Neonatal Malaria with Hyperglycemia and Hyperlipedemia: A Case Report


Surat Municipal Institute of Medical Education Research (S.M.I.M.E.R.) affiliated to Veer Narmad South Gujarat University, India.


Introduction: Neonatal Malaria manifests most commonly as fever ,anemia, hepatospleenomegaly, jaundice, loosestools and poor feeding however hyperglycemia and hyperlipedemia associated with malaria is not mentioned in literature.
Case Presenttion : A full term neonate was admitted in December, in N.I.C.U. as fever and anemia with spleenohepatomegaly ,his peripheral smear was positive for falciparum malaria with negative sepsis screen however there was hyperglycemia ,glucosuria and hyperlipedemia associated with it, malaria was and hyperglycemia was treated with antimalarials and Insulin respectively although Hyperlipedemia persisted on discharge.



Congenital or Neonatal Malaria is a rare disease and is associated with significant mortality1-2.Malaria involves multisystem infection. Haematological, renal & central nervous system adds to the mortality3. However association of hyperglycemia and or hyperlipedemia with malaria are rarely encountered .

Case Report:

A 18 days old full term, normally delivered male newborn, weighing 2.5 kg (birth weight 2.4 Kg) on breast feeding was admitted in December, in N.I.CU. with  history of high fever since five days. Mother was 24 yr. old, second para with normal antenatal history but had a post partum c/o of fever since 5 days. Her peripheral smear was positive for Falciparum malaria parasite +++ with platelet count 39,000, Her TORCH infections was negative . On clinical examination the neonate was active, feeding well but had icterus and hepato-spleenomegaly (liver 3cm and spleen 4cm), congenital anomalies, other systems and fundus was also normal. His initial investigations were Hb 6.1 gm ,TLC 10700, platelets 18000, Blood group O+ve, corrected reticulocyte count 4% and peripheral smear positive for falciparum + 4 while sepsis screen and Lumber puncture, was normal, random blood sugar was 711mg% with high Glucosuria but  ketoacids were absent, however, blood sample was reported to be highly Lipemic. U.S.G. and C.T. of abdomen showed hepatospleenomegaly but X-ray chest was normal. Other blood investigations such as CRP, G-6-PD ,TSH ,T3, T4, Blood Urea Creatinine and Electrolytes were normal, urine was positive for reducing substance ,SGOT 350u/l ,SGPT 384u/l, Total Bilirubin 8.0 mg/dl, Direct and indirect fraction being 6.3mg/dl, and 1.7 mg/dl and Alkaline Phosphatase 1950 u/l .TORCH titre, only CMV-IgG was positive IgM negative HSV-I (IgM) was positive and HSV-II (IgM) was equivocal but these tests were carried out on a sample which was highly lipemic. A second fasting blood sample on 3rd Dec. was also reported to be Highly lipemic, lipid profile being Cholesterol 305 mg/dl, Triglycerides 1691mg/dl HDL 13mg/dl (low) and LDL 72mg/dl (low), Random Blood sugar was 892 mg%. Insulin infusion was started initially as Blood glucose was very high @ 0.02U/kg/hour and later it was increased up to 0.1 U/Kg/hour but on 6thDec, it was stopped as the levels approached towards normoglycemia, a comparatively low Cholesterol and Triglycerides were reported but they were still above normal levels (Cholesterol 285mg/dl Triglycerides 989mg/dl, HDL 17mg/dl (low), LDL 70mg/dl (low). Mother’s RBS and fasting lipid profile was Cholesterol 195mg/dl, Triglicerydes 81mg/dl, HDL 59mg/dl ,LDL 94mg/dl. Neonate was not given any intravenous fluids (except insulin infusion) neither any parentral nutrition during the stay in hospital. Post prandial C-peptide levels was low 0.52 ng/ml (range1.2- 3.4ng/ml). Patient was treated with Inj. Ampicillin  and Inj. Gentamycin initially but as the sepsis screen was negative it was stopped, Inj. Artesunate and Clindamycin, was completed. Packed RBC transfusion was given. Patient responded to intravenous insulin infusion as the blood sugar levels came to normal prior to one day of discharge, however surprisingly there was no polyuria, no dehydration  in spite of blood sugar levels remained high for few days. Patient remained active and continued on breast feeding during period of admission. On Dec8th patient was discharged against medical advice due to economic reasons.



Hyperglycemia is inversely related to gestational age and weight in neonates , it is more common in premature and very low birth babies as compare to term neonates. Etiology of Hyperglycemia may be, due to antenatal h/o  drugs such as Theophylline, Dexamethasone and Glucose infusions especially in preterm newborns, Total parentral nutrition , Stress, infections, transient neonatal diabetes mellitus. In our case, the child was full term ,weighing normally, on  breast feeding ,with normal antennal history, and no sepsis with normal maternal lipid profile,  peripheral smear positive for falciparum malaria hence the diagnosis was Full term appropriate for gestational age with severe anemia, complicated falciparum malaria, hyperlipedemia with   hyperglycemia. Transient Diabetes of newborn is accompanied by Hyerglycemia which responds to insulin, remains for few weeks or months and then it resolves ,however few cases may have abnormal glucose tolerance test or recurrence of diabetes in older childhood; in some cases there is no remission and is known as permanent neonatal diabetes. The newborns in such cases are usually IUGR and have dehydration ,it is thought to be due to be either inadequate secretion or some degree of insulin insensitivity, in our case the newborn was fullterm normal with no such manifestations, had hyperlipedemia, although C-peptide level was low but insulin levels could not be done.10 Usually Hypoglycemia is a complication in severe malaria. however in our case it was hyperglycemia, which may be because of associated hyperlipedemia, although a few cases  of malaria associated with hyperglycemia in older children  have been reported 4,5. Neonatal Hyperglycemia due to Hyperlipedemia is attributed to an increase in free fatty acid levels which decrease peripheral glucose utilization primarily by substituting carbon and altering enzymatic activity that preferentially leads to fatty acid carbon oxidation rather than glucose oxidation. Fatty acids also inhibit the effect of insulin to suppress hepatic glucose production. These two conditions increase glucose concentrations in the plasma6. Hyperlipedemia as a complication of  congenital or neonatal malaria may be  rare ,as we could not find literature on malaria associated with both hyperglycemia with hyperlipedemia in neonates, although dyslipedemia  has been reported with the malaria in adults7-9.Other possible diagnosis might have been Familial hyperlipedemia, but as father and other family members lipid profile was not available diagnosis of familial hyperlipedemia was not confirmed. Though presentation of familial hyperlipedemia is usually late in childhood and is associated with obesity and increased insulin levels but it is not associated with hyperglycemia. But exact cause of hyperlipdmia could not be confirmed that is, whether it was due to malaria or some other condition.Limitations: As the samples were highly lipemic values of certain investigations might have been altered. Father’s Lipid profile, Newborn insulin  and free fatty acid levels and a repeat C-peptide level, could not be done as the facility was not available in our Institute, in addition there was economic restrictions ,newborn was not available for follow up.



Newborns presenting with hyperglycemia with hyperlipedemia are rare with possible differential diagnoses of Transient Neonatal Diabetes Mellitus , Familial Dyslipedemia and probably Neonatal malaria in such cases. However in our case was difficult to conclude that, whether hyperglycemia with hyperlipedemia was per se or it was due to associated Malaria.

Conflict of interests: None



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