Endocrine Abstracts

Case history: A 67 year-old male was referred from GP to Endocrine clinic due to incidental high Calcium level in a routine bone profile. Adjusted Serum Calcium was 2.69 mmol/l. In Endocrine clinic, a detailed history was taken. The patient denied all symptoms of hypercalcemia.

Past medical history: Alcohol-related cirrhosis (complicated with Varices banded by OGD), Diverticular disease, Type 2 diabetes mellitus, Hypertension, Hyperlipidemia.

Alcohol history: one to two bottles of wine per day for five years

Family history: no family history of known hypercalcaemia

Medications: Hydrochorothiazide-Metformin.

On examination: BMI 36. BP 170/80. No lymphadenopathy. Heart/chest normal. Mild Hepatomegaly. Tinge Jaundice.

Investigations: The aim of investigations was:

1. Confirm Hypercalcemia (Adjusted to Albumin)

2. Determine the mechanism (PTH dependent or independent)

3. Seek underlying illness/cause (CXR, FBC, ESR, liver and kidney functions, electrolytes, TFT, myeloma screen, Vitamin D, serum cortisol, CT chest/abdomen/pelvic, ACE level)

4. To Determine end-organ damage (24 h urine calcium, urine creatinine, renal US)

Results and treatment: Adjusted Calcium: 2.69 mmol/l – PTH: <1 – Phosphate: 0.83 – Alkaline Phosphatase: 82 – Calcium/I (urine): 7.4 mmol/l – Fractional excretion of Calcium: 0.016 mol/mol – Creatinine/I (urine): 12.4 mmol/l

Gamma GT: 234 – ALT 200 – Bilirubin 70

Serum Mg: 0.50 mmol/l

• And ALL the following tests were within normal range:

1. Kidney function Tests-Sodium and Potassium

2. FBC– ESR

3. Immunoglobulin assay

4. Urinary Metanephrines

5. Autoimmune screen

6. Vitamin D 1.25 and 25Oh Vitamin D

7. Thyroid function and cortisol

8. Tumor markers

9. HBA1C

10. Insulin Like G.F1

11. Vitamin A

CT Chest–Abdomen–pelvis: No Malignancy-cirrhosis- Portal hypertension

Gastroscopy: Esophageal Varices

Skeletal Survey: Normal

The first impression was this hypercalcaemia is likely related to thiazide diuretics. Hydrochlorothiazide stopped then adjusted calcium level repeated afterwards and was higher (2.71 mmol/l). Despite extensive evaluation, no cause for hypercalcemia was identified. This was a PTH-independent hypercalcemia with normal vitamin D metabolites. He was ambulatory. He had not used vitamin A supplementation, lithium or antacids. He was managed with fluids and cut off alcohol drink and no specific medication was given for hypercalcemia. His ionized Calcium levels returned back to normal limits.

Conclusions and points for discussion: Hypercalcemia with CLD is a diagnosis of exclusion. Hypercalcemia is more reported with CLD with hepatic neoplasm but less reported in absence of neoplasm. 2 points for discussion:

1) Mechanism of Hypercacemia in CLD

2) Relation between the etiology of CLD and Hypercacemia (e.g., Alcohic, NASH, Viral hepatitis, Neoplasm)