Background After a strong epidemiological link to diet was established in an outbreak of pancytopenia in cats in spring 2021 in the United Kingdom, 3 dry diets were recalled. Concentrations of the hemato‐ and myelotoxic mycotoxins T‐2, HT‐2 and diacetoxyscirpenol (DAS) greater than the European Commission guidance for dry cat foods were detected in the recalled diets. Objectives To describe clinical and clinicopathological findings in cats diagnosed with suspected diet induced pancytopenia. Animals Fifty cats presenting with pancytopenia after exposure to a recalled diet. Methods Multicenter retrospective case series study. Cats with known exposure to 1 of the recalled diets were included if presented with bi‐ or pancytopenia and underwent bone marrow examination. Results Case fatality rate was 78%. Bone marrow aspirates and biopsy examination results were available in 23 cats; 19 cats had a bone marrow aspirate, and 8 cats had a biopsy core, available for examination. Bone marrow hypo to aplasia—often affecting all cell lines—was the main feature in all 31 available core specimens. A disproportionately pronounced effect on myeloid and megakaryocytic cells was observed in 19 cats. Myelofibrosis or bone marrow necrosis was not a feature. Conclusion and Clinical Importance Mycotoxin induced pancytopenia should be considered as differential diagnosis in otherwise healthy cats presenting with bi‐ or pancytopenia and bone marrow hypo‐ to aplasia.

BackgroundHypoadrenocorticism is an important differential for hypercalcemia. The etiology of hypercalcemia in hypoadrenocorticism in dogs is unclear.ObjectiveTo review the prevalence of hypercalcemia and use statistical models to identify clinical, demographic, and biochemical variables associated with hypercalcemia in dogs with primary hypoadrenocorticism.AnimalsOne hundred ten dogs with primary hypoadrenocorticism; 107 with recorded total calcium (TCa), 43 recorded ionized calcium (iCa).MethodsMulticenter retrospective observational study at 4 UK referral hospitals. Univariable logistic regression analyses were performed to assess the association between independent variables of signalment, hypoadrenocorticism type (glucocorticoid only deficient hypoadrenocorticism [GHoC] vs glucocorticoid and mineralocorticoid deficient hypoadrenocorticism [GMHoC]), clinicopathological variables and hypercalcemia. Hypercalcemia was defined as elevated TCa, an elevated iCa, or both elevated TCa and iCa (Model 1) or as elevated iCa (Model 2).ResultsOverall prevalence of hypercalcemia was 34.5% (38/110). The odds of hypercalcemia (Model 1) were increased (P < .05) in dogs with GMHoC ([vs GHoC], OR [odds ratio] = 3.86, 95% confidence interval [CI] 1.105‐13.463), higher serum creatinine (OR = 1.512, 95% CI 1.041‐2.197), and higher serum albumin (OR = 4.187, 95% CI 1.744‐10.048). The odds of ionized hypercalcemia (Model 2) were increased (P < .05) with reduced serum potassium concentration (OR = 0.401, 95% CI 0.184‐0.876) and younger age (OR = 0.737, 95% CI 0.558‐0.974).Conclusions and Clinical ImportanceThis study identified several key clinical and biochemical variables associated with hypercalcemia in dogs with primary hypoadrenocorticism. These findings aid understanding of the pathophysiology and etiology of hypercalcemia in dogs with primary hypoadrenocorticism.