Syed Ahmed Zaki, Preeti Shanbag , Prithi Shenoy

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J Vector Borne Dis 47, June 2010, pp. 123–125Unusual presentation of malaria as tetany: a case reportSyed Ahmed Zaki, Preeti Shanbag & Prithi ShenoyDepartment of Pediatrics, Lokmanya Tilak Municipal Medical College and General Hospital, Mumbai, IndiaKey words  Calcium; magnesium; malaria; phosphate; tetanyMalaria is a major disease of public health impor-tance with a high morbidity and mortality. Variousatypical presentations of malaria have been describedin literature1. Physicians should be aware of the dif-ferent ways in which malaria can present to ensureits early diagnosis and treatment. We herein describean unusual presentation of malaria as tetany and dis-cuss in brief regarding calcium, phosphate and mag-nesium metabolism in malaria.Case report: A 12-year old Indian boy hailing fromMumbai was admitted in Lokmanya Tilak MunicipalMedical College and General Hospital, Mumbai, In-dia with fever for four days and painful, intermittentmuscle spasm of the left foot since one day. Feverwas high-grade, intermittent and associated with rig-ors. There was no history of loss of consciousness,altered sensorium, paresthesia, trauma, drug intakeor convulsion. His past, development and family his-tory was normal. His dietary history was normal withan adequate calcium intake. On admission, the childwas febrile with a heart rate of 140/min, respiratoryrate of 28/min and blood pressure of 100/78 mm Hg.There was pallor and mild icterus on examination.Chvostek sign and Trousseau sign were negative.Intermittent muscle spasm of the left foot was seenon examination. The liver was tender and palpable4 cm below the right costal margin with a span of7 cm. The spleen was palpable 3 cm below the leftcostal margin. On central nervous examination, hewas conscious and well-oriented in time, place andperson. His motor and sensory examination was nor-mal. Superficial reflexes were normal with bilateralbrisk knee and ankle reflexes. There were no cer-ebellar or meningeal signs. Other systems werenormal.Investigations done on the day of admission revealed:hemoglobin 7.8 g/dL, total leukocyte count 12,600ml, and platelet count 70,000/ml. Peripheral bloodsmear showed ring-form trophozoites of Plasmodiumfalciparum. OptiMal test was positive for P.falciparum malaria and the parasite index was 3%.Other investigations showed: serum calcium 7.1mg/dL (normal range 8.8–10.5 mg/dL), serum phos-phorous 3 mg/dL (normal range 3.4–4.5 mg/dL),serum magnesium 1.4 mg/dL (normal range 1.8–3mg/dL), alkaline phosphatase 200 U/L, serum albu-min 3 mg/dL (normal range 3.5–5.5 mg/dL). The cor-rected calcium was 7.8 mg/dL {Corrected calcium =Calcium + (normal albumin – serum albumin) x 0.8}.Serum parathormone was 9.2 pg/ml  (normal range9–65 pg/ml), urinary calcium/creatinine ratio was 0.5(normal <0.2). Urinary phosphorous could not bedone due to non-availability of this facility at our in-stitution. Electrocardiography and arterial blood gasanalysis were normal. The total serum bilirubin was1.8 mg/dL with a conjugated fraction of 0.7 mg/dL.The serum concentrations of aspartate aminotrans-ferase, alanine aminotransferase, and lactate dehy-drogenase were 160 U/L, 225 U/L and 598 IU/Lrespectively. Serum sodium, serum potassium, renalfunction tests, coagulation profile and random bloodsugar were normal. Serological tests for dengue andleptospirosis were negative. Intravenous artesunatewas started at a dose of 2.4 mg/kg at 0, 12 and 24 hfollowed by once a day for total seven days. Intrave-nous calcium gluconate (10 ml of 10% solution thrice J  VECTOR  BORNE  DIS  47, JUNE 2010 124a day) was also started in the patient.As the muscle spasm did not respond to calciumsupplements, intravenous magnesium (0.2 cc/kg ofa 50% solution) was started resulting in symptom-atic improvement within four days. The patient be-came afebrile on the third day of treatment. Repeatserum levels of calcium, magnesium, phosphorous,and urinary calcium/creatinine done on the seventhday were normal. Serum parathormone levels hadincreased on the seventh day (63 pg/ml). The childwas discharged on the seventh day and was asymp-tomatic on follow-up after one month.The maintenance of plasma concentration of calcium,phosphate and magnesium within a narrow physi-ological range is vital to the integrity of a variety ofcellular metabolic processes. Mild asymptomatichypocalcemia is commonly seen in malaria regard-less of the severity of infection2. However, in somecases hypocalcemia can be severe and symptomatic3.Hypocalcemia in malaria can cause prolonged Q-Tcinterval which could be a risk factor for quininecardiotoxicity and sudden death3, 4. It has been foundthat with clinical recovery and parasite clearance, theserum calcium level returns to normal. Thus, moni-toring serum calcium can have prognostic value insevere malaria3. Various hypotheses have been putforward for the explanation of hypocalcemia in ma-laria. The main reason cited is the ‘sick euparathyroidsyndrome’ which describes a state in which the par-athyroid response to hypocalcemia is depressed dur-ing active infection, with recovery of the glandularfunction as the parasitaemia gets cleared5.Another hypothesis for malaria-associated hypocal-cemia relates to the changes in phosphate metabo-lism. A lowered renal threshold for phosphate ap-pears to be a major contributing factor forhypophosphatemia in malaria5. Hypophosphatemiais associated with hypercalciuria as seen in our pa-tient6. Hypophosphatemia can cause encephalopa-thy, depressed leucocyte function, increased suscep-tibility to gram-negative infections, plateletdysfunction, coagulation abnormalities andhaemolytic anaemia5. These abnormalities are alsoseen in severe and complicated malaria7. Reducederythrocyte concentration of 2, 3, diphosphoglyceratein hypophosphatemia can further impair the tissueoxygen delivery and vital organ function in severemalaria8. Thus, hypophosphatemia contributes to andin some cases may even aggravate a variety of clini-cal and laboratory abnormalities associated with se-vere malaria. However, routine administration ofphosphate is not recommended in view of the poten-tial risk of hyperphosphatemia and the fact that nor-mal serum concentrations are restored within daysof initiation of treatment2. Mild asymptomatic hypo-magnesemia is also known to occur in malaria5. Itcan cause secondary hypocalcemia by impairing therelease of parathormone by the parathyroid gland andthrough blunting the tissue response to parathor-mone9.In conclusion, we wish to highlight that alteration incalcium, phosphate and magnesium metabolism canoccur in patients with malaria. Also, quinine shouldbe used cautiously in patients with severe malariaassociated with hypocalcemia and prolonged Q-Tcinterval.AcknowledgementThe authors would like to thank Dr Sandhya Kamath,Dean, Lokmanya Tilak Municipal Medical Collegeand General Hospital, for permitting us to publishthis paper.References1. Irving KG, Kemp E, Olivier BJ, Mendelow BV. Unusualpresentation of malaria as a leukemoid reaction: a case re-port. S Afr Med J 1987; 71: 597–8.2. Davis TM, Li GQ, Guo XB, Spencer JL, St John A. Se-rum ionized calcium, serum and intracellular phosphate,and serum parathormone concentrations in acute malaria.Trans R Soc Trop Med Hyg 1993; 87: 49–53.3. Prabha MR, Pereira P, Chowta N, Hegde BM. Clinicalimplications of hypocalcemia in malaria. Indian J MedRes 1998; 108: 62–5. 125 ZAKI ET AL: MALARIA AND TETANY4. Soni CL, Kumhar MR, Gupta BK, Singh VB, Srimali L,Nayak KC, et al. Prognostic implication of hypocalcemiaand QTc interval in malaria. Indian J Malariol 2000; 37:61–7.5. Davis TM, Pukrittayakamee S, Woodhead JS, HollowayP, Chaivisuth B, White NJ. Calcium and phosphate me-tabolism in acute falciparum malaria. Clin Sci (London).1991; 81: 297–304.6. Massary SG. Effect of phosphate depletion on renal tu-bular transport. In: Avioli LV, editor. Phosphate metabo-lism: kidney and bone. Paris: Armour Montague 1976;p. 25–32.7. Guidelines for the treatment of malaria. Geneva: WorldHealth Organization. Available from: http://www.who.int/malaria/doc/TreatmentGuidelines2006.pdf.8. Lichtman MA, Miller DR, Cohen J, Waterhouse C. Re-duced red cell glycolysis, 2, 3-diphosphoglycerate andadenosine triphosphate concentration, and increased hae-moglobin-oxygen affinity caused by hypophosphatemia.Ann Intern Med 1971; 74: 562–8.9. Greenbaun LA. Electrolytes and acid-base disorders. In:Behrman RE, Kliegman RM, Jenson HB, editors. Nelsontextbook of pediatrics, 17th edn. Philadelphia, PA: WBSaunders Company 2004; p. 218.Corresponding author: Dr Syed Ahmed Zaki, Department of Pediatrics, Lokmanya Tilak Municipal Medical College andGeneral Hospital, Mumbai–400 022, India.E-mail: drzakisyed@gmail.comReceived: 24 October 2009 Accepted in revised form: 12 March 2010

Unusual presentation of malaria as tetany: a case report

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