C A S E S T U D I E S

Case Study: Atypical Antipsychotic Use Associated

With Severe Hyperglycemia
Marguerite J. McNeely, MD, MPH

Downloaded from http://diabetesjournals.org/clinical/article-pdf/20/4/202/497928/0202.pdf by guest on 07 November 2022

Presentation range is negative). A toxicology screen Commentary
A.T. is a 50-year-old woman who devel- was negative. No evidence of infection, Hyperosmolar hyperglycemic nonketotic
oped acute hyperosmolar crisis. She first myocardial ischemia, or other acute ill- syndrome (HHNS) is defined as glucose
presented for primary care 5 months ness was found. During the hospital stay, >600 mg/dl and serum osmolality >320
before the event. Medical history was A.T. reported earlier treatment with gly- mOsm/kg in the absence of significant
notable for longstanding schizo-affective buride (DiaBeta, Micronase, and Gly- ketoacidosis.1 Signs and symptoms
disorder and hyperlipidemia. She denied nase) and metformin (Glucophage), but include acute or subacute changes in
a history of diabetes. She reported her stated that those medications had been mentation, temperature dysregulation
medication regimen had not changed in stopped more than 1 year ago for (hyperthermia or hypothermia), relative
more than 1 year; medications included unknown reasons. hypotension, and renal insufficiency.
divalproex (Depakote), gabapentin The patient was discharged from The condition typically affects patients
(Neurontin), olanzapine (Zyprexa), and the hospital on a regimen of 14 units of with type 2 diabetes who are over age
gemfibrozil (Lopid). NPH insulin with 14 units of regular 50. HHNS is often triggered by a physi-
A.T.’s weight was 235 lb. A random insulin before breakfast, and 10 units of ological stress that causes hyper-
plasma glucose was 103 mg/dl. Liver NPH insulin with 10 units of regular glycemia and dehydration, such as
function tests, blood urea nitrogen, and insulin before dinner. Olanzapine and infection, myocardial infarction, stroke,
creatinine were also normal. One month hydrochlorothiazide were stopped, and or heat stroke. Medications associated
before the event, hydrochlorothiazide, 25 haloperidol (Haldol) was started. with HHNS include glucocorticoids and
mg daily, was started for hypertension, A few days after hospital discharge, diuretics. Recently, the newest genera-
and simvastatin (Zocor) was substituted A.T. presented to the clinic. She had tion of antipsychotic agents, referred to
for gemfibrozil to treat hypercholes- skipped lunch, and her glucose was 48 as “atypical antipsychotics,” have been
terolemia. mg/dl. Insulin was stopped. associated with diabetes, severe hyper-
One month later, A.T. presented to Three months after stopping all glycemia, and diabetic ketoacidosis.2
clinic with 1 day of urinary incontinence hypoglycemic agents, she weighed 233 A.T. clearly met the criteria for
but no other symptoms of illness and lb, her random glucose was 136 mg/dl, HHNS, since her calculated serum
was hospitalized for severe hyper- and her A1C was 7.5%. osmolality was 340 mOsm/kg, using the
glycemia. Her weight was 219 lb. Uri- About 4 months after hospital dis- formula: serum osmolality = 2(Na + K)
nalysis showed no white blood cells but charge, A.T. weighed 241 lb, and review + (blood urea nitrogen/2.8) + (glu-
was strongly positive for glucose and of her glucose meter memory function cose/18). She did not have obvious acute
weakly positive for ketones (trace). Her showed random glucose levels were all mental status changes, but subtle deficits
glucose level was 1,572 mg/dl, and her >200 mg/dl. Her A1C was 10.3%. She may have been masked by her chronic
hemoglobin A1c (A1C) result was >14%. was started on repaglinide (Prandin), and psychosis.
Her serum sodium was 113 mEq/l, within a few months, a fixed dose of Why she developed HHNS is less
potassium was 4.8 mEq/l, and carbon ultralente insulin was added. clear. It seems unlikely that low-dose
dioxide (bicarbonate) was 36 mEq/l. hydrochlorothiazide alone triggered such
A.T. was severely volume-depleted as Questions severe hyperglycemia. Olanzapine, an
evidenced by postural hypotension, ele- 1. Why did this patient develop severe atypical antipsychotic medication, was
vated blood urea nitrogen of 47 mg/dl, hyperglycemia? likely a major factor.
and elevated creatinine of 2.5 mg/dl. A 2. How is diabetes best managed in Atypical antipsychotics cause weight
semiquantitative blood acetone level was patients with severe psychiatric disor- gain, and this is thought to be the pri-
positive at a dilution of 1:8 (reference ders? mary reason that mild to moderate

CLINICAL DIABETES • Volume 20, Number 4, 2002 195

 C A S E S T U D I E S

hyperglycemia is often associated with atric conditions. Ideally, such patients ✔ Using oral agents and/or long-act-
these medications.3 However, severe would live with a responsible person ing insulin to control severe
hyperglycemia that resolves with discon- who helps manage their diabetes. For chronic hyperglycemia.
tinuation of the medication has also been patients without a close friend or relative ✔ Before using metformin, deter-
reported. The mechanism for acute, tran- who is willing to assume this role, alter- mining whether the patient is like-
sient hyperglycemia remains unclear, natives include a paid caretaker or assist- ly to stop it if dehydration occurs.
although one study demonstrated that ed living. ✔ Before using short-acting insulin,
these medications inhibit glucose trans- However, poor judgment and lack of determining whether the patient is
port into cells.4 insight are inherent features of many likely to take it with food.
Atypical antipsychotics offer many psychiatric disorders. Therefore, some ✔ Prescribing small quantities of
benefits over older antipsychotics, and psychiatric patients will refuse help with insulin using pre-filled syringes or
they are now commonly used to treat diabetes management. State laws vary insulin pens when appropriate.

Downloaded from http://diabetesjournals.org/clinical/article-pdf/20/4/202/497928/0202.pdf by guest on 07 November 2022

many psychiatric conditions, including with regard to the involuntary confine- ✔ Encouraging patients to wear a
agitation in elderly patients with demen- ment and treatment of psychiatric medical alert bracelet or necklace
tia. Patients who use these medications patients who are unable to care for them- that lists diabetes.
should be monitored for hyperglycemia. selves. • In patients for whom tight glucose
However, as this case demonstrates, Concerns about a patient’s capacity control is not realistic, other aspects of
severe, acute derangement of glucose for self-care should be discussed with the diabetes care may be especially impor-
control can occur even when a patient patient and the patient’s psychiatric team. tant, such as treatment of hypertension
has been stable on medication for If appropriate, judicial review of the and hyperlipidemia; regular screening
months to years.5 patient’s situation should be considered. for retinopathy, neuropathy, and
This case also illustrates the chal- nephropathy; and aspirin therapy.
lenges of treating diabetes in patients Clinical Pearls
with severe psychiatric disorders. • Atypical antipsychotics appear to REFERENCES
Members of a multidisciplinary psy- increase the risk of type 2 diabetes by 1
Genuth S: Diabetic ketoacidosis and hyperos-
chiatric team see A.T. several times a inducing weight gain. Less commonly, molar hyperglycemic nonketotic syndrome in
adults. In Therapy for Diabetes Mellitus and Relat-
week. Nevertheless, she has persistent they have been associated with severe ed Disorders. Lebovitz HE, Ed. Alexandria, Va.,
problems with tangential thoughts, hyperglycemia that resolves or American Diabetes Association, p.83–96, 1998
2
poor judgment, and delusions. Despite improves when the medication is Mir S, Taylor D: Atypical antipsychotics and
hyperglycaemia. Int Clin Psychopharmacol
inpatient and outpatient diabetes edu- stopped. 16:63–73, 2001
cation and frequent reinforcement from • Managing diabetes in patients with 3
McIntyre RS, McCann SM, Kennedy SH:
her medical providers, she has been severe psychiatric disorders is espe- Antipsychotic metabolic effects: weight gain, dia-
unable to apply this knowledge in her cially challenging. Although diabetes betes mellitus, and lipid abnormalities. Can J
Psychiatry 46:273–281, 2001
daily life. For example, she can test her education is important, not all patients 4
Ardizzone TD, Bradley RJ, Freeman AM
blood glucose and identify whether the will be capable of applying this infor- 3rd, Dwyer DS: Inhibition of glucose transport in
result is low, acceptable, or high. When mation appropriately. The diabetes PC12 cells by the atypical antipsychotic drugs
risperidone and clozapine, and structural analogs
faced with a low blood glucose, she is treatment plan should be realistic and of clozapine. Brain Res 923:82–90, 2001
able to state that consuming juice and a account for the patient’s situation. 5
Bechara CI, Goldman-Levine JD: Dramatic
snack is advisable. However, she may • Strategies to minimize the risks of worsening of type 2 diabetes mellitus due to olan-
then begin to focus on her desire to treating diabetes in psychiatric zapine after 3 years of therapy. Pharmacotherapy
21:1444–1447, 2001
lose weight or her frustration with dia- patients include:
betes in general and decide not to fol- ✔ Enlisting the help of a caretaker
low any advice for treating the hypo- whenever possible. Marguerite J. McNeely, MD, MPH, is an
glycemia. ✔ Treating mild hyperglycemia with assistant professor in the Division of
Very little is written about managing medications only in carefully General Internal Medicine at the Uni-
diabetes in patients with severe psychi- selected patients. versity of Washington in Seattle.

196 Volume 20, Number 4, 2002 • CLINICAL DIABETES

 C A S E S T U D I E S

Case Study: Necrotizing Fasciitis in a Patient With

Obesity and Poorly Controlled Type 2 Diabetes
Anca M. Avram, MD

Presentation Questions of hours. Frequently, the severity and the

E.N. is a 60-year-old white woman who 1. What is the diagnosis? extent of the infection are not initially

Downloaded from http://diabetesjournals.org/clinical/article-pdf/20/4/202/497928/0202.pdf by guest on 07 November 2022

presented at the hospital with high fever, 2. How should this patient be managed? appreciated. Delay in accurate diagnosis
chills, and severe pain at the base of her 3. What are the microorganisms pro- is associated with poor prognosis.
neck. She was unable to flex or rotate ducing this fulminating infection? In E.N.’s case, surgery revealed
her neck because of pain and swelling. 4. How is the patient predisposed to extensive soft tissue necrosis of the cer-
She recalled that 3 days before admis- developing this condition? vical fascia extending to the carotid
sion, there was an unusually warm win- sheath, with involvement of the right
ter day, and she walked in a nearby park Commentary trapezius and right sternocleidomastoid
enjoying the weather. She recalled an E.N. underwent computed tomography muscle. There was a large quantity of
itching and painful sensation that she (CT) imaging of the neck and chest, necrotic, foul-smelling tissue and thin,
initially attributed to a spider/insect bite which showed extensive gas formation watery, brown discharge (classically
on her upper back, which gradually pro- in the soft tissues of the right back neck described as “dishwater pus”). Gram
gressed to severe pain and swelling over dissecting along the fascial planes stain of necrotic tissue specimens
the next 2 days. toward the front neck and upper back. showed a polymicrobial bacterial popu-
Her medical history was significant Based on clinical presentation and CT lation (many Gram-positive and Gram-
for type 2 diabetes for the past 5 years, images (Figures 1 and 2), E.N. was negative cocci and many Gram-negative
class 2 obesity (body mass index 37.5 diagnosed with necrotizing fasciitis. bacilli), and the culture identified
kg/m2), and hypertension for the past 10 CT diagnostic criteria for necrotiz- staphylococcus epidermidis, streptococ-
years. Her medications were glyburide ing fasciitis are asymmetric fascial cus viridans, bacteroides ureolyticus,
(Micronase), 5 mg twice daily, and vera- thickening associated with fat stranding pseudomonas aeruginosa, proteus
pamil (Calan SR), 240 mg daily. She did and gas tracking along the fascial mirabilis, and enterococcus faecalis.
not smoke or drink alcohol. Her family planes. In advanced cases, the infection E.N. underwent multiple surgical
history was significant for mother with can extend to the adjacent muscles, with debridements and was treated with large
type 2 diabetes and hypertension. gas present within the muscle mass doses of intravenous antibiotics: clin-
At admission, E.N. was febrile (tem- characteristic of myonecrosis. Imaging damycin (Cleocin), 900 mg every 8
perature 40C), tachypneic (respiratory modalities detecting the presence of gas hours, and gentamicin (Garamycin), 450
rate 20), tachycardic (heart rate 120), in the soft tissues are plain radiography mg every 24 hours. Blood cultures were
and hypertensive (blood pressure 164/69 of the involved areas, ultrasonography repeatedly negative. Despite aggressive
mmHg). Physical examination revealed a of the scrotum in the case of Fournier’s surgical and medical management, the
large area of wood-like induration (5  gangrene, CT imaging, and magnetic patient developed septic shock and car-
6 inches) extending from the back of the resonance imaging. CT imaging has the diac arrest, unresponsive to resuscitation
neck forward to the chin and downward advantage of being readily available and attempts.
to the upper back. The skin was darkly offering an excellent depiction of the This case illustrates the evolution of
erythematous, and there was a central extent of soft tissue necrosis and of pos- necrotizing fasciitis, which is a deep and
area of excoriation with yellow crust. sible coexisting deep abdominal or devastating soft tissue infection. In 80%
Admission laboratory studies revealed pelvic abscesses. of cases, the infection develops as an
hemoglobin 13.7 g/dl, white blood count With the diagnosis established, E.N. extension from a skin lesion (i.e., minor
13.6 K/mm3, bands 10%, plasma glucose was immediately taken to the operating abrasion, insect bite, or injection site),
356 mg/dl, and hemoglobin A1c 10.2%. room for incision and debridement. but in 20% of cases, there is no visible
Blood cultures were performed, and the Necrotizing fasciitis is a surgical emer- skin lesion. The etiology can be
patient was treated with high-dose intra- gency because the infection can spread monomicrobial (i.e., group A -hemolyt-
venous antibiotics. in the subcutaneous tissue over a period ic streptococcus pyogenes, staphylococ-

198 Volume 20, Number 4, 2002 • CLINICAL DIABETES

 C A S E S T U D I E S

extensive soft tissue necrosis. Early and

aggressive surgical debridement of all
involved tissues, combined with combi-
nation intravenous antibiotic therapy
with broad spectrum coverage, is the
cornerstone of therapy.
Early diagnosis based on clinical
presentation and imaging modalities is
essential in initiating medical and surgical
treatment. In the absence of rapid control
of the spread of the infection, necrotizing
fasciitis progresses to disseminated vas-

Downloaded from http://diabetesjournals.org/clinical/article-pdf/20/4/202/497928/0202.pdf by guest on 07 November 2022

cular coagulation, septic shock, and death
(cumulative mortality rate 34%).

Clinical Pearls
• Necrotizing fasciitis is a severe soft
Figure 1. Extensive gas formation in the soft tissues of the right posterior neck dis- tissue infection occurring in patients
secting along the fascial planes toward the anterior neck and upper back. with diabetes, morbid obesity, alco-
holism, advanced atherosclerotic dis-
ease, and decubitus ulcers.
• Early diagnosis is essential for
patients’ survival.
• CT imaging is very useful in identify-
ing the presence of gas in soft tissues
and gas tracking along the fascial
planes.
• Aggressive surgical debridement and
combination, broad-spectrum cover-
age intravenous antibiotic therapy are
the cornerstones of therapy.

SUGGESTED READINGS
Gonzalez MH: Necrotizing fasciitis and gan-
grene of the upper extremity. Hand Clinics
14:635–645, 1998
McArdle P, Gallen I: Necrotising fasciitis in
diabetics. Lancet 348:552, 1996
Figure 2. Soft tissue gas tracking along the cervical fascia and extending to the McHenry CR, Piotrowski JJ, Petrinic D,
Malangoni MA: Determinants of mortality for
right carotid sheath. Gas present within the right sternocleidomastoid and trapezius necrotizing soft tissue infections. Ann Surg
muscles is characteristic of myonecrosis. 221:558–565, 1995
Rajbhandari SM, Wilson RM: Unusual infec-
tions in diabetes. Diabetes Res Clin Pract
cus aureus, or peptostreptococcus) or necrotizing fasciitis by the tissue hypox- 39:123–128, 1998
polymicrobial (mixed aerobe and anaer- ia caused by arteriosclerosis and the
Wysoki MG, Santora TA, Shah RM, Fried-
obe bacteria). Risk factors for develop- immunodeficiency associated with poor man AC: Necrotizing fasciitis: CT characteristics.
ing necrotizing fasciitis are uncontrolled glycemic control. Neutrophil chemo- Radiology 203:859–863, 1997
diabetes, alcoholism, morbid obesity, taxis, adherence, phagocytosis, and intra-
advanced atherosclerotic disease, and cellular oxidative killing have been
decubitus ulcers. shown to be defective in diabetes. Anca M. Avram, MD, is a fellow in the
Diabetes is the underlying illness in The pathological hallmark of necro- Division of Endocrinology and Metabo-
half of all cases of necrotizing fasciitis. tizing fasciitis is thrombosis of subcuta- lism at the University of Michigan in
Diabetic patients may be predisposed to neous arteries and arterioles leading to Ann Arbor.

200 Volume 20, Number 4, 2002 • CLINICAL DIABETES

 C A S E S T U D I E S

Case Study: A Woman With Type 2 Diabetes and

Severe Hypertriglyceridemia Sensitive to
Fat Restriction
Deborah Thomas-Dobersen, RD, MS, CDE

Downloaded from http://diabetesjournals.org/clinical/article-pdf/20/4/202/497928/0202.pdf by guest on 07 November 2022

Presentation Questions terol Education Program (NCEP III)
L.S. is a 52-year-old Caucasian woman 1. What nutritional modification would guidelines, the first goal for this patient
who was diagnosed with type 2 diabetes be effective in rapidly lowering is to lower triglycerides to prevent pan-
in 1988. She developed hypertriglyc- serum triglycerides when the patient creatitis, which not only can result in
eridemia 3 years later and hypertension is at risk of pancreatitis? hospitalization, but also is potentially
9 years later. Other medical problems 2. What treatment strategies can be lethal.4 Although L.S. is already on the
include obesity and diverticulosis. She employed to lower triglycerides, and maximum dose of gemfibrozil, her
presents now for screening to determine how effective are they? triglycerides are still inadequately con-
eligibility for a clinical research protocol 3. How can nutritional modifications trolled.
using once-daily insulin. improve insulin resistance? With triglycerides in this range, she
Physical exam reveals a height of 64 should be alerted immediately to the fact
inches, a weight of 181 lb, a body mass Discussion that any alcohol, even that found in over-
index of 31 kg/m2, and a waist circum- Type 2 diabetes carries a two- to four- the-counter cold remedies can trigger
ference of 40 inches. Blood pressure, fold excess risk of coronary heart dis- pancreatitis until her serum triglycerides
well controlled on 20 mg lisinopril ease. The most common pattern of dys- are brought down to a safer range (<500
(Prinivil) daily, is 104/70 mmHg. lipidemia in patients with type 2 dia- mg/dl). In addition, a single high-fat
Laboratory results reveal a fasting betes is elevated triglycerides and meal can also trigger pancreatitis.
lipid panel as follows: total cholesterol decreased HDL levels.1 Although coex- A severely restricted fat intake
214 mg/dl, triglycerides 940 mg/dl, istent increases in small, dense LDL (<10% of daily kcal) can effectively
direct HDL cholesterol 24 mg/dl, an cholesterol particles—not the triglyc- bring down serum triglycerides by 20%
invalid LDL cholesterol unobtainable erides themselves—may be responsible per day until triglycerides are <500
because of the hypertriglyceridemia, for the increase in cardiovascular risk, mg/dl. A diet in which fat is so severely
and a free fatty acid of 1.1 mEq/l (nor- hypertriglyceridemia poses a significant restricted usually brings about weight
mal range 0.1–0.6 mEq/l). Hemoglobin burden on society.2 loss as well. A loss of 2.5 kg body
A1c (A1C) is 9.5%, and fasting blood In type 2 diabetes, characterized by weight would bring an expected 15–20%
glucose (FBG) is 304 mg/dl. When insulin resistance and insulin deficiency, decrease in serum triglycerides. In addi-
called to discuss the finding of severe the pathophysiology of hypertriglyc- tion, aerobic exercise can help to lower
hypertriglyceridema, the patient com- eridemia is an increased hepatic produc- serum triglycerides by 10–15%.2
mented that she had previously had fast- tion of triglycerides as well as a Interventions to further decrease
ing triglycerides as high as 3,000 mg/dl. decreased lipoprotein lipase activity serum triglycerides to <200 mg/dl,
L.S. is currently taking metformin leading to slower breakdown of VLDL increase HDL to 45 mg/dl, and decrease
(Glucophage), 1,000 mg twice daily, and cholesterol and chylomicrons.3 The LDL to <100 mg/dl should be attempted
glipizide (Glucatrol XL), 10 mg twice American Diabetes Association (ADA) to decrease the risk of coronary heart
daily, to control her blood glucose. She Clinical Practice Recommendations list disease.
is also on gemfibrizol (Lopid), 600 mg serum triglycerides ≥400 mg/dl and an At the first clinic visit, L.S. was
twice daily, for hypertriglyceridemia and HDL level <45 mg/dl for women as advised of the risk of pancreatitis and
estradiol (Estraderm) for menopause indicative of high risk of coronary heart advised to forego any alcohol and to
(topical estrogen does not induce hyper- disease.1 adhere to severe fat restriction until she
triglyceridemia). By both ADA and National Choles- has a fasting serum triglyceride level

202 Volume 20, Number 4, 2002 • CLINICAL DIABETES

 C A S E S T U D I E S

<400 mg/dl. She and her husband are Commonly, controlling hyper- empowerment approach through which
both from the South, and their traditional glycemia leads to a decrease in triglyc- patients are the primary decision makers
Southern fare used quite a bit of salt erides.1 However, in this patient, the is important.
pork, which deleteriously augmented the clearing of serum triglycerides, the Although lifestyle changes are
saturated as well as total fat in her diet. restricted saturated fat, and the weight always recommended as first-line thera-
She had been advised to “watch her loss had a substantial impact on improv- py, the approach to helping patients
weight” when her triglycerides were in ing glucose tolerance without adding achieve these lifestyle changes in busy
the 3,000 mg/dl range, but she had been further diabetes oral agents. Studies office practices is too often insufficient.
unable to follow that recommendation. have shown that dietary fat, primarily A new Medicare benefit effective Janu-
Between clinic visits, L.S. was given saturated fat, has adverse effects on ary 2002 allows patients with diabetes
written information about a low-fat (10% insulin sensitivity.5 Restricting fat access to insurance coverage for MNT.
of kcal) diet, including lists of foods to intake, especially saturated fat, resulted Evidence-based research shows that

Downloaded from http://diabetesjournals.org/clinical/article-pdf/20/4/202/497928/0202.pdf by guest on 07 November 2022

restrict and foods to encourage until a in a better metabolic profile in regard to MNT provided by a registered dietitian
more thorough meal plan could be devel- both glucose tolerance and fasting experienced in the management of dia-
oped based on an assessment of her pre- serum triglycerides. betes is clinically effective.6
vious dietary patterns. She was advised Lifestyle changes had been recom-
that this was a short-term, severe dietary mended previously; why was L.S. suc- Clinical Pearls
change. She had already instituted an cessful this time when she hadn’t been • Reducing dietary fat improves body
exercise program, walking for 1 hour, before? The patient offered the following weight, which in turn improves glu-
five times a week regularly. comments when asked this question. cose tolerance and hypertriglyc-
Two weeks later, when L.S. returned eridemia.7–9
to clinic after following the suggested fat • “I was handed written information, • There is evidence that saturated fat
restriction, her lab results showed the but concern about the numbers may elevate plasma glucose by way of
following lipid profile: serum total cho- (hypertriglyceridemia) was never con- increasing insulin resistance.
lesterol 193 mg/dl, serum triglycerides veyed.” • MNT for hypertriglyceridemia may be
355 mg/dl, direct HDL cholesterol 32 • “They tell you what you need to do, divided into three parts:
mg/dl, and LDL cholesterol 90 mg/dl. but not how or why to do it.” 1. When fasting triglycerides are
Her A1C had dropped to 8.8% with no • “No one sat down and talked with me. ≥1,000 mg/dl, restrict dietary fat to
change in therapy for her diabetes, and I never received individualized atten- 10% of kcal until fasting triglyc-
her FBG was 158 mg/dl. Her fasting free tion.” erides fall to <500 mg/dl.
fatty acid level was 0.7 mEq/l. Her • “If my triglycerides were potentially 2. For fasting triglycerides between
weight had dropped by 3 lb. harmful, why did they not see me 1,000 and 500 mg/dl, a) reduce
At this visit, medical nutrition thera- sooner than 3 months? Three months saturated fat to <7% of energy and
py (MNT) was initiated, and the patient was the usual time between visits and dietary cholesterol to 200 mg/day;
was put on 10 units of 75/25 insulin again they conveyed no concern.” b) increase viscous (soluble) fiber
before dinner. to 10–25 mg/day; c) encourage
Six weeks later, her A1C had In previous attempts to encourage this modest weight loss (5–7% of body
dropped further, to 7%, her FBG was patient make lifestyle changes, the com- weight); and d) increase physical
110 mg/dl, and her weight was down pliance approach was used, but the ben- activity.10 Monounsaturated fats or
another 2 lb. Her lipid profile was as efits of self-care, the costs of not com- carbohydrates can be used to sub-
follows: total cholesterol 181 mg/dl, plying, the susceptibility to pancreatitis stitute for the decrease in saturated
triglycerides 299 mg/dl, direct HDL and cardiovascular disease, and the fats.
cholesterol 32 mg/dl, and LDL choles- severity of such elevated triglycerides 3. For fasting triglycerides <500
terol 89 mg/dl. Her fasting free fatty were not conveyed. A referral to an edu- mg/dl, encourage weight loss and
acid level was now 0.6 mEq/l, the upper cator, time spent in assessing eating pat- a decrease in simple sugars in
level of normal. Meal plan records terns and teaching alternatives, and more addition to the above reduction in
showed that she was consuming ~1,500 frequent visits or follow-up serve to con- saturated fat.
kcal/day and getting ~25% of daily kcal vey the importance of recommended
from fat. lifestyle changes. MNT coupled with an Continued on page 216

CLINICAL DIABETES • Volume 20, Number 4, 2002 203