Relative Incidence of Antipsychotic Adverse Effects
Sedation EPS Anticholinergic Orthostasis Weight Gain
Risperidone + ++ 0 to + ++ +++
0, no effect; +, low; ++, moderate; +++, high; ++++, very high; EPS, extrapyramidalside effects.
Reprinted from Facts & Comparisons eAnswers. http://online.factsandcomparisons.com/MonoDisp.aspx?
monoID=fandc-hcp10202. Accessed May 15, 2016, with permission.
Akathisia can present alone or in combination with drug-induced parkinsonism, or
It presents as an inability to remain still combined with an
intense feeling of internal restlessness that can make the patient appear quite
In the unfortunate event akathisia is incorrectly interpreted as agitation,
increased or “as needed” antipsychotic doses to target agitation will worsen the
syndrome. Akathisia is best treated by a small reduction in antipsychotic dosage,
addition of low dosage β-adrenergic blockers (i.e., propranolol 10 mg bid or tid), or
addition of anticholinergic agents (especially if drug-induced parkinsonism is also
present). Benzodiazepines can also be used in patients not responsive to the
aforementioned strategies (Table 85-11).
experiencing at this time? What information in her presentation supports this finding?
J.J. is most likely experiencing akathisia. As her symptoms did decrease when
brexpiprazole was initiated, it is unlikely that it is agitation due to her schizophrenia
that is causing the restlessness. Antipsychotics, even those that are D2 partial agonists
such as brexpiprazole, are known to cause akathisia as an adverse effect. Her
symptoms also appear to be akathisia: constant pacing/movement, always fidgety,
and feeling of inner restlessness. Although lorazepam would be expected to treat
agitation, it is also a potential treatment for akathisia as well.
CASE 85-1, QUESTION 9: What would be the appropriate treatment for J.J.’s akathisia?
Agents to Treat Antipsychotic-Induced Parkinsonism and Akathisia
Medication Equivalent Dose (mg) Dose/Day (mg/day)
Procyclidine (Kemadrin) 1.5 10–20
Trihexyphenidyl (Artane) 1 2–15
Propranolol (Inderal) — 20–60 (max = 120)
aOral dose or intramuscular (IM) injection can be used.
Adapted from Facts & Comparisons eAnswers. http://online.factsandcomparisons.com/MonoDisp.aspx?
monoID=fandc-hcp10202. Accessed May 15, 2016, with permission.
First and foremost, it should be determined whether J.J. can be stabilized on a
lower dose of her medication. Often a reduction in antipsychotic dose will resolve
any EPS symptoms. If this is not possible and J.J. would destabilize as a result, then
an additional medication will be needed to manage the problem. Although lorazepam
would serve this purpose, the concerns about chronic daily administration of
benzodiazepines must be considered. As J.J. may have akathisia with brexpiprazole
as long as she is on the medication, she could require treatment for akathisia this
entire time. Another option for treating this problem would be propranolol, the
nonselective β-blocker. Propranolol has been found to be helpful in alleviating
akathisia in low, subcardiac doses such as 10 to 20 mg twice daily. If this treatment
is selected, then her blood pressure and heart rate should be monitored accordingly.
Ideally, we would keep J.J. on the medication that stabilized her during her
hospitalization. It might be possible to contact her insurance to obtain a prior
authorization for this medication. If that cannot be done, then they should be asked
whether aripiprazole is available for use with J.J. Aripiprazole is also a D2 partial
agonist, like brexpiprazole, so theoretically it should work in a similar manner as
brexpiprazole. If her insurance will not pay for aripiprazole, then another atypical
antipsychotic with a similar adverse effect profile should be considered. As
brexpiprazole has lower rates of EPS and metabolic adverse effects, an agent such as
ziprasidone might be considered as it has similar rates of EPS and metabolic effects
but is available as a generic medication.
improve JJ’s prognosis once she is discharged?
Although J.J.’s symptoms should start to decrease within a few days of starting the
medication, it may take a week or longer to see significant improvement. At this point
she may be stable enough for discharge from the hospital, but still show some
functional deficits. It may take several more weeks, possibly months, for her to return
to her baseline prior to her symptoms starting, and she may never fully reach this
point. The utilization of nonpharmacologic methods, including individual and group
therapy modalities, could also help J.J.’s continued improvement and stabilization.
Education for both her and her family could also be of benefit to her.
J.J. should not stop her medication at this time. Although a medication adjustment
might be needed, depending upon the nature and cause of her concentration, that is not
a reason to stop the medication altogether. Most treatment guidelines recommend a
minimum of 6 months, and preferably one year, of treatment after a psychotic
episode. As she has only been symptom-free for 5 months, J.J.’s risk of relapse is
very high without medication treatment.
antipsychotics (LAIAs) at this time?
J.J. is not a candidate for a LAIA currently as she has never tried an oral
formulation of any of them to this point. Recommendations for use of a LAIA require
at a minimum repeated dosages of the oral form of the medication to ensure a lack of
an allergy to the med, or in some instances for the patient to be stable on an oral dose
of the medication and the converted over to the LAIA form. However, she might
benefit from the use of a LAIA if she truly intends to be nonadherent with oral forms
of antipsychotics. As she has only shown nonadherence to one medication trial due to
a potential misunderstanding of her illness and her treatment, she could benefit from
education in these areas to improve her adherence. In addition, her family could be
educated to help J.J. maintain her med adherence as well.
agent for JJ, and why or why not?
Assuming that J.J. has been administered oral risperidone in the past which
ensures a lack of an allergy to the medication, it still would not be an appropriate
option at this time. Due to the unique pharmacokinetic parameters of risperidone
LAIA, it requires 3 weeks of overlap of oral medication (risperidone or otherwise)
as the initial dose does not begin releasing medication until this time. Assuming J.J.’s
nonadherence to oral medications will continue, this could lead to a poor outcome,
especially if she is discharged from the hospital. J.J.’s insurance should be contacted
to attempt to find an alternative atypical antipsychotic LAIA.
One of the more troubling potential adverse effects from chronic treatment with
antipsychotics is the development of persistent choreoathetoid (sometimes described
as snake-like) movements of the tongue, hands, feet, and in severe cases even the
149 Chronic blockade of striatal D2
results in these receptors becoming supersensitive to available dopamine. Changes in
interconnected neurotransmitter systems, such as GABAergic or muscarinic,
result in dyskinesias that can often appear on withdrawal of antipsychotics, upon
lowering of the dosage, or when a patient is changed to clozapine or quetiapine
treatment from another antipsychotic. If these withdrawal dyskinesias persist, then the
condition of persistent or tardive dyskinesia can result. Tardive dyskinesia can also
present without any change in medication dose after many years of treatment. FGAs
are considered to have a much greater risk (5% yearly incidence in long-term use in
adults) of causing tardive dyskinesia than the SGAs, but reported incidences vary
151 Risk of developing tardive dyskinesia increases with
cumulative lifetime dosage and duration of antipsychotic treatment, increased age,
comorbid diabetes mellitus, traumatic brain injury, having an affective disorder,
anticholinergic medication use, a history of drug-induced parkinsonism, and female
152–155 Although the incidence rate for patients treated with typical
antipsychotics is more substantial,
the atypical antipsychotics also carry this risk
albeit at a lower but still not negligible rate.
Although all dyskinetic movements seen on withdrawal of antipsychotic
medication are not necessarily persistent or tardive dyskinesia, there are those cases
of patients who do retain the potentially stigmatizing movements long after
antipsychotic medications are tapered or changed. When this occurs, it is often very
difficult to remediate these movements. Medication changes which decrease the
effects of dopamine on striatal receptors tend to cause immediate improvement
followed by long-term worsening of dyskinetic symptoms. Few double-blind studies
show any benefit of augmenting with various agents, and agents which often have
shown promise in early case reports and open studies (i.e., diazepam, donepezil,
branched chain amino acids) often do not bear up to the scrutiny of a double-blind
157–159 Even accepted strategies such as lowering antipsychotic dosages (or
stopping them when possible) or changing to less offending second-generation agents
such as clozapine or quetiapine do not always yield the desired outcome. Some
limited evidence suggests that clonazepam and ginkgo biloba may prove helpful.
However, a better course of strategy appears to do what we can to prevent the
occurrence of tardive dyskinesia by strategies such as keeping antipsychotic dosages
as low as possible and using medications that are less likely to induce this
150,151,160 and incorporating close monitoring for development of symptoms
utilizing the Abnormal Involuntary Movement Scale (AIMS) examination. However,
we do have the option to tailor our medication choice to the vulnerability of the
patient. As the severity and prevalence of tardive dyskinesia is apparently on the
there may be cause to be optimistic.
The low-potency FGAs and certain SGAs, particularly olanzapine and clozapine, are
potent muscarinic receptor antagonists. The resultant anticholinergic effects can range
from bothersome to potentially life-threatening. These effects include dry mouth,
blurred vision, mydriasis, tachycardia, urinary retention, constipation, paralytic ileus,
confusion, and delirium. Something that may appear merely bothersome, like dry
mouth, can have more serious consequences if not addressed. Dry mouth can lead to
dental caries or weight gain if thirst is quenched with sugary beverages. Additional
sugar, in the form of gum or liquids, can also increase the risk of oral fungal
infections. Patients can utilize sugar free hard candies or gum, or saliva substitute
products if anticholinergic medication dosage cannot be reduced.
patients with schizophrenia should be encouraged to connect with regular dental
services. Another often overlooked anticholinergic adverse effect is constipation.
Patients may not draw the connection between constipation and a medication that they
are taking for their mental health. Consistent monitoring of patient’s bowel habits and
unaddressed bowel discomfort progressing to paralytic ileus and patient expiration
due to bowel rupture or aspiration of gastric contents.
The patient’s overall anticholinergic burden is often increased by the addition of
anticholinergic medications, such as benztropine, for EPS prophylaxis or treatment.
Indication for use of anticholinergic agents should be re-evaluated periodically
during treatment and upon transitions in care. Failure to taper unnecessary
anticholinergic medications can lead to decreased quality of life and preventable
Antipsychotic medications are thought to exert cardiovascular effects through direct
antagonism of adrenergic and cholinergic receptors, as well as through indirect
central autonomic effects and baroreceptor reflexes.
Orthostatic hypotension occurs in up to 40% of patients treated with antipsychotic
It occurs frequently during the initial dose titration and
disproportionately affects elderly patients. Orthostasis results from the blockade of
vascular α1A-adrenoceptors, which makes it difficult for patients to adapt to
positional changes in blood pressure. Tolerance to orthostasis will usually develop
within 2 to 3 weeks of antipsychotic initiation or dose increase. Antipsychotic agents
with high affinity for α1A-adrenoceptors relative to D2
risperidone) clinically display greater rates of orthostasis than agents with low α1A
affinity relative to D2 affinity (i.e., haloperidol).
164 The risk for falls secondary to
orthostasis can be mitigated by (1) slowing the rate of titration, (2) splitting the dose,
and (3) counseling the patient to make slow transitions from prone and seated
positions. Increasing fluid and salt intake and using support stockings are other
nonpharmacologic interventions that may help alleviate orthostasis whereas the
patient adapts to a change in dosage. More persistent orthostasis resulting from
clozapine treatment can be managed with fludrocortisone or ephedrine if
nonpharmacologic interventions are not clinically feasible.
Antipsychotic-associated tachycardia can occur as a direct effect of anticholinergic
activity on vagal activity or as a compensatory mechanism related to orthostatic
hypotension. Patients treated with clozapine tend to have a dose-related increase in
bothersome to the patient or symptomatic.
Prolongation of the QT interval, or QTc
interval when corrected for heart rate, is a
variable risk associated with all antipsychotics. QTc
interval prolongation increases
the risk for torsades de pointes (TdP), a malignant polymorphic ventricular
tachycardia that is associated with syncope and sudden cardiac death.
potential mechanism for this effect is believed to be mediated through blockade of the
rapidly activating delayed rectifying current (IKr
) which conducts potassium out of
the cardiomyocytes to cause cardiac repolarization.
The Pfizer 054 study, developed in consultation with the FDA, demonstrated QTc
prolongation as a class effect for SGAs.
peak plasma concentrations of haloperidol 15 mg/day (n = 27), thioridazine 300
mg/day (n = 30), ziprasidone 160 mg/day (n = 31), quetiapine 750 mg/day (n = 27),
olanzapine 20 mg/day (n = 24), or risperidone 6 to 8 mg/day increased to 16 mg/day
interval in the presence or absence of metabolic inhibitors in
patients with stable psychotic disorders. No patients were observed to have a QTc
interval greater than 500 ms, and mean QTc changes from baseline were similar for
monotherapy and with concomitant administration of a metabolic inhibitor. The
antipsychotics associated with the greatest change in mean baseline QTc were
thioridazine (30.1 ms) and ziprasidone (15.9 ms). Haloperidol, quetiapine,
risperidone 6 to 8 mg/day, risperidone 16 mg/day, and olanzapine were associated
with mean QTc changes of 7.5, 5.7, 3.9, 3.6, and 1.7 ms, respectively.
context, the mean diurnal variation in QTc
is approximately 75 to 100 ms and this
may vary further based on sleep, diet, obesity, electrolyte disturbances, endocrine
164,167 No cases of torsades de pointes were observed in
the 4,571 ziprasidone-treated patients included in the Pfizer 054 study and the
168 One of the newer SGAs, iloperidone, has also demonstrated
a dose-dependent and drug interaction-dependent risk of QTc prolongation similar to
that of ziprasidone in both short- and long-term randomized trials.
In clinical practice, concomitant administration of QTc
be avoided. If coadministration is necessary in a patient with no underlying cardiac
abnormalities or risk factors for TdP, the patient should be monitored closely. The
interacting medication should be discontinued if the QTc
ms. Use of antipsychotics with higher risk of QTc prolongation, chlorpromazine or
ziprasidone, should be avoided in patients with underlying cardiac issues, electrolyte
abnormalities (hypokalemia or hypomagnesaemia), congenital long-QT syndrome, or
those comedicated with agents affecting cardiac function (particularly
antiarrhythmics of class Ia—disopyramide, procainamide, quinidine—and class III—
amiodarone, dofetilide, sotalol).
time? What information in her presentation supports this finding?
J.J. is most likely suffering from drug-induced parkinsonism, a type of EPS. All the
abnormal findings noted in J.J. at this time, stiffness, tremor, and shuffling gate, are
characteristic findings for drug-induced parkinsonism. Although risperidone, as an
atypical antipsychotic, is less likely to cause this problem compared to the older,
conventional antipsychotics, it can still cause it. One risk factor of parkinsonism with
risperidone is increasing the dose, which occurred in J.J. recently. Although she was
fine on the lower dose, the increase in dose to 6 mg/day caused enough D2
blockade in the nigrostriatal pathway to induce this EPS type.
CASE 85-1, QUESTION 16: How can J.J.’s drug-induced parkinsonism be treated?
Ideally the first choice would be to decrease the dose of the offending agent. As
J.J.’s dose of risperidone was just increased to 6 mg/day due to lingering symptoms,
this is most likely not an option as it is highly likely those symptoms would return. A
change in antipsychotics could also be considered, but it appears that other than the
EPS, J.J. is currently stable on this medication and dose. The only other option would
be to add another medication to treat her parkinsonism. Some options include the use
of anticholinergic medications, such as benztropine, or the use of amantadine.
mg twice daily. WillJJ need to stay on this medication indefinitely?
J.J. should be maintained on benztropine for at least 3 months once her
parkinsonism resolves. If there are no other changes in her clinical status or her
not return, then she should not need the medication any longer. Should the EPS return,
however, then she may need continued anticholinergic treatment.
CASE 85-1, QUESTION 18: What are some other adverse effects that should be monitored for in JJ, both
specific to risperidone and for antipsychotics in general?
Any patient receiving an antipsychotic should be monitored for all types of EPS,
including parkinsonism. Other EPS types, such as dystonia and akathisia, should be
watched for as well as the development of any tardive dyskinesia. Although the risk
of these concerns is lower with an atypical antipsychotic, such as risperidone, it is
still possible. J.J.’s weight and serum glucose and lipids should also be monitored
regularly both during the initiation of antipsychotic treatment and periodically
throughout. Risperidone also can cause drug-induced orthostasis, so she should be
monitored for dizziness, especially upon standing.
Prolactin is a polypeptide hormone secreted by lactotroph cells in the anterior
pituitary. Dopamine acts as an inhibitor of prolactin release in the tuberoinfundibular
from the hypothalamus to the anterior pituitary. Blockade of D2
pathway leads to increased release of prolactin and potential effects on multiple
organ systems and gene expression throughout the body. Agents that cause more
potent D2 blockade are associated with a greater risk of hyperprolactinemia.
multiple-treatment meta-analysis by Leucht and associates stratified select
antipsychotics based on their effect on the standardized mean difference in prolactin
from baseline as follows: paliperidone (highest), risperidone, haloperidol,
lurasidone, ziprasidone, iloperidone, chlorpromazine, olanzapine, asenapine,
quetiapine, and aripiprazole (lowest/decreased prolactin).
baseline prolactin monitoring at the discretion of the clinician, screening for
symptoms of excess prolactin at every visit for the first year of treatment and annually
thereafter if symptoms are stable, and follow-up prolactin levels only if clinically
45,173,174 The upper limit of normal prolactin levels is 18 to 20 ng/mL in
males and 24 ng/mL in females who are not pregnant or lactating.
Clinical sequelae from excess prolactin release include sexual dysfunction,
gynecomastia, galactorrhea, amenorrhea, hypogonadism, and potential bone mineral
density changes with long-term elevations. However, prolactin levels do not directly
correlate with these adverse events and patients may remain asymptomatic.
Considerations for treatment should only be addressed in actively symptomatic
In symptomatic patients, dose reduction or switching to an agent with
less potent D2 blockade would be recommended first line. If these strategies fail to
improve the symptoms or cannot be undertaken for clinical reasons, a dopamine
agonist, such as bromocriptine, cabergoline, or amantadine, may be considered.
However, the risk of potential exacerbation of psychosis must be weighed against
45,171,174,175 There is also growing evidence to support the use of
adjunctive aripiprazole, a partial D2 agonist, to improve hyperprolactinemia in
patients who cannot be switched from a more potent agent.
CASE 85-1, QUESTION 19: Over time J.J.’s dose of risperidone is increased to 4 mg twice a day due to
level is 115 ng/mL. What could explain why J.J. believes she is pregnant?
The negative pregnancy test proves J.J. is not pregnant (assuming no error by the
laboratory). Her symptoms are indicative of hyperprolactinemia, another potential
receptor antagonism from antipsychotic therapy. As her prolactin
level increased, it caused J.J. to become amenorrheic and cause her to lactate.
Although not a common adverse effect of most atypical antipsychotics, risperidone
(and paliperidone) is similar to the typical antipsychotics in their propensity to
CASE 85-1, QUESTION 20: How should J.J.’s hyperprolactinemia be treated?
Ideally the treatment of antipsychotic-induced hyperprolactinemia involves a dose
reduction of the offending agent. As J.J. was increased to 4 mg twice daily due to an
insufficient response to a lower dose, this may not be possible. If a dose reduction
cannot be done safely, then a change in antipsychotic to one with a lower risk of
hyperprolactinemia should be considered. If this too is not clinically appropriate for
the patient, then addition of a dopaminergic agonist may be considered, such as
amantadine. This should be done cautiously as a strong dopaminergic agonist, such as
bromocriptine, may exacerbate her psychosis. There are also data available on using
aripiprazole augmentation to treat hyperprolactinemia from antipsychotics, but this
might be considered after other agents have been tried, unless J.J. appears to need a
stronger antipsychotic regimen.
Although the development of the SGAs was supposed to free us from the concern of
the extrapyramidal adverse effects of the FGAs, many of the newer agents such as
clozapine, olanzapine, quetiapine, and risperidone showed a tendency to, like the
low-potency typical first-generation agents, cause substantial weight gain.
substantial weight gain tended to occur to the greatest extent in the first few months of
treatment, with a certain segment of those treated gaining more than 20 lb.
study showed that 15.4% of those patients treated with olanzapine had weight gain
greater than or equal to 7% of their body weight in the first 6 weeks of treatment.
soon became apparent that clozapine and these newer SGAs had the potential to
increase body weight and serum triglyceride levels,
65–68 and therefore potentially
cause glucose dysregulation as well.
71,181,182 Patients suffering from schizophrenia are
already prone to an earlier death than nonmentally ill patients due to their physical
health and inherent sedentary lifestyle; therefore, weight gain may be an even more
critical issue than the potentially stigmatizing occurrence of tardive dyskinesia.
Numerous mechanisms have been theorized to explain the weight gain induced by
the SGAs. These include histamine (H1
antagonism at 5-HT2c with a possible genetic predisposition in some,
muscarinic antagonism which could possibly lead to increased consumption of sugary
beverages or “thirsty” calories,
188 and impairments in plasma leptin secretion.
Concomitant medications, such as valproic acid, lithium, mirtazapine, some
antihistamines, and tertiary tricyclic antidepressants, can also increase body weight
by synergistic pharmacologic effects.
Hyperglycemia and Diabetes Mellitus
It is unclear whether there are direct actions by SGAs involved in the development of
diabetes mellitus. However, it is clear that weight gain, increased triglycerides, or
decreased insulin sensitivity due to SGAs may cause an increased frequency or
earlier onset of this endocrine disorder.
71,181,193–195 An early study showed a moderate
correlation (r = 0.60, p =.03) between serum insulin and clozapine levels,
Lund and associates showed an approximately 2.5 times greater risk of diabetes
mellitus and hyperlipidemia in patients agents 20 to 34 years old treated with
197 Other retrospective studies in veterans also suggested a
slightly greater prevalence of diabetes in patients less than 40 years old on the SGAs
clozapine, olanzapine, quetiapine, or risperidone (OR =1.09; CI=1.03–1.15) than
181 and an incidence of diabetes mellitus approximately 1.5 times
greater in patients treated with olanzapine, risperidone, or quetiapine than with
typical, mostly low-potency, antipsychotics.
71 Guidelines stress the need to monitor
these patients routinely for glucose dysregulation, weight gain, and
Treatment-emergent increases in both serum triglycerides and total serum cholesterol
may occur with use of antipsychotics. The initial reports were of increased serum
66,68,199 a notation of this phenomenon in the package
insert for quetiapine, and reports of this occurring in patients taking olanzapine.
Risperidone does not raise serum triglycerides as
, and ziprasidone has negligible effects on serum
200,201 Aripiprazole resulted in lowered serum triglyceride levels
compared to placebo in pooled double-blind trials.
202 Average serum triglycerides
with clozapine, olanzapine, or quetiapine tended to increase by approximately 60 to
66–67,70 Extreme elevations in serum triglycerides (>1,000
mg/dL) have been noted in some patients and were often associated with acute
J.J., as with all patients receiving antipsychotics, is at risk of developing
potentially significant weight gain, glucose irregularities including diabetes mellitus
type 2, and dyslipidemia, especially hypertriglyceridemia. The risk varies among the
agents, with SGAs generally thought to be at a higher risk than with FGAs.
factors include the patient’s diet and exercise, family history of diabetes and
cholesterol problems, and others.
What would be the appropriate monitoring for J.J. upon initiation of olanzapine?
As olanzapine has a high risk of causing metabolic adverse effects in patients, J.J.
should be monitored closely for the development of these effects. Her weight should
be checked very closely, especially at baseline and over the first few months of
treatment. Monthly, if not more frequently, weights should be measured during this
time. In addition, her serum glucose and/or HbA1c along with her serum lipid panel
should be checked at baseline and then in 3 months for any changes, with an interim
serum glucose measurement around 1 to 2 months. Her blood pressure should also be
monitored for any changes, especially if her weight increases significantly. If any
increases or abnormalities are noted in these parameters, they should be addressed
appropriately before becoming a medical concern.
an increase from her weight prior to olanzapine of 139 lb (BMI = 23.9 kg/m
). J.J.’s parents are also concerned
olanzapine, and whether there is anything that can be done about it.
Olanzapine could certainly be the cause of her recent weight gain, because it has
one of the higher risks of causing weight gain among the SGAs. A 12-lb weight gain
is certainly possible with this medication. As J.J., and her parents, has noticed an
increase in her appetite since starting the medication, this makes it even more likely
should be given an appointment with a nutritionist to review her diet, and she should
also be encouraged to increase her exercise on a regular basis, whether at a gym or
even by adding 20- to 30-minute walks 4 to 5 days a week.
Metabolic Monitoring Protocol for Antipsychotics
More frequent assessments may be warranted based on clinicalstatus.
patients with schizophrenia and related disorders. J Clin Psychopharmacol. 2005;25(3):255–258.
of schizophrenia. Schizophr Bull. 2002;28(1):5–16.
CASE 85-1, QUESTION 24: A month later, J.J. returns to the clinic. Blood work done a few days ago
Increases in serum glucose and lipids, especially triglycerides, are possible with
SGAs, and olanzapine in particular. As her glucose and A1c have increased since
starting the medication, this makes it highly likely this is the cause. Although J.J.’s
LDL and HDL cholesterol measurements are not ideal, they are not as concerning as
her very elevated triglyceride level. At this high of a level of triglycerides, there is
the concern of possible pancreatitis. J.J. should be asked about any upper abdominal
pain or other possible symptoms.
Although we could treat her increased serum glucose and lipids with appropriate
medications for each concern, another consideration would be to change J.J. from
olanzapine to another SGA with a lower risk of metabolic problems. This would
need to be done after considering the risk of J.J.’s possible psychiatric
decompensation from changing her antipsychotic treatment.
Currently, metabolic syndrome is seen as a major concern when treating
schizophrenia, and it is recommended that patients receiving SGAs must be routinely
monitored for weight gain, changes in fasting serum lipids, or signs of glucose
193,198,203 Some estimates of the prevalence of metabolic syndrome in
patients with schizophrenia range from 18.8% to approximately 40% of those
204 As medication-naïve patients are already at a high risk for developing
205 we should strive to minimize the chance or worsening their
situation. Furthermore, since weight gain with antipsychotic medication and its
secondary metabolic complications tends to occur rapidly, patients should receive
more frequent assessments for this when they are first started or switched to a new
antipsychotic medication. Medication use evaluations to make sure this necessary
monitoring is performed may be helpful.
Moreover, effective pharmacotherapy carries with it a potential for serious
adverse metabolic effects such as obesity, hypertriglyceridemia, and resulting
glucose dysregulation as well as movement disorders such as akathisia, drug-induced
parkinsonism, and tardive dyskinesia. One study showed metabolic disorders occur
more than 3 times (3.7; 95% CI = 1.5–9.0) as much in patients with schizophrenia as
compared to nonpsychiatrically ill controls.
In fact, cardiovascular disorders are
the main reason patients with schizophrenia tend to die at a younger age than their
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