LETTERS TO THE EDITOR Spier SA, Frontera MA (199 I), Unexpected deaths in depressed medical inpatients treated with fluoxetine. ] Clin Psychiatry 52:377-382 Zarzar MN, Kingsley RS (1990), Use of fluoxetine in a person with cardiac arrrhyrnias. Psychosomatics 31:235-236
COCAINE CRAVING
Kaminer Y (1992a), Desipramine facilitation of cocaine abstinence in an adolescent. ] Am Acad Child Adolesc Psychiatry 31:312-317 Kaminer Y (I 992b), Clinical implications of the relationship between attention deficit hyperactivity disorder and psychoactive substance use disorders. American ]ournal ofAddictions 1:257-264 Kosten TR, Gawin FH, Kosten TA et aI. (1992), Six-rnonth follow up of short-term pharmacotherapy for cocaine dependence. American
]ournal ofAddictions 1:40-49
To the Editor: The special article by Ambrosini and colleagues (1993) was comprehensive and educational. However, the authors omitted noting the therapeutic use of desipramine (OMI) in facilitating cocaine abstinence in adults (Gawin et al., 1989; Kosten et al., 1992) and in a 6-month follow-up study of an adolescent (Kaminer, 1992a). Kosten and colleagues (1992) presented 6-month followup data on 43 of the 72 patients originally studied by Gawin et al. (1989) and reported that cocaine abstinence was significantly greater in patients treated with OMI (44%) than in those treated with lithium (19%) or placebo (27%). The reduction/elimination of cocaine abstinence-related craving by OMI is attributed to a probable desensitization of presynaptic inhibitory dopaminergic autoreceptors. This is essential to improve relapse prevention rates and to ensure treatment retention that can be utilized for the introduction of additional therapeutic interventions. Since the publication of the adolescent case study (Kaminer, 1992a), I have treated two more adolescents with OMI for cocaine craving. The first patient responded favorably to the treatment; however, the other patient developed postural hypotension and the medication was discontinued. It is noteworthy that the second patient reported a regular abuse of Elavil® (amitrypryline) for its sedative effects in order to reduce the high from stimulants. This confirms verbal reports by adult substance abusers about the abuse potential ofcertain tricyclic antidepressants. Patients reported that the street value of amitriptyline is five dollars as compared to only one dollar for other tricyclic antidepressants. Child and adolescent psychiatrists need to be aware of this phenomenon in order to prevent abuse by adolescents who are substance abusers, their siblings, parents, and peers who are also at high risk for substance abuse. A similar caution was reported regarding a potential abuse of therapeutic stimulants (Kaminer, 1992b).
MPH AND THROMBOCYTOSIS
To the Editor:
Ambrosini PJ, Bianchi MD, Rabinovich H, Elia J (1993), Antidepressant treatment in children and adolescents.] Am AcadChildAdolesc Psychiatry, 32:483-493 Gawin FH, Kleber HD, Byck R et al. (1989), Desipramine facilitation of initial cocaine abstinence. Arch Gen Psychiatry 46:117-121
Stimulant drugs account for 99% of medications prescribed in children with attention-deficit hyperactivity disorder and are the primary pharmacological agents used in adults with narcolepsy (Wilens, 1992; Kales et al., 1987). Methylphenidate is the most commonly used stimulant in these disorders in the United States. Though effective in these conditions, methylphenidate is known to produce several behavioral and physiological side effects. The only reported hematological adverse effect of methylphenidate is idiopathic thrombocytopenic purpura (Grossman and Grossman, 1985). We are describing a case of a 7-year-old boy who was referred to our sleep disorders center with a complaint of excessive daytime sleepiness. Complete physical exam done on initial visit was normal except for enlarged tonsils and adenoids. All-night diagnostic polysomnography (PSG) and multiple sleep latency test (MSLT)-standardized testingconfirmed the diagnosis of narcolepsy with shortened rapid eye movement (REM) latency, frequent arousals on PSG, and sleep-onset REM in three of five naps in MSLT. A complete blood count done prior to the initiation of methylphenidate was normal except for a slight elevation of platelet count, 607 X 1Q3/ mm3 (normal, 140 to 440 X 1Q3/ mm3). He was started on methylphenidate 10 mg and was gradually increased to 40 mg/day over the next several months to decrease daytime sleepiness. Repeat blood count was done after approximately 9 months of therapy with methylphenidate. This showed the platelet count to be abnormally high at 913 X 1Q3/ mm3. No abnormal clinical symptoms were reported. The methylphenidate was then reduced to 30 mg/day. Thereafter there was a gradual decline in platelet count over several months and it came close to normal (489 X 1Q3/ mm3) after 2 years of therapy with methylphenidate. To our knowledge, thrombocytosis has never been reported with methylphenidate. Thrombocytosis, a platelet count in excess of 400 X 1Q3/ mm3, is classified as primary or secondary. Primary thrombocytosis results directly from a myeloproliferative disorder. Thrombosis and hemorrhage are potential complications of thrombocytosis (Kutri, 1990).
592
J. AM. ACAD. CHILD ADOLESC. PSYCHIATRY, 33:4, MAY 1994
Yifrah Kaminer, M.D. University of Connecticut Health Center Farmington, CT