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Hypercalcemia of Malignancy Associated With Extensive Lytic Bone Lesions in B-Cell Acute Lymphoblastic Leukemia (All) : Not So Malignant
Hypercalcemia of Malignancy Associated With Extensive Lytic Bone Lesions in B-Cell Acute Lymphoblastic Leukemia (All) : Not So Malignant
Hypercalcemia of Malignancy Associated With Extensive Lytic Bone Lesions in B-Cell Acute Lymphoblastic Leukemia (All) : Not So Malignant
12(03), 1094-1101
RESEARCH ARTICLE
HYPERCALCEMIA OF MALIGNANCY ASSOCIATED WITH EXTENSIVE LYTIC BONE LESIONS IN
B-CELL ACUTE LYMPHOBLASTIC LEUKEMIA (ALL): NOT SO MALIGNANT
Priyanka Ahirwar, Narendra K Chaudhary, Bhavna Dhingra, Girish C Bhatt, Mahesh Maheshwari and
Shikha Malik
Department of Pediatrics, All India Institute of Medical Sciences, Bhopal, Madhya Pradesh, India.
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Manuscript Info Abstract
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Manuscript History
Received: 30 January 2024
Final Accepted: 29 February 2024
Published: March 2024 Copy Right, IJAR, 2024,. All rights reserved.
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Introduction:-
Hypercalcemia of malignancy is an unusual but serious complication of childhood malignancy.
We report a case of thirteen-year-old female with B-cell acute lymphoblastic leukemia (B-ALL) who presented with
severe hypercalcemia with radiological evidence of osteolytic lesions.
Case History:
A thirteen-year-old previously healthy female.
Presented to our hospital with history of multiple joint and bone pains for 1 month, which started from hip, gradually
involved knee, ankle, shoulder, elbows and wrist. There was history of morning stiffness and pain was so severe that
she was not able to do routine activities.
She also had generalised weakness, abdominal pain, nausea, vomiting, cough and fever of 2-3 days. She had pallor
with signs of congestive cardiac failure.
Her Complete blood count was suggestive of pancytopenia with 40% blast cells. Her other investigations revealed
serum urea 50 mg/dl, creatinine 1.22 mg/dl, potassium 2.3 mmol/l, uric acid 14 mg/dl, phosphorus 3.6mg/dl, total
calcium 19.8 mg/dl and alkaline phosphatase 323 U/L.
X-ray skull showed multiple small lytic lesions giving salt and pepper appearance. X-ray long bones was showing
lytic lesions.
Further workup for hypercalcemia revealed normal PTH(31.5pg/ml) and vitamin-D level.
USG abdomen did not show nephrocalcinosis but showed grade II renal parenchymal changes.
She was diagnosed to have B-ALL by flow cytometry but cytogenetics was normal and molecular studies were
negative for common translocations including t(17;19).
She was treated for hypercalcemia with intravenous (iv) hydration, iv pamidronate for 3 doses and frusemide and
started on prephase steroid.
IV hydration with normal saline and iv furesemide were started at presentation. There was no significant change in
calcium values. and iv pamidronate was given after 24hrs.There was decreasing calcium values noted. Steroids
started on fourth day once the diagnosis was confirmed.Calcium level was normal after 3 doses of pamidronate and
1 dose of steroid.
She responded well with combined therapy and calcium was normal by two days of pamidronate and after day one
of steroid. There was no hypocalcemia noted during first few weeks of steroid. Calcitonin was not needed.
Discussion:-
Hypercalcemia of malignancy is rare metabolic finding
The differential for hypercalcemia can be divided into PTH or non PTH mediated causes.
1. Osteolysis due to proliferation and bone tissue invasion by tumor cells
2. Osteoclastic bone resorption induced by tumor humoral factors(PTH Rp) and cytokines.
In our case the PTH level was normal, and vitamin D was normal, so the etiology of hypercalcemia was believed to
be massive bony calcium release due to extensive metastasis.
First step in diagnostic algorithm is biochemical evaluation including plasma and urine level of calcium(with
calcium/creatinine ratio),PTH, vitamin D and phosphate. A standard biological checkup(hematologic, renal, hepatic,
electrolytes and acidbase is also required, along with adrenal and thyroid measurements.
The second step is Imaging workup, abdominalultrasound , whole skeletal radiography, CT, bone scintigraphy and
PETCT.
Third step, particularly if suppressed PTH is tissue biopsy and immunological analysis.
Once identified, severe hypercalcemia can be rapidly and effectively treated with combination of highly effective
therapies including high volume saline, furesemide, bisphosphonates and chemotherapy.
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In 1977 Aldinger and co-workers showed that malignancy induced hypercalcemia is frequently associated with
hypokalemia.
Conclusions:-
Hypercalcemia associated with acute leukemia respond well with combination treatment with hydration,
bisphosphonates, frusemide and earliest initiation of cytoreductive therapy.
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