Journal Pre-proof

Case Report: Plasmapheresis as an early treatment for Severe Hypertriglyceridemia,

Acute Pancreatitis, and Diabetic Ketoacidosis

Ayesha Monga Kravetz, Pooja Sanghavi, Vidit Bhargava, Run Zhang Shi, Laura M.
Nally
PII: S2376-0605(21)00049-3
DOI: https://doi.org/10.1016/j.aace.2021.03.009
Reference: ACCR 93

To appear in: AACE Clinical Case Reports

Received Date: 7 January 2021

Revised Date: 8 March 2021
Accepted Date: 24 March 2021

Please cite this article as: Kravetz AM, Sanghavi P, Bhargava V, Shi RZ, Nally LM, Case Report:
Plasmapheresis as an early treatment for Severe Hypertriglyceridemia, Acute Pancreatitis, and Diabetic
Ketoacidosis, AACE Clinical Case Reports (2021), doi: https://doi.org/10.1016/j.aace.2021.03.009.

This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition
of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of
record. This version will undergo additional copyediting, typesetting and review before it is published
in its final form, but we are providing this version to give early visibility of the article. Please note that,
during the production process, errors may be discovered which could affect the content, and all legal
disclaimers that apply to the journal pertain.

© 2021 Published by Elsevier Inc. on behalf of the AACE.

 Case Report:

Plasmapheresis as an early treatment for Severe

Hypertriglyceridemia, Acute Pancreatitis, and Diabetic
Ketoacidosis
5 Ayesha Monga Kravetza,b, Pooja Sanghavic , Vidit Bhargavad, Run Zhang Shie , Laura M. Nallyb,f

a Frank H. Netter MD School of Medicine, North Haven, CT, United States

b Department of Pediatrics, Division of Pediatric Endocrinology, Yale University School of

of
10 Medicine, New Haven, CT, United States

ro
cDepartment of Pediatrics, Stanford University School of Medicine, Stanford, CA, United States

15 Medicine, Stanford, CA, United States

-p
dDepartment of Pediatrics, Division of Pediatric Intensive Care, Stanford University School of
re
eDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, United States
lP

f Department of Pediatrics, Division of Pediatric Endocrinology, Stanford University School of

20 Medicine, Stanford, CA, United States
na

Short Title: Plasmapheresis treatment for Severe Hypertriglyceridemia, Acute Pancreatitis, and
Diabetic Ketoacidosis
ur

Corresponding Author:
Jo

25 Laura M. Nally
Department of Pediatrics
Yale University School of Medicine
Pediatric Diabetes Research Program, One Long Wharf Drive, Suite 503
New Haven, CT, 06511, United States
30 Tel: 203-785-5831
E-mail: laura.nally@yale.edu
Number of Tables: 2, Number of Figures: 1, Word count: 1583
Keywords: pediatric diabetes, diabetes mellitus type 1, lipid metabolism, severe
hypertriglyceridemia, acute pancreatitis, plasmapheresis, diabetic ketoacidosis
35
 Abstract (215/250 words)

Background: Severe hypertriglyceridemia (plasma triglycerides >1000 mg/dL) is a rare but

serious complication in children who develop diabetic ketoacidosis (DKA) from uncontrolled or

new onset type 1 diabetes mellitus (T1D).

40 Case Presentation: We present the case of a severely malnourished 16-year-old with a 10-

month history of presumed type 2 diabetes mellitus (T2D) managed with lifestyle modifications

and Metformin, who presented with severe hypertriglyceridemia (SHTG), acute pancreatitis, and

of
DKA. On examination, there was no evidence of lipemia retinalis, cutaneous xanthomas, or

ro
xanthelasma. He was initially treated with an insulin infusion and intravenous fluids. Despite this

45 treatment, his pancreatitis symptoms and lipase worsened, necessitating 2 courses of

-p
plasmapheresis; this treatment led to immediate resolution of his symptoms and dramatic
re
improvement of his overall clinical status. He was discharged on hospital day 5. During his
lP

hospital admission, ICA-512, insulin, GAD-65, and ZnT8 autoantibodies were positive in the
na

presence of insulinopenia, consistent with T1D. Hypertriglyceridemia and hypercholesterolemia

50 did not recur during follow up, suggesting that the underlying mechanism for SHTG was insulin
ur

deficiency.
Jo

Conclusions: This report of SHTG, DKA, and pancreatitis in an adolescent highlights the safe,

early initiation of plasmapheresis as effective treatment. To our knowledge, plasmapheresis has

rarely been used so early on in the course of treatment for an adolescent with SHTG, DKA, and

55 acute pancreatitis.

Keywords: type 1 diabetes, diabetic ketoacidosis, severe hypertriglyceridemia, acute

pancreatitis, plasmapheresis

60
 Introduction
Diabetic ketoacidosis (DKA) is a serious metabolic complication of uncontrolled type 1

diabetes (T1D) and, rarely, type 2 diabetes (T2D) [1]. DKA is defined as hyperglycemia,

ketonemia or moderate or large ketonuria, and metabolic acidosis occurring from insulin

65 deficiency [1]. Severe hypertriglyceridemia (triglycerides >1000 mg/dL) and pancreatitis

secondary to severe hypertriglyceridemia (SHTG) are very rare but serious complications in

pediatric patients with DKA. While standard treatment of SHTG involves intravenous fluids and

of
insulin infusion, plasmapheresis is rarely reported in the pediatric literature with this clinical triad

[2, 3]. We present our experience with laboratory discrepancies that complicated the diagnosis

ro
70 and with the utilization of plasmapheresis early in the disease course, which led to rapid

stabilization of the patient and early discharge.

-p
re
Case Presentation
lP

A 16-year-old Hispanic male presented to his physician with decreased appetite and

foul-smelling urine. His BMI was 17.2 kg/m2 (7%ile), point of care glucose level was 283 mg/dL
na

75 and urine dipstick was positive for glucose and ketones. Despite ketonuria, he was diagnosed
ur

with T2D and initially managed with lifestyle modifications. Three months after his initial
Jo

presentation, his HbA1c reached 8.6% (<5.7%), and he was started on Metformin. A fasting lipid

panel was normal (cholesterol 146 mg/dL (<170 mg/dL), high-density lipoprotein (HDL) 58

mg/dL (>40 mg/dL), low-density lipoproteins (LDL) 66 mg/dL (<110 mg/dL), very-low density

80 lipoprotein (VLDL) 22 mg/dL, and triglycerides 111 mg/dL (<90 mg/dL)). The family reported

excellent compliance with Metformin and dietary modifications.

Ten months after his diagnosis, he presented to the emergency room with severe

malnutrition, nausea, vomiting, and abdominal pain for 4 days and worsening hyperglycemia

over 3 weeks (glucose levels 200-300 mg/dL). His weight on admission was 47 kg (2%ile) and

85 BMI 15 kg/m2 (<1%ile). Pertinent family history included a father with hypercholesterolemia and

T2D diagnosed at age 37 and managed with metformin, as well as a paternal uncle and
 paternal grandmother with T2D. There was no family history of myocardial infarction, early

stroke, or pancreatitis.

On exam, the patient had moderate abdominal tenderness in both upper quadrants. He

90 was alert and oriented, with no focal neurological deficits. He had no eruptive cutaneous

xanthomas, lipemia retinalis, tuberous xanthomas, or palmar crease xanthomas. Laboratory

results showed mild acidosis based on an arterial blood gas (ABG) with pH 7.32 (7.35-7.45),

however a metabolic panel revealed bicarbonate 8 mmol/L (20-30 mmol/L) (Table 1). A

of
urinalysis was positive for glucose and ketones. His blood was noted to be milky, prompting

ro
95 additional testing that revealed severely elevated triglycerides 28,040 mg/dL with elevated

cholesterol, LDL, and ALT. A repeat lipase showed increase from 40 U/L to 744 U/L over the
-p
course of a few hours, suggesting acute pancreatitis. Alcohol and drug testing were not
re
completed due to low suspicion in this patient. Medications known to cause pancreatitis or
lP

hypertriglyceridemia were also excluded. He received 1 L of intravenous (IV) fluids and

na

100 morphine for pain.

Upon arrival to the pediatric intensive care unit, pH decreased to 7.23, despite fluid
ur

resuscitation. His β-hydroxybutyrate level was 8.9 mmol/L (0.2-0.8 mmol/L), c-peptide 0.2 ng/mL
Jo

(0.8-4.0 ng/mL), and insulin <1 µIU/mL (<20 µIU/mL). He continued to have elevated liver

enzymes, with aspartate aminotransferase 80 U/L (<40 U/L) and alanine transaminase 420 U/L

105 (<60 U/L). HbA1c returned elevated to 12.9%. An abdominal ultrasound showed an abnormal,

enlarged, inhomogeneous pancreas and no evidence of hepatosplenomegaly or gallstones.

W ith an elevated anion gap acidosis and ketones raising concern for DKA, he received

IV hydration and was started on a Regular insulin infusion at 0.1 U/kg/hr that was increased to

0.15 U/kg/hr the following morning when triglycerides did not improve (Figure 1). Twenty hours

110 after initiating DKA therapy, his triglyceride levels remained >2,000 mg/dL and his lipase levels

remained elevated at 768 U/ L. His abdominal pain acutely worsened and was no longer
 controlled by narcotic medications. As a result, 21 hours after admission he received his first

course of plasmapheresis, dramatically decreasing triglycerides to 451 mg/dL and improving his

pain. He received a second course of plasmapheresis at 40 hours based on current practice

115 guidelines [4], which decreased triglycerides to 69 mg/dL. He started a low-fat diet 42 hours

after admission, which he tolerated well. While clinically stable for discharge, he remained

inpatient for 2 additional days to receive diabetes education and initiation of insulin, and was

discharged on hospital day 5. Diabetes autoantibodies returned positive for ICA-512, insulin,

of
GAD-65, and ZnT8, confirming a diagnosis of T1D. Hypertriglyceridemia did not recur during 19

ro
120 months of follow up.

Discussion
-p
The exact mechanisms involved in the triad of DKA, SHTG, and acute pancreatitis are
re
not entirely understood. As observed in our patient, patients with DKA have abnormal glucose
lP

and lipid metabolism that can result in hypertriglyceridemia [5]. Insulin deficiency prevents the
na

125 synthesis of lipoprotein lipase, an enzyme that hydrolyzes triglycerides in lipoproteins into free

fatty acids and glycerol [6, 7, 8]. Therefore, during DKA, increased fat mobilization by activation
ur

of lipolysis and inhibition of lipoprotein lipase leads to an increase in triglycerides [7, 9]. Insulin
Jo

also promotes storage of free fatty acids into adipocytes, preventing high concentrations of

potentially toxic free fatty acids in the plasma. Acute pancreatitis secondary to SHTG may be

130 explained by elevated concentrations of cell-damaging free fatty acids produced from the

hydrolysis of triglycerides by pancreatic lipase [10].

While there are various primary causes of SHTG, including polygenic and monogenic

disorders of hypertriglyceridemia, in our patient, there was strong support for insulin deficiency

as the cause given his hyperglycemia, a severely elevated β-hydroxybutyrate level, and a low

135 bicarbonate level. However, his initial bicarbonate level did not correlate with the pH, leading to

uncertainty about the presence of metabolic acidosis. Additionally, triglyceride levels reaching

40,176 mg/dL due to uncontrolled T1D is not commonly seen. Given the likelihood of DKA,
 treatment with insulin infusion and hydration was initiated. After rehydration, arterial pH levels

met the diagnostic criteria for DKA and insulin infusion was continued. When triglyceride levels

140 did not significantly improve, the insulin infusion was increased further. However, triglyceride

levels remained severely elevated, and the patient had worsening acute pancreatitis symptoms,

prompting plasmapheresis.

There are no clear guidelines in the literature on managing the triad of DKA, SHTG, and

acute pancreatitis in the pediatric population [11]. In patients with SHTG, immediate lowering of

of
145 triglycerides is possible with insulin infusion [6]. Additionally, previous pediatric case reports on

ro
this clinical triad have noted reductions of triglyceride levels with IV fluids and insulin therapy

alone (Table 2) [12, 13, 14, 15, 16, 17, 18, 19, 20, 21]. However, a study by Richardson et al.
-p
[11], noted that in pediatric patients with SHTG, diabetes and/or DKA who received IV insulin,
re
the average time for triglycerides to decline to <1,000 mg/dL was 3 days and to decline to <500
lP

150 mg/dL was 23.8 days. The first reported case of plasmapheresis in a pediatric patient with DKA,
na

SHTG, and acute pancreatitis was prompted by renal insufficiency, while the second one was

prompted by altered mental status [2, 3]. In our patient, the acute increase in severe abdominal
ur

pain unresponsive to narcotics and lack of responsiveness to hydration and insulin led to
Jo

initiation of plasmapheresis, avoiding risks of prolonged SHTG (i.e., stroke, ischemia, infection).

155 The risks of plasmapheresis, including stroke, ischemia, infection, and anaphylaxis, were also

considered by the team.

To our knowledge, only 13 cases of pediatric DKA, hypertriglyceridemia, and pancreatitis

have been reported to date (Table 2). As previously mentioned, treatment for pediatric patients

with the triad of DKA, SHTG, and acute pancreatitis has focused on IV fluids and insulin

160 therapy; however, two patients with this triad have been successfully treated with

plasmapheresis, resulting in triglyceride reduction and significant improvement of clinical status

[2, 3]. The longest reported hospital stay for the triad was 20 days [21], while the shortest stay

was 5 days [12]. In our case, early initiation of plasmapheresis, stabilized the patient for
 discharge on day 3, preventing significant morbidity. The remaining 2 days in the hospital were

165 devoted to diabetes education and initiating insulin therapy.

As alluded to previously, this case presented some challenges in the diagnosis of DKA.

Severely elevated triglyceride levels may artificially elevate or lower other laboratory results,

requiring cautious interpretation [22, 23, 24]. The patient’s initial ABG did not strictly meet

diagnostic criteria for the diagnosis of DKA. However, a metabolic panel revealed a low

170 bicarbonate, an anion gap, and significantly elevated β-hydroxybutyrate and ketones, which was

of
consistent with DKA. When interpreting laboratory results in the setting of SHTG, it is important

ro
to recognize that hypertriglyceridemia can falsely lower bicarbonate levels [22, 23, 24] through a

“space occupying effect” in which the volume displaced by lipids causes a decrease in the
-p
aqueous phase of the sample. This interference can occur with both the enzymatic and the
re
175 indirect ion-selective electrode methods [23]. The discordance between pH and bicarbonate
lP

values presented an initial challenge in determining the severity of DKA and safest course of
na

treatment. In this case, the safest option was to treat the patient for presumed DKA.

Severe hypertriglyceridemia can also result in pseudonormoglycemia when measuring

ur

blood glucose levels using a glucometer. As explained by the space occupying effect, with
Jo

180 triglycerides accounting for approximately 1/3 of our patient’s blood volume, this artificially

decreased the blood sugar concentration detected on his home glucometer. Therefore, patients

with diabetes and SHTG may delay checking for ketones and seeking medical care, along with

delayed diagnosis of DKA [24]. In the outpatient setting, practitioners should cautiously interpret

glucose readings if a patient has suspected SHTG, as they are likely to underestimate the true

185 glucose concentration. Apart from aforementioned tests impacted by hypertriglyceridemia,

including glucose and bicarbonate, other spectrophotometric method-based tests may also be

affected. In the context of this case report, tests such as AST and ALT may be severely

affected, and results should be interpreted with caution. The “space occupying effect” of severe

hypertriglyceridemia will inevitably impact electrolyte readings by the indirect ion-selective

190 electrode methods, most significantly affecting sodium results, the so-called

pseudohyponatremia. Retesting by using a direct method measuring electrolyte activity, such as

the blood gas instrument, would provide accurate results and guide clinical IV fluid decisions.

When considering plasmapheresis in the clinical triad, hydration and insulin should be

the first therapeutic steps, as resolution of DKA can generally improve SHTG [9]. Based on our

195 experience, once DKA resolves, it may be beneficial to initiate plasmapheresis in the treatment

of SHTG and acute pancreatitis, especially if the clinical status deteriorates. In our case,

of
therapeutic plasma exchange was initiated early and appropriately in the course of acute

ro
pancreatitis, which led to faster resolution of symptoms, advancement of diet, and early

discharge [25]. The best candidates for plasmapheresis may be those with severe acute

200
-p
pancreatitis, triglyceride levels ≥1000 mg/dL after initial resuscitation with IV fluids, and those
re
with signs of organ failure [26]. The ideal timing for initiation of apheresis is within 24 to 96 hours
lP

after the onset of symptoms and after glycemic control measures have been initiated. With
na

limited data on its use, pediatric randomized controlled trials are needed to determine if

plasmapheresis is an effective and safe tool in the management of SHTG, DKA, and
ur

205 pancreatitis.
Jo

210
 Declarations

215 Ethics approval and consent to participate

Ethics approval and consent was not required to publish this case report by our institutional

review board.

Consent for Publication

The case report was discussed with the mother and all questions were answered. Verbal

220 informed consent to publish was given to the corresponding author by the patient’s mother.

of
Availability of data and material

ro
All of the data presented in the study is available and can be verified through the patient’s

electronic medical record.

Competing Interests
-p
re
225 The authors declare that there is no conflict of interest.
lP

Funding
na

This manuscript was supported by National Institutes of Health Grant K12 DK094714. The

content is solely the responsibility of the authors and does not necessarily represent the official
ur

view of the NIH.

Jo

230 Author’s Contributions

L.M.N. and V.B. conceived of and presented the idea. A.M.K., P.S., V.B., L.M.N. performed an

extensive literature search. L.M.N. collected the patient data. A.M.K. and L.M.N. drafted the

manuscript and designed the figure. R.Z.S. reviewed and edited the manuscript. All authors

approved the manuscript for publication.

235
 References

1 Wolfsdorf JI, Glaser N, Agus M, Fritsch M, Hanas R, Rewers A, et al. ISPAD Clinical Practice

Consensus Guidelines 2018: Diabetic ketoacidosis and the hyperglycemic hyperosmolar state.

Pediatr Diabetes. 2018;19 Suppl 27:155-77.

240

2 Lutfi R, Huang J, Wong HR. Plasmapheresis to treat hypertriglyceridemia in a child with

diabetic ketoacidosis and pancreatitis. Pediatrics. 2012;129(1):e195-8.

of
ro
3 Lee JM, Razavi A, Le AV, Williams R. Severe hypertriglyceridemia: a rare and harmful

245 complication in diabetic ketoacidosis, treated successfully with plasmapharesis. Pediatrics.

2019;144(2 MeetingAbstract):390-390.
-p
re
lP

4 Schwartz J, Padmanabhan A, Aqui N, Balogun RA, Connelly-Smith L, Delaney M, et al.

na

Guidelines on the Use of Therapeutic Apheresis in Clinical Practice-Evidence-Based Approach

250 from the Writing Committee of the American Society for Apheresis: The Seventh Special Issue.
ur

J Clin Apher. 2016;31(3):149-62.

Jo

5 Simons-Linares CR, Jang S, Sanaka M, Bhatt A, Lopez R, Vargo J, et al. The triad of diabetes

ketoacidosis, hypertriglyceridemia and acute pancreatitis. How does it affect mortality and

255 morbidity?: A 10-year analysis of the National Inpatient Sample. Medicine (Baltimore).

2019;98(7):e14378.

6 Poonuru S, Pathak SR, Vats HS, Pathak RD. Rapid reduction of severely elevated serum

triglycerides with insulin infusion, gemfibrozil and niacin. Clin Med Res. 2011;9(1):38-41.

260
 7 Sharma PK, Kumar M, Yadav DK. Severe Hypertriglyceridemia Causing Pancreatitis in a

Child with New-onset Type-I Diabetes Mellitus Presenting with Diabetic Ketoacidosis. Indian J

Crit Care Med. 2017;21(3):176-8.

265 8 Hahn SJ, Park JH, Lee JH, Lee JK, Kim KA. Severe hypertriglyceridemia in diabetic

ketoacidosis accompanied by acute pancreatitis: case report. J Korean Med Sci.

2010;25(9):1375-8.

of
ro
9 Donelli D, Morini L, Trenti C, Santi R, Arioli D, Negri EA. Plasma Exchange for the Treatment

270 of Transient Extreme Hypertriglyceridemia Associated with Diabetic Ketoacidosis and Acute
-p
Pancreatitis. Eur J Case Rep Intern Med. 2018;5(5):000853.
re
lP

10 Yang F, Wang Y, Sternfeld L, Rodriguez JA, Ross C, Hayden MR, et al. The role of free fatty
na

acids, pancreatic lipase and Ca+ signalling in injury of isolated acinar cells and pancreatitis

275 model in lipoprotein lipase-deficient mice. Acta Physiol (Oxf). 2009;195(1):13-28.

ur
Jo

11 Richardson T, Aslibekyan S, Ashraf AP. Clinical Characteristics and Sequelae of Severe

Hypertriglyceridemia in Pediatrics. Endocr Pract. 2018;24(9):789-95.

280 12 Bouchaala K, Bahloul M, Bradii S, Kallel H, Chtara K, Bouaziz M. Acute Pancreatitis Induced

by Diabetic Ketoacidosis with Major Hypertriglyceridemia: Report of Four Cases. Case Rep Crit

Care. 2020;2020:7653730.

13 Zaher FZ, Boubagura I, Rafi S, Elmghari G, Elansari N. Diabetic Ketoacidosis Revealing a

285 Severe Hypertriglyceridemia and Acute Pancreatitis in Type 1 Diabetes Mellitus. Case Rep

Endocrinol. 2019;2019:8974619.
 14 Yagnik PJ, Desai PH, Modem VM. Hypertriglyceridemia with Acute Pancreatitis in Pediatric

Diabetic Ketoacidosis: A Case Report. Cureus. 2019;11(1):e3844.

290

15 Sharma PK, Kumar M, Yadav DK. Severe Hypertriglyceridemia Causing Pancreatitis in a

Child with New-onset Type-I Diabetes Mellitus Presenting with Diabetic Ketoacidosis. Indian J

Crit Care Med. 2017;21(3):176-8.

of
ro
295 16 Aboulhosn K, Arnason T. Acute pancreatitis and severe hypertriglyceridaemia masking

unsuspected underlying diabetic ketoacidosis. BMJ Case Rep. 2013;2013.

-p
re
17 Wolfgram PM, Macdonald MJ. Severe Hypertriglyceridemia Causing Acute Pancreatitis in a
lP

Child with New Onset Type I Diabetes Mellitus Presenting in Ketoacidosis. J Pediatr Intensive

300
na

Care. 2013;2(2):77-80.
ur

18 Rodriguez Santana Y, Nimo Roman A, Garcia Saez I, Lopez Alvarez JM, Consuegra Llapur
Jo

E, Gonzalez Jorge R. Treatment of severe hypertriglyceridemia with continuous insulin infusion.

Case Rep Crit Care. 2011;2011:293917.

305

19 Slyper AH, Wyatt DT, Brown CW. Clinical and/or biochemical pancreatitis in diabetic

ketoacidosis. J Pediatr Endocrinol. 1994;7(3):261-4.

20 Winter RJ, Herr TJ, Stone NJ, Traisman HS. Diabetic lipemia in childhood diabetic

310 ketoacidosis: a clue to coexisting acute pancreatitis. Diabetes Care. 1980;3(6):706-7.

 21 Cywinski JS, Walker FA, White H, Traisman HS. Juvenile diabetes mellitus associated with

acute pancreatitis. Acta Paediatr Scand. 1965;54(6):597-602.

315 22 Cartier JL, Look DC, Dunn JP. PSEUDOHYPOBICARBONATEMIA IN A PATIENT

PRESENTING WITH SUSPECTED DIABETIC KETOACIDOSIS. AACE Clinical Case Reports.

2018;4(2):e108-e11.

of
23 Rifkin SI, Shaub B. Factitious hypobicarbonatemia associated with profound hyperlipidemia.

ro
320 Ren Fail. 2014;36(7):1155-7.

-p
24 Rumbak MJ, Hughes TA, Kitabchi AE. Pseudonormoglycemia in diabetic ketoacidosis with
re
elevated triglycerides. Am J Emerg Med. 1991;9(1):61-3.
lP

325
na

25 Zhang KY, Cox KL, Sellers ZM. Plasmapheresis for Hypertriglyceridemia-Induced Acute

Pancreatitis in a Child: A Case Report and Brief Review of the Literature. Pancreas.
ur

2017;46(7):e58-e9.
Jo

26 Click B, Ketchum AM, Turner R, Whitcomb DC, Papachristou GI, Yadav D. The role of

330 apheresis in hypertriglyceridemia-induced acute pancreatitis: A systematic review.

Pancreatology. 2015;15(4):313-20.
Table 1. Laboratory results upon arrival to the ER with reference ranges.

Laboratory Test (Reference Range)

of
ro
-p
re
lP
na
ur
Jo
 Table 2. Reported cases of hypertriglyceridemia, diabetic ketoacidosis, and pancreatitis, including patient presentation,
treatment, and length of hospital stay. F indicates female; M indicates male.
340
Title (year)

of
ro
-p
re
lP
na
ur
Jo
(2017) [15]

Acute pancreatitis
and severe
hypertriglyceridemia
masking unsuspected
underlying diabetic
ketoacidosis (2013)
[16]

of
ro
-p
re
lP
na
ur
Jo
345 Figure 1. Triglyceride levels, noted in mg/dL, during the patient’s hospital stay are shown. The

treatments that the patient received are also noted.

of
ro
-p
re
lP
na
ur
Jo
Jo
ur
na
lP
re
-p
ro
of
 Teaching Points

• Πλασµ απηε ρε σισ ισ σαφε ωηε ν ινιτιατε δ ε αρλψ ιν τηε τρε ατµ ε ντ οφ αδολε σχε ντσ ωηο

πρε σε ντ ωιτη σε ϖε ρε ηψπε ρτριγ λψχε ριδε µ ια, αχυτε πανχρε ατιτισ, ανδ διαβε τιχ

κε τοαχιδοσισ.

5 • Ω ηε ν ιντε ρπρε τινγ βλοοδ τε στσ ιν α πατιε ντ ωιτη διαβε τε σ ανδ σε ϖε ρε

ηψπε ρτριγ λψχε ριδε µ ια, πατιε ντσ µ αψ ηαϖε πσε υδονορµ ογ λψχε µ ια, τηυσ, ηοµ ε

of
γ λυχοµ ε τε ρσ µ αψ νοτ βε α ρε λιαβλε µ ε ασυρε οφ ηψπε ργ λψχε µ ια ιν τηισ ποπυλατιον.

ro
• ∆ υε το ε ξαγ γ ε ρατε δ λε ϖε λσ οφ αχιδοσισ ιν τηε σε ττινγ οφ σε ϖε ρε
-p
ηψπε ρτριγ λψχε ριδε µ ια, χλινιχιανσ σηουλδ χαυτιουσλψ ιντε ρπρε τ λαβορατορψ ϖαλυε σ,
re
10 ε σπε χιαλλψ βιχαρβονατε λε ϖε λσ, ιν ανψ πε διατριχ πατιε ντ τηατ πρε σε ντσ ωιτη σε ϖε ρε

ηψπε ρτριγ λψχε ριδε µ ια.

lP
na

Clinical Relevance
ur

This case demonstrates the importance of carefully interpreting laboratory values

Jo

when assessing for hyperglycemia and acidosis in cases of severe

15 hypertriglyceridemia (SHTG). Additional tests, such as beta-hydroxybutyrate, c-

peptide, and insulin may help establish the diagnosis of DKA. To avoid serious

morbidity, plasmapheresis should be considered in pediatric diabetes cases when

SHTG causes clinical deterioration.

20
Declaration of interests

☒ The authors declare that they have no known competing financial interests or personal relationships
that could have appeared to influence the work reported in this paper.

☒The authors declare the following financial interests/personal relationships which may be considered
as potential competing interests:

of
ro
-p
re
lP
na
ur
Jo