Difficult-to-Diagnose Diabetes in a Patient Treated With Cyclophosphamide

The Contradictory Roles of Immunosuppressant Agents: A Case Report

Manuel García-Sáenz; Daniel Uribe-Cortés; Claudia Ramírez-Rentería; Aldo Ferreira-Hermosillo

Disclosures

J Med Case Reports. 2019;12(364) 

In This Article

Background

Most patients with diabetes mellitus (DM) are classified into the commonly accepted groups: type 1 DM (T1DM), type 2 DM, gestational DM, latent autoimmune diabetes of the adult (LADA), or maturity-onset diabetes of the young (MODY). However, almost 10% of patients may prove difficult to classify, especially in the younger groups.[1]

T1DM is usually associated with other autoimmune diseases. In this type of diabetes the CD4+ and CD8+ T cells play an important role in the initiation and progression of the disease. The recruitment and activation of these lymphocytes stimulates further secretion of inflammatory cytokines that accelerate beta cell destruction, resulting in insulin depletion.[2] Due to the lack of insulin and the effect of counterregulatory hormones, diabetic ketoacidosis (DKA) may occur.[3]

Cyclophosphamide (CY) is a cytotoxic chemotherapeutic agent used in the treatment of hematological diseases. A possible relation between CY and T1DM has been suggested in experimental animal models due to its immunomodulatory properties. It has been shown to promote susceptibility to T1DM in young prediabetic non-obese diabetic (NOD) mice.[2,4–7] Although the mechanism of action is not clear, some reports have suggested that CY may cause the destabilization of the local immune-regulatory balance by temporarily depleting suppressor cells. Paradoxically, CY has been used in addition to other immune modulators as a treatment for type B insulin resistance syndrome.[8,9]

We present the case of a patient with systemic lupus erythematosus (SLE), not previously diagnosed as having diabetes and with no evidence of autoimmune DM, who developed DKA after six cycles of CY therapy.

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