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Table of Contents
CASE REPORT
Year : 2022  |  Volume : 11  |  Issue : 2  |  Page : 115-118

A rare presentation of type 1 diabetes mellitus: Diabetic ketoacidosis with severe dyslipidaemia and eruptive xanthomas


Department of Internal Medicine, College of Health Sciences, University of Abuja, Abuja, Nigeria

Date of Submission16-Jul-2021
Date of Decision21-Oct-2021
Date of Acceptance14-Dec-2021
Date of Web Publication14-Apr-2022

Correspondence Address:
Yakubu Lawal
Department of Internal Medicine, College of Health Sciences, University of Abuja, Abuja
Nigeria
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jcsr.jcsr_44_21

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  Abstract 


Diabetic ketoacidosis (DKA) is the most common life-threatening complication of diabetes, especially in type 1 diabetes mellitus (T1DM). Severe dyslipidaemia causing extensive xanthomas is very rarely reported in DKA. We report the case of a 30-year-old male with T1DM who presented with features of ketoacidosis and had extensive eruptive xanthomas. Blood samples drawn on admission showed excessively lipemic serum and marked dyslipidaemia after analysis. The patient was treated with insulin, rehydration and statins with good clinical outcome. The present case highlights the importance of serial monitoring of lipids and early lipid-lowering therapy in DKA presenting with severe dyslipidaemia, especially when occurring with cutaneous symptoms.

Keywords: Diabetic ketoacidosis, dyslipidaemia, statins, xanthomas


How to cite this article:
Ateko OA, Lawal Y, Mshelia-Reng R, Ugwuneji UO, Julius IU, Anumah FE. A rare presentation of type 1 diabetes mellitus: Diabetic ketoacidosis with severe dyslipidaemia and eruptive xanthomas. J Clin Sci Res 2022;11:115-8

How to cite this URL:
Ateko OA, Lawal Y, Mshelia-Reng R, Ugwuneji UO, Julius IU, Anumah FE. A rare presentation of type 1 diabetes mellitus: Diabetic ketoacidosis with severe dyslipidaemia and eruptive xanthomas. J Clin Sci Res [serial online] 2022 [cited 2022 May 21];11:115-8. Available from: https://www.jcsr.co.in/text.asp?2022/11/2/115/343246




  Introduction Top


Diabetic ketoacidosis (DKA) is an acute life-threatening complication of diabetes defined by the triad of hyperglycaemia, ketonemia/ketonuria and metabolic acidosis.[1] It accounts for about 30% of first presentations in newly diagnosed T1DM.[2] Mild hyperlipidaemia occurring in association with DKA is common.[3] However, DKA complicated by severe dyslipidaemia resulting in extensive eruptive xanthomas has been rarely described in T1DM. We report the case of a young adult diagnosed with T1DM for 7 months with poor glycaemic control presenting with the triad of DKA, severe dyslipidaemia and eruptive xanthomas.


  Case Report Top


A 30-year-old male presented with abdominal pain, vomiting and confusion for 2 days duration. His partner also provided additional history of polyuria and polydipsia preceding his presenting symptoms. There were no fever or risk factors for dyslipidaemia. He was diagnosed with T1DM 7 months earlier and was on premixed insulin however with poor adherence. Family history was negative for diabetes and hyperlipidaemia.

On arrival at the emergency department, he was severely dehydrated and had rapid shallow breathing (Kussmaul breath) with acetone breath. Further, systemic examination revealed a heart rate of 112 beats/min, blood pressure of 90/60 mmHg, temperature of 37.2 °C, respiratory rate of 44 cycles/min and oxygen saturation of 97%. Glasgow Coma Scale was 13. The chest was clear on auscultation with equal air entry bilaterally. Abdomen was soft and tender with no palpable organomegaly or masses. He had crops of red-yellow papules on the extensor surfaces of his elbows, hands and knees [Figure 1]. Anthropometric measurements were as follows: height 1.7 m, weight 55 kg and body mass index 20 kg/m2. Other examinations were unremarkable.
Figure 1: Clinical photographs showing eruptive xanthoma affecting extensor surfaces of the elbows (a and b), hands (c) and knees (d)

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Blood samples drawn for laboratory examination appeared grossly lipemic [Figure 2]. Serum chemistry analysis revealed abnormal values for triglyceride (75.6 mmol/L, reference range 0.4–1.52 mmol/L), total cholesterol (28.2 mmol/L, reference range 0–5.2 mmol/L), high-density lipoprotein (HDL) cholesterol (0.1 mmol/L, reference range > 0.9 mmol/L) and low-density lipoprotein (LDL) cholesterol could not be estimated using the Friedewald formula (the Friedewald formula is inaccurate at extremely high triglyceride and total cholesterol levels).[4] Serum sodium level was (160 mmol/L, reference range 136–148 mmol/L), potassium (1.9 mmol/L, reference range 3–5 mmol/L), chloride (125 mmol/L, reference range 98–110 mmol/L), bicarbonate (10 mmol/L, reference range 20–30 mmol/L), urea (12.3 mmol/L, reference range 2.1–7.1 mmol/L) and serum creatinine (29umol/L, reference range 64–104 umol). Uric acid level was 5000umol/L (reference range 204–410 umol/L). Random blood glucose check using a meter was (21.3 mmol/L, reference range 7.8–10 mmol/L). Calculated serum osmolality was (329 mOsm/kg, reference range 275–286 mOsm/kg) and his urinalysis showed 3+ of ketones and glucose. Initial glycosylated haemoglobin was 15% (reference range <6%) and he had a positive anti-glutamic acid decarboxylase 65 antibody. Abdominal ultrasound was unremarkable. Skin biopsy showed infiltration of the papillary dermis with foamy macrophages with overall features in keeping with eruptive xanthomas.
Figure 2: Lipaemic serum due to severe hyperlipidaemia

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He was admitted and rehydrated with intravenous fluid alongside insulin infusion according to the standard protocol for DKA. He was also commenced on statins and xanthine oxidase inhibitor. The patient was started on statin to treat hyperlipidaemia consisting of hypercholesterolaemia and hypertriglyceridemia. This is because the levels of cholesterol and triglyceride were extremely high coupled with the presence of eruptive xanthomas. Considering most of the guidelines, it is recommended to commence treatment with statin in a situation of combined hypercholesterolaemia and hypertriglyceridemia, fibrates may be added later. In this case, since the patient was responding to rehydration, insulin and statin; there was no need to add fibrates. The xanthomas, hyperlipidaemia, hyperuricaemia and electrolyte values improved with the pharmacologic treatment and resolution of DKA [Figure 3]. He was discharged on premixed insulin with good blood glucose control after 16 days on admission. The laboratory parameters during the course of admission can be seen in [Table 1].
Figure 3: Clinical photographs showing healed eruptive xanthoma lesions over elbows (a and b) and knees (c) following resolution of DKA and hyperlipidaemia

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Table 1: Serial serum lipid profiles and electrolytes/urea/creatinine of the patient

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  Discussion Top


Impaired lipid metabolism in diabetes has been described in the literature for many years. The most common forms of dyslipidaemia in diabetes include elevated triglyceride, total cholesterol and LDL cholesterol levels.[5] Although approximately 30%–50% of patients with DKA may have associated hypertriglyceridemia, severe dyslipidaemia resulting in eruptive xanthomas is a rare occurrence in DKA.[6]

The mechanism of dyslipidaemia in DKA and T1DM is triggered by insulin deficiency. In lipid metabolism, insulin promotes lipogenesis and inhibits both lipolysis and ketogenesis. However, in conditions of severe deficiency, lipolysis is activated in the adipocytes leading to the release of free fatty acids which are taken up by the liver to produce triglyceride-rich lipoproteins.[3],[7] The activity of lipoprotein lipase, an extracellular enzyme responsible for the catabolism of triglycerides is also decreased resulting in poor clearance of triglyceride-rich lipoproteins (very LDL [VLDL] and chylomicrons) from the plasma and causing hypertriglyceridemia.[8] Elevated triglyceride-rich lipoprotein levels, in turn, lead to an increase in cholesteryl ester transfer protein-mediated transfer of triglycerides to HDL and LDL forming both triglyceride-rich HDL and LDL which are then further hydrolysed by hepatic lipase resulting in low plasma levels of HDL cholesterol levels and increase production of small dense LDL cholesterol which is highly atherogenic.[3],[7],[9] However, it is important to state that in addition to insulin deficiency, the occurrence of severe dyslipidaemia may have also been aggravated by an underlying genetic predisposition to dyslipidaemia.

High levels of circulating lipids (cholesterol and triglycerides) can result in diverse clinical manifestations due to abnormal deposition in various tissues. Deposition in the skin leads to eruptive xanthomas commonly on the extensor surfaces of the extremities and buttocks. Eruptive xanthomas occurs almost only in the presence of hyperlipidaemia (mixed hypercholesterolaemia and hypertriglyceridemia in the index case) and has a prevalence of 18 cases in 100,000 people, making it a rare presentation.[6],[10]

Furthermore, hyperlipidaemia has been reported by various studies to be associated with hyperuricaemia which is in keeping with our findings.[11],[12] In a different vein, severe dyslipidaemia has been shown to interfere with the measurements of other laboratory parameters accurately.[13] This may have contributed to the extremely low potassium levels, even though some potassium depletion occurs as a result of DKA. Pseudohyponatremia was not observed in our case, most likely due to the overriding effect of severe dehydration causing hyperchloremic hypernatremia.

The management of DKA with severe dyslipidaemia includes adequate rehydration and continuous infusion of insulin according to the DKA management protocol because the underlying mechanism of dyslipidaemia is insulin deficiency. However, in the presence of severe hyperlipidaemia with accompanying eruptive xanthomas, early therapy with lipid-lowering agents may hasten the healing of cutaneous lesions and also significantly reduce the risk of more grievous complications like pancreatitis as well as long-term cardiovascular risk.[14],[15] This was the experience in the case of our patient.

The weakness of our case was that an appropriate genetic study could not be performed in the patient and first-degree relatives to detect the presence of a coexisting genetic predisposition to severe dyslipidaemia. DKA patients can also present with features of severe hyperlipidaemia such as eruptive xanthomas. Early recognition and treatment of the accompanying severe dyslipidaemia are important to ensure quick healing of these cutaneous lesions and avert long-term cardiovascular complications.

Acknowledgement

We acknowledge the nurses of the Department of Medicine, the laboratory staff, and the Medical Record Officers of the University of Abuja Teaching Hospital for the various roles they played in the successful management and discharge of the index case.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crises in adult patients with diabetes. Diabetes Care 2009;32:1335-43.  Back to cited text no. 1
    
2.
Smith CP, Firth D, Bennett S, Howard C, Chisholm P. Ketoacidosis occurring in newly diagnosed and established diabetic children. Acta Paediatr 1998;87:537-41.  Back to cited text no. 2
    
3.
Schofield JD, Liu Y, Rao-Balakrishna P, Malik RA, Soran H. Diabetes dyslipidemia. Diabetes Ther 2016;7:203-19.  Back to cited text no. 3
    
4.
Seth SM, Blaha MJ, Elshazly MB, Brinton EA, Toth PP, McEvoy JW, et al. Friedewald-estimated versus directly measured low-density lipoprotein cholesterol and treatment implications. J Am Coll Cardiol 2013;62:732-9.  Back to cited text no. 4
    
5.
Hassan MM, Sharaf AS, Soliman MH, Al-Wakeel AN. Dyslipidemia in type 1 diabetes mellitus: Relation to diabetes duration, glycemic control, body habitus, dietary intake and other epidemiological risk factors. Egypt Pediatr Assoc Gaz 2015;63:63-8.  Back to cited text no. 5
    
6.
Zak A, Zeman M, Slaby A, Vecka M. Xanthomas clinical and pathophysiological relations. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub 2014;158:181-8.  Back to cited text no. 6
    
7.
Hirano T. Pathophysiology of diabetic dyslipidemia. J Atheroscler Thromb 2018;25:771-82.  Back to cited text no. 7
    
8.
Radhakutty A, Shen J, Hooper AJ, Miller SA, Burnett JR, Mah PM, et al. Quantification and genotyping of lipoprotein lipase in patients with diabetic lipaemia. Diabet Med 2014;31:1702-7.  Back to cited text no. 8
    
9.
Ivanova EA, Myasoedova VA, Melnichenko AA, Grechko AV, Orekhov AN. Small dense low-density lipoprotein as biomarker for atherosclerotic diseases. Oxid Med Cell Longev 2017;2017:1273042.  Back to cited text no. 9
    
10.
Nair S, Yadav D, Pitchumoni CS. Association of diabetic ketoacidosis and acute pancreatitis: observations in 100 consecutive episodes of DKA. Am J Gastroenterol 2000;95:2795-800.  Back to cited text no. 10
    
11.
Hou YL, Yang XL, Wang CX, Zhi LX, Yang MJ, You CG. Hypertriglyceridemia and hyperuricemia: A retrospective study of urban residents. Lipids Health Dis 2019;18:81.  Back to cited text no. 11
    
12.
Peng TC, Wang CC, Kao TW, Chan JY, Yang YH, Chang YW, et al. Relationship between hyperuricemia and lipid profiles in US adults. Biomed Res Int 2015;2015:127596.  Back to cited text no. 12
    
13.
Soleimani N, Mohammadzadeh S, Asadian F. Lipemia interferences in biochemical tests, investigating the efficacy of different removal methods in comparison with ultracentrifugation as the gold standard. J Anal Methods Chem 2020;2020:9857636.  Back to cited text no. 13
    
14.
Preiss D, Tikkanen MJ, Welsh P, Ford I, Lovato LC, Elam MB, et al. Lipid-modifying therapies and risk of pancreatitis: A meta-analysis. JAMA 2012;308:804-11.  Back to cited text no. 14
    
15.
Lee MM, Sattar N, McMurray JJ, Packard CJ. Statins in the prevention and treatment of heart failure: A review of the evidence. Curr Atheroscler Rep 2019;21:41.  Back to cited text no. 15
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
    Tables

  [Table 1]



 

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