Calcium carbonate

Direct observations: clinical cases, poisoning incidents and other

Administrative data

Endpoint:

direct observations: clinical cases, poisoning incidents and other

Type of information:

other: Clinical case

Adequacy of study:

supporting study

Reliability:

2 (reliable with restrictions)

Rationale for reliability incl. deficiencies:

study well documented, meets generally accepted scientific principles, acceptable for assessment

Data source

Reference

Reference Type:

publication

Title:

Calcium Carbonate Consumption During Pregnancy: An Unusual Cause of Neonatal Hypocalcemia

Author:

Robertson WC

Year:

2002

Bibliographic source:

J Child Neurol, 17: 853-855

Materials and methods

Study type:

clinical case study

Endpoint addressed:

developmental toxicity / teratogenicity

Test guideline

Qualifier:

no guideline required

Principles of method if other than guideline:

The paper reports a clinical case of neonatal hypocalcaemia possibly caused by the maternal ingestion of antacids.

GLP compliance:

no

Test material

Test material information

Constituent 1

Reference substance name:

Calcium carbonate

EC Number:

207-439-9

EC Name:

Calcium carbonate

Cas Number:

471-34-1

Molecular formula:

CH2O3.Ca

IUPAC Name:

calcium carbonate

Test material form:

solid: bulk

Details on test material:

- Name of test material: Tums EX tablet each containing 750 mg calcium carbonate

Method

Subjects:

The mother was a healthy 24 year old who developed significant acid indigestion early in pregnancy and treated the dyspepsia by taking 10 to 14 extra strength Tums daily. The calcium carbonate was started midway through the first trimester and continued until the onset of labour.
The child was delivered at 39 weeks of gestation, appeared healthy and was sent home on the second day of life. During the first week of life the infant was active, alert and fed without difficulty.
At 8 days old the previously healthy infant was evaluated following five 30 second episodes of jerking movements of all limbs.

Route of exposure:

other: via the mother during pregnancy

Reason of exposure:

intentional

Exposure assessment:

estimated

Results and discussion

Clinical signs:

Examination revealed an active, healthy appearing 3.6 kg male infant with mild icterus. General physical examination and neurologic assessment were appropriate for age. Carpopedal spasm, Chvostek's sign and stridor were not present.
Admission laboratory values were normal except for a total calcium of 6.3 mg/dL. Blood glucose was 82 mg/dL and cerebrospinal fluid studies were unremarkable. Initial haematological studies did not include serum phosphorus.
There were three additional spells of generalised clonic activity lasting approximately 30 seconds during the first 10 hours of hospitalisation. There was no subsequent seizure activity.

Results of examinations:

Brain magnetic resonance imaging was normal except for probable decreased flow through the right transverse sinus. An EEG contained frequent temporal and occipital spike discharges.
Serologic tests for hypercoagulability were negative and chest radiographs revealed a typical thymic shadow. Liver function studies were normal except for a total bilirubin of 12.1 mg/dL. Serum pH, magnesium levels, total protein and creatinine were unremarkable. Free thyroxine, 1,25-dihydroxyvitamin D and parathormone values were also normal.

Effectivity of medical treatment:

The child received 20 mg/kg of iv phenobarbital shortly after admission and 180 mg of intravenous calcium gluconate soon after the laboratory reported his serum calcium. Three additional doses of 360 mg of calcium gluconate were given 6 hours apart during the first day of hospitalisation.
The infant received a single intravenous dose of 360 mg of calcium gluconate on the second hospital day.

Outcome of incidence:

The child's ionised calcium gradually improved and his serum phosphorus levels slowly decreased to near normal values. After 6 days of hospitalisation, the child's total calcium was 8.8 mg/dL and haemoglobin and haematocrit were 14.3 g/L and 41.3%, respectively. He was discharged at 2 weeks of age on phenobarbital, calcium carbonate and low-phosphate formula.
After discharge, the infant was gradually removed from calcium supplementation and placed on regular formula by 9 weeks of age. Calcium and phosphorus levels remained normal and there was no additional seizure activity. Evaluation at 3 months of age revealed a healthy child with no abnormalities on physical examination. Follow-up EEG was normal and the infant was weaned from phenobarbital without incident.

Applicant's summary and conclusion

Conclusions:

The paper reports the clinical case of a child whose mother took large doses of calcium carbonate throughout pregnancy. The infant developed seizures on the 8th day of life which appeared to be secondary to hypocalcaemia. Obvious causes for hypocalcaemia were excluded. Our observations suggest that maternal ingestion of excessive amounts of calcium may temporarily suppress neonatal parathormone production causing late neonatal hypocalcaemia.