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Year : 2022  |  Volume : 6  |  Issue : 2  |  Page : 152

Calcinosis cutis in chronic myeloid leukemia

Department of Dermatology, Venereology and Leprosy, Shri B M Patil Medical College, Hospital and Research Centre, Bangaramma Sajjan Campus, Vijayapura, Karnataka, India

Date of Submission15-Feb-2021
Date of Decision15-May-2021
Date of Acceptance19-Nov-2021
Date of Web Publication26-Aug-2022

Correspondence Address:
Arun C Inamadar
Department of Dermatology, Venereology and Leprosy, Shri B M Patil Medical College, Hospital and Research Centre, Bangaramma Sajjan Campus, Vijayapura - 586 103, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/cdr.cdr_12_21

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Calcinosis cutis is a rare condition of calcium deposition in skin and subcutaneous tissue. Multiple underlying diseases have been implicated for calcification, the pathogenesis of which is poorly understood. We report a case of calcinosis cutis secondary to chronic myeloid leukemia. The case is being reported for its rarity of association.

Keywords: Calcinosis cutis, chronic myeloid leukemia, mediated hypercalcemia, metastatic calcinosis, parathyroid hormone-related protein

How to cite this article:
Inamadar AC, Lingaiah A, Janagond AB. Calcinosis cutis in chronic myeloid leukemia. Clin Dermatol Rev 2022;6:152

How to cite this URL:
Inamadar AC, Lingaiah A, Janagond AB. Calcinosis cutis in chronic myeloid leukemia. Clin Dermatol Rev [serial online] 2022 [cited 2023 Jan 31];6:152. Available from: https://www.cdriadvlkn.org/text.asp?2022/6/2/152/354735

  Introduction Top

Calcinosis cutis is a condition characterized by deposition of calcium salts in the skin and subcutaneous tissue. It is classified into five main types: metastatic, dystrophic, idiopathic, iatrogenic, and calciphylaxis.[1] Overall the most common type of calcinosis cutis is dystrophic calcification with normal laboratory values of calcium and phosphorus.[2] Dystrophic calcification occurs in pancreatic panniculitis associated with pancreatitis. Other associated underlying diseases include systemic sclerosis, dermatomyositis, mixed connective tissue disease, or lupus, which induce tissue damage and create a nidus for calcification. Metastatic calcification occurs when the serum calcium-phosphate product exceeds 70 mg/dL.[3] It usually presents over periarticular regions and most commonly associated with chronic kidney failure. Hypervitaminosis D, hyperparathyroidism, milk-alkali syndrome, sarcoidosis, and rarely malignant neoplasms are implicated as other causes.[3] Idiopathic calcification has no underlying tissue damage or abnormal laboratory values. It includes tumoral calcinosis, subepidermal calcified nodules, and scrotal calcinosis. Iatrogenic calcification is caused by administration of calcium or phosphate-containing agent that induces local precipitation of calcium salts. Chronic renal failure and dialysis-associated calcification of small and medium-sized vessels are termed as calciphylaxis.[3]

  Case Report Top

A 65-year-old male patient presented to us with a complaint of difficulty in prolonged sitting due to burning sensation over both buttocks for 1 year. A detailed history and review of his past medical records revealed that the patient was diagnosed with chronic myeloid leukemia (CML) 9 months back and was on oral imatinib for 3 months for the same. The patient denied having similar lesions elsewhere, trauma or receiving injection at the sites of burning sensation. There was no history of underlying bone pain, associated co-morbid conditions, or connective tissue disorders.

Examination revealed the presence of ill-defined hyperpigmented patch approximately measuring 4 cm × 5 cm present over lower medial quadrant of bilateral gluteal areas and a small nontender, indurated plaque measuring 0.5 cm × 0.5 cm over right buttock overlying the hyperpigmented patch. There was no hepato-spleenomegaly or lymphadenopathy.

On X-ray, no soft tissue opacity was appreciated, however, ultrasonography showed multiple microcalcification in the skin and the subcutaneous tissue. A small nick was made over the plaque through which hard whitish material was visualized on application of mild pressure over the surrounding area.

Histopathology revealed normal epidermis with subepithelium showing fibrocollagenous tissue with areas of amorphous deposits of acellular basophilic material suggestive of calcification and sparse inflammatory infiltrate comprised of lymphocytes. Von Kossa stain for calcium was positive thereby confirming the diagnosis of calcinosis cutis.

Complete hemogram, renal function test, and serum calcium had been done 2 days earlier as a part of his monthly routine investigations for continuation of imatinib which was normal except for mild anemia (Hb was 10.4 g% [N-13–17 g%] and serum calcium 1.12 mmol/L [N 1.0–1.30 mmol/L]). Hence, laboratory investigations were not repeated at consultation.

Considering the ill-defined nature and small size of the lesion and the fact that surgical trauma itself may stimulate calcification, the patient was started on treatment with laboratory prepared topical 25% sodium metabisulfite emulsion cream for twice daily application and advised to follow-up after a month.

  Discussion Top

Paraneoplastic hypercalcemia usually occurs as a part of a malignancy syndrome where there is an alteration in the calcium and bone metabolism due to bony metastases or production of an abnormal hormone.[4] Few case reports have described calcinosis cutis in CML with hypercalcemia and hyperphosphatemia consistent with typical metastatic calcinosis cutis.[2],[4]

Humoral factors mediated by parathyroid hormone-related protein (PTHrP) are thought to cause hypercalcemia during accelerated phase of CML.[4],[5],[6] PTHrP is a protein that exerts certain PTH-like effects and is implicated in hypercalcemia by stimulating bone resorption and increasing renal calcium reabsorption and releasing calcium into serum. Although uncommon, the elevation of PTHrP mRNA in cultured leukemic cells, as well as increased plasma levels in patients with T-cell leukemia and B-cell lymphoma has been demonstrated in previous studies.[7] This possibly explains the occurrence of calcinosis cutis in our patient in the background of CML.

  Conclusion Top

Hypophosphatemia and hypocalcemia is an unanticipated side effect of imatinib therapy which in part has been attributed to drug-mediated changes to renal and gastrointestinal handling of phosphate and calcium. Emerging data suggest that imatinib also targets cells of the skeleton, causing decreased circulating levels of calcium and phosphate as a consequence of stimulation of retention and sequestration of these minerals into the bone.[8],[9] This can probably be attributed to our patients serum calcium level being normal at the time of evaluation. We thereby diagnosed the patient to be having metastatic calcinosis cutis secondary to CML even though the typical elevated serum calcium and phosphate levels were not observed.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Reiter N, El-Shabrawi L, Leinweber B, Berghold A, Aberer E. Calcinosis cutis: Part I. Diagnostic pathway. J Am Acad Dermatol 2011;65:1-12.  Back to cited text no. 1
Altman I, Lee IH, Burns MR, Rondelli D, Ennis WJ. Calcinosis cutis presenting in the context of long-term therapy for chronic myeloid leukemia: A case report and review of the literature. Wounds 2015;27:20-5.  Back to cited text no. 2
Le C, Bedocs PM. Calcinosis Cutis. United States: Stat Pearls Publishing LLC; 2020.  Back to cited text no. 3
Samdani A. Calcinosis cutis: A rare complication of chronic myeloid leukemia. Ann Saudi Med 2006;26:62-4.  Back to cited text no. 4
[PUBMED]  [Full text]  
Toro-Tobón D, Agosto S, Ahmadi S, Koops M, Bruder JM. Chronic myeloid leukemia associated hypercalcemia: A case report and literature review. Am J Case Rep 2017;18:203.  Back to cited text no. 5
Kakihana K, Mizuchi D, Yamaguchi M, Sakashita C, Fukuda T, Yamamoto K, et al. Hypercalcemia mediated by parathyroid hormone-related protein in the blastic phase of chronic myelogenous leukemia. Rinsho Ketsueki. 2002;43:102-6.  Back to cited text no. 6
Kubonishi I, Asahi Y, Machida H, Uemura Y, Hatakeyama N, Kubota T, et al. PTHrP-mediated hypercalcaemia in a case of CML blast crisis. Br J Haematol 1997;96:165-7.  Back to cited text no. 7
Vandyke K, Fitter S, Dewar AL, Hughes TP, Zannettino AC. Dysregulation of bone remodeling by imatinib mesylate. Blood 2010;115:766-74.  Back to cited text no. 8
Miyoshi N, Tanaka H, Ito T, Katayama Y, Niimi H, Hyodo H, et al. Use of imatinib mesylate for favorable control of hypercalcemia mediated by parathyroid hormone-related protein in a patient with chronic myelogenous leukemia at blast phase. Int J Hematol 2005;82:333-7.  Back to cited text no. 9


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