatment with amitriptyline (100-300 mg/day) was effective in reducing hypochondriacal concerns among 20 consecutive nonpsychotic inpatients with DSM-III (American Psychiatric Association 1980) melancholic major depression, one-third of whom had scores on the Illness Attitude Scale that were characteristic of patients with hypochondriasis before treatment.

Panic disorder. Noyes et al. (1986) reported that pharmacologic treatment of 60 patients with panic disorder and agoraphobia resulted in a diminution of panic attacks as well as a significant decrease in hypochondriasis, as measured by the Illness Behavior Questionnaire dimensions of disease fear, disease conviction, and bodily preoccupation.

Obsessive-compulsive disorder. Bodkin and White (1989) reported that clonazepam was very helpful in ameliorating a man's OCD symptoms and hypochondriasis about AIDS. Fallon et al. (1991) reported that fluoxetine at doses of 60 mg/day, but not 20-40 mg/day, were effective in reducing DSM-III-R hypo-chondriasis and OCD. Similar to the pharmacotherapy of OCD, this case suggested that hypochondriasis patients with a stronger obsessional component may preferentially respond to the higher doses of fluoxetine often needed to treat OCD successfully.

Delusional disorder, somatic subtype. This disorder, also known as "atypical psychosis" or "monosymptomatic hypochondriacal psychosis," refers to hypochondriasis of delusional intensity. Often the disease the patient fears he or she has is rare, such as spongiform encephalitis (mad cow disease). Case reports suggest that antipsychotic medications, such as haloperidol (Fishbain et al. 1992), pimozide (Lippert 1986; Scarone and Gambini 1991), and thioridazine (Scarone and Gambini 1991), may reduce convictions of delusional intensity to nonpsychotic proportions.

Pharmacotherapy for Primary Hypochondriasis

In a retrospective study, Pilowsky (1968) identified 66 psychiatric inpatients with primary hypochondriasis, half of whom had been given either electroconvulsive therapy or antidepressants. Half of the patients had good outcome after 2 years, with good prognosis associated with a shorter duration of hypochondriacal fears and the absence of a comorbid personality disorder.

Imipramine. Imipramine, a medication that exhibits both sero-tonergic and noradrenergic reuptake inhibition, has been reported to be effective in case reports and a small open series. In a case report, Lippert (1986) found that 150 mg/day of imipramine was helpful for a man who, for 3 months, had hypochondriasis about AIDS compounded by major depression. In a small open series, Wesner and Noyes (1991) conducted an 8-week prospective open trial of imipramine at a mean final dose of 144 mg/day and reported that all patients showed at least moderate improvement by 4 weeks, with one patient symptom free. Using the data from the Fallon et al. (1996) placebo-controlled fluoxetine study and the Wesner and Noyes data on imipramine, a comparison of virtually symptom-free patients showed the following: 50% of patients had been given fluoxetine, 20% placebo, and 12.5% imipramine. Although these results suggest a lack of effectiveness of imipramine, a direct comparison with more selective serotonin reuptake inhibitors (SSRIs) and placebo in a larger number of patients will help determine whether imipramine is effective in treating hypochondriasis.

Clomipramine. Clomipramine has been reported as being helpful in treating hypochondriasis in several case reports, at doses ranging from 25 mg/day (Kamlana and Gray 1988) to 200 mg/day (Stone 1993). In Stone's report, a 31-year-old man with a 10-year history of primary hypochondriasis did not show improvement despite many previous pharmacologic treatments, including treatment with benzodiazepines, mood stabilizers, beta-blockers, anti-psychotics, and tricyclic antidepressants.

Fluvoxamine. Fluvoxamine was reported to be effective for treating hypochondriasis in a case report and an uncontrolled open-label trial. In the case report (Fallon et al. 1996), a 38-year-old woman experienced hypochondriacal fears of breast cancer, engaged in repeated self-checking, and underwent medical evaluations for 3 years. The woman experienced no improvement with a 12-week trial of fluoxetine (80 mg/day); however, she did experience improvement after 8 weeks of treatment with fluvoxamine (300 mg/day). This progress was sustained over the ensuing 3 years. This case suggested that failure to respond to one SSRI does not preclude response to a different SSRI.

In a 10-week open-label trial of fluvoxamine with a 2-week placebo run-in (Fallon 2001), patients completed the Heightened Illness Concern Diary, measures of hypochondriasis (Analog Scale,

Whiteley Index, Illness Attitude Scale), and a measure of functional status (Medical Outcomes Study 36-Item Short-Form Health Survey [SF-36]) before treatment with fluvoxamine, which was increased gradually to 300 mg/day. In this study, 4 (22%) of 18 patients were excluded during the placebo run-in phase either because of marked improvement or noncompliance with the medication or study visits. Three patients discontinued treatment before 6 weeks. Eight (73%) of 11 patients who completed the minimum treatment of at least 6 weeks responded to treatment and 8 (57%) of 14 patients given active fluvoxamine responded. Even though these results suggest that fluvoxamine may be effective for treating hypochondriasis, the greater than 25% dropout rate in active treatment suggests that pharmaco-therapy may be less acceptable to patients than psychotherapy. This suggestion is supported by a 4.6% dropout rate reported by Clark et al. (1998) in their study of cognitive therapy and behavioral stress management therapy, as well as by Walker et al. (1999) in an opinion survey, which indicated that 17 (74%) of 23 patients with DSM-IV hypochondriasis preferred cognitive-behavioral therapy to pharmacotherapy.

Fluoxetine. Fluoxetine for the treatment of hypochondriasis has been well studied. Two separate case reports (Fallon et al. 1991; Viswanathan and Paradis 1991) suggested that fluoxetine (40-80 mg/day) is beneficial for patients with treatment-refractory hypochondriasis. Each of the patients in these case reports did not respond to previous treatments, including psychotherapy (which included behavioral therapy in one case), nonserotoner-gic antidepressants, antianxiety agents, and antipsychotic medications.

Fallon et al. (1993) reported the results of a 12-week open-label trial of fluoxetine for 16 patients with hypochondriasis without major depression, with doses starting at 20 mg/day, increasing every 2 weeks by 20 mg/day as tolerated and needed, to 80 mg/ day. Only 2 patients dropped out of the trial during the initial weeks of active medication treatment, and 14 completed all 12 weeks. Among patients who completed treatment, the response rate at 12 weeks (71.4%) was twice the rate at 6 weeks (35.7%), suggesting that longer courses of therapy might be needed for hypochondriasis. Alternatively, because the mean dose of fluoxetine was higher at 12 weeks than at 6 weeks (52 mg/day versus 39 mg/day), the critical factor may be medication dose rather than duration. Four of the patients who responded to fluoxetine were virtually symptom free at the end of treatment. Patients with primary hypochondriasis appeared to respond at a higher rate than patients with hypochondriasis complicated by another major comorbid Axis I disorder: 6 (86%) of 7 patients and 4 (57%) of 7 patients, respectively. Although improvement occurred in nearly all measures of hypochondriasis and mood, there was no statistical improvement in bodily preoccupation.

Fallon et al. (1996) reported the results of a mid-study analysis of the first 25 patients to enter a double-blind 12-week placebo-controlled study of fluoxetine for DSM-IV hypochondriasis, with doses starting at 20 mg/day and increasing as needed to 80 mg/ day. During the 2-week placebo run-in, 5 patients were excluded either because of a placebo response or noncompliance with the protocol. Of the 20 patients assigned randomly to placebo or fluoxetine, 16 (80%) completed a minimum treatment of 6 weeks and 15 (75%) completed the full 12 weeks. Eight (80%) of 10 patients randomized to fluoxetine responded at 6 and 12 weeks versus a placebo response of 3 (50%) of 6 patients at 6 weeks and 3 (60%) of 5 patients at 12 weeks on the Clinical Global Improvement (CGI) Scale. These response rates, although high for fluoxetine at 6 and 12 weeks, also indicated a robust placebo response at 6 and 12 weeks, respectively. When the data were reexamined to rate response as a score of "very much improved" on the CGI Scale (virtually symptom free), the response rate was higher for fluoxetine than placebo at 12 weeks: 5 (50%) of 10 fluoxetine-randomized patients versus 1 (20%) of 5 placebo-randomized patients. This mid-study analysis of a double-blind placebo-controlled study suggested preferential efficacy for fluoxetine but also raised critical questions about the nonspecific therapeutic effects of placebo and patient-clinician encounters. A similar concern emerged from the Clark et al. (1998) study of cognitive therapy versus behavioral stress management therapy for treating hypochondriasis.

Therapeutic Suggestions for Pharmacologic Treatment

Patients with hypochondriasis who are considering a medication trial benefit from a careful explanation of how the medicine might reduce illness obsessions and distress over bodily symptoms by acting on the neurochemistry of the brain, correcting an imbalance that would otherwise allow the hypochondriasis to continue. Because patients with hypochondriasis are often fearful of the unknown long-term consequences of medication, an honest and open discussion about the risks and benefits of medication treatment should be conducted, with the physician being careful not to provide excessive detail that would only further frighten the patient. As part of the discussion of pharmacothera-py, the physician should emphasize that therapeutic action may take 6 weeks or longer and that initial side effects often decrease after the first several weeks.

Although pharmacotherapy may not be the preferred choice of treatment for most people with hypochondriasis, 70-80% of patients participating in hypochondriasis trials appear to benefit from them.

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