A description of equine cutaneous mastocytosis is given. The lesion was characterized by focal aggregates of mast cells, and by eosinophils, fibrinoid necrosis of collagen, and focal necrosis with dystrophic mineralization of necrotic debris. This is an uncommon, previously undescribed lesion in horses. The authors encountered 14 cases in a 16-year period. The etiology and nature of the lesion are undetermined. Morphologic similarities to canine cutaneous mast-cell tumors, cutaneous lesions of collagen diseases, and calcinosis circumscripta are noted and the possibility of relationships to these lesions is discussed.

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Batracylin (NSC-320846) is a dual inhibitor of DNA topoisomerases I and II. Batracylin advanced as an anticancer agent to Phase I clinical trials where dose limiting hemorrhagic cystitis (bladder inflammation and bleeding) was observed. To further investigate batracylin’s mechanism of toxicity, studies were conducted in Fischer 344 rats. Once daily oral administration of 16 or 32 mg/kg batracylin to rats for 4 days caused overt toxicity. Abnormal clinical observations and adverse effects on clinical pathology, urinalysis, and histology indicated acute renal damage and urothelial damage and bone marrow dysfunction. Scanning electron microscopy revealed sloughing of the superficial and intermediate urothelial layers. DNA damage was evident in kidney and bone marrow as indicated by histone γ-H2AX immunofluorescence. After a single oral administration of 16 or 32 mg/kg, the majority of batracylin was converted to N-acetylbatracylin (NAB) with a half-life of 4–11 hr. mesna (Mesnex™), a drug known to reduce the incidence of hemorrhagic cystitis induced by ifosfamide or cyclophosphamide, was administered to rats prior to batracylin, but did not alleviate batacylin-induced bladder and renal toxicity. These findings suggest that batracylin results in DNA damage-based mechanisms of toxicity and not an acrolein-based mechanism of toxicity as occurs after ifosfamide or cyclophosphamide administration.

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