Literature Review of COVID-19 Related CVT Reports in 2020

Iffat Jamal^* Department of Medical Sciences, University of Cambridge, England, United Kingdom
^*Correspondence: Iffat Jamal, Department of Medical Sciences, University of Cambridge, England, United Kingdom, Email:

Received: Mar 08, 2022, Manuscript No. JEBMH-21-46460; Editor assigned: Mar 11, 2022, Pre QC No. JEBMH-21-46460 (PQ); Reviewed: Mar 25, 2022, QC No. JEBMH-21-46460; Revised: Mar 30, 2022, Manuscript No. JEBMH-21-46460; Published: Apr 05, 2022, DOI: 10.18410/jebmh/2022/9.5.1

Citation: Jamal I. Literature review of COVID-19 related CVT reports in 2020. J Evid Based Med Healthc 2022;9(05):01.

Keywords

Musculoskeletal feet, Imatinib mesylate, Hypocalcemia

Introduction

Imatinib mesylate is a tyrosine kinase inhibitor targeted to BCR-ABL, PDGFR, and KIT mutations. It plays a pivotal role in treatment of Chronic Myelogenous Leukaemia (CML) and Gastrointestinal Stromal Tumours (GISTs), and has dramatically changed the clinical management of these tumour types.^1-4

The adverse effects of imatinib are mostly mild and manageable.

Various side effects are as follows : Various side effects are as follows :

• Anemia

• Oedema

• Fatigue

• Nausea

• Diarrhoea

• Cramps

• Rash

• Myalgia

• Arthralgia ⁵

• Granulocytopenia

Musculoskeletal effects of imatinib are reported in 25 % of GIST patients and 20 % – 40 % of CML patients, including arthralgia, myalgia, and muscle cramps, but are rarely dose-limiting.^5-8

The pathophysiology of these effects is uncertain. Various pathophysiological mechanisms proposed are :

Secondly, imatinib is a member of a family of protein tyrosine kinase inhibitors which can induce marked changes in cell excitability and ion homeostasis. Indeed, imatinib blocks low voltageactivated T-type calcium channels in human embryonic kidney cells.⁹ Thus imatinib could have a nonspecific effect on calcium homeostasis that is not KIT receptor-mediated.

Thirdly Imatinib might be causing nonspecific inhibition of calcium channels in tubule which might be leading to hypocalcemia.

Musculoskeletal complaints are a common side effect of Imatinib and are manifested as muscle cramps and bone pain. The muscle cramps occur mainly in the hands, feet, calves, and thighs. The pattern, frequency, and severity of cramps are usually constant over time, and they may resemble titanic contractions. Some patients relate cramps to exertion or describe night time occurrence. Bone pain and arthralgias have been reported by 20 % to 40 % of patients. Their onset tends to be in the first month of therapy, and they frequently abate after a few months. The symptoms most frequently affect the femurs, tibias, hips, and knees. Bone or joint pain can be severe and disabling and may be strikingly asymmetric. In some cases, imaging studies were done but failed to detect abnormalities.^9,10

Various electrolyte imbalances common in Imatinib treatment:

Hypophophatemia: This is the most common electrolyte imbalance associated with Imatinib. The clinical manifestations of mild hypophosphatemia include myalgias, weakness, anorexia. Chronic severe depletion may be manifested by pain in muscles and bones.

Hypocalcemia: This is the second most common abnormality which was detected in patients on Imatinib, Hypocalcemia increases excitation of nerve and muscle cells, primarily affecting the neuromuscular and cardiovascular systems. Extensive spasm of skeletal muscle causes cramps and tetany.⁹

Hypokalemia: Described only in case reports in patients who are on Imatinib, this is also a possible cause of myalgia and muscle spasms but does not cause arthralgia /bony pains.

The treatment which has been advised by NCCN and other literature evidence states that calcium supplementation is an important treatment aspect in the management of musculoskeletal pain along with fluids supplementation.^10-12

Myalgia and musculoskeletal is the one of the common nonhematological side effect in patients of chronic myeloid leukemia who is initiated on imatinib. This side effect must be efficiently taken care of inorder to increase the compliance of patients for better outcome.

References

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2. Deininger MW, O’Brien SG, Ford JM, et al. Practical management of patients with chronic myeloid leukemia receiving imatinib. J Clin Oncol 2003;21(8):1637–1647.

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3. O’Brien SG, Guilhot F, Larson RA, et al. Imatinib compared with interferon and low-dose cytarabine for newly diagnosed chronic-phase chronic myeloid leukemia. The New England J Med 2003;348(11):994 –1004.

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7. Debiec-Rychter M, Dumez H, Judson I, et al. Use of cKIT/PDGFRA mutational analysis to predict the clinical response to imatinib in patients with advanced gastrointestinal stromal tumours entered on phase I and II studies of the EORTC Soft Tissue and Bone Sarcoma Group. European J Cancer 2004;40(5):689–695.

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9. Marin D, Marktel S, Bua M, et al. The use of imatinib (STI571) in chronic myelod leukemia: some practical considerations. Haematologica 2002;87(9):979–988.

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10. Blay JY, Berthaud P, Perol D, et al. Continuous vs intermittent imatinib treatment in advanced GIST after one year: a prospective randomized trial of the French Sarcoma Group. Am J Clin Oncol 2004;23.

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11. Steegmann JL, Alaez C, Granda A, et al. Phosphate, calcium ` balance, and renal function in CML patients previously resistant or intolerant to interferon alpha and treated with STI571. Blood 2002;100.

12. Cataldi M, Gaudino A, Lariccia V, et al. Imatinib-mesylate blocks recombinant T-type calcium channels expressed in human embryonic kidney-293 cells by a protein tyrosine kinaseindependent mechanism. J Pharmacol Experim Therapeutics 2004;309(1):208–215.

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