Amyloid deposits localized to the islets of Langerhans are typical of non-insulin-dependent human diabetes mellitus and of diabetes mellitus in adult cats. Amyloid deposits also commonly occur in insulin-producing pancreatic tumors. We have purified a major protein-insulinoma or islet amyloid polypeptide (IAPP)-from human and cat islet amyloid and from amyloid of a human insulinoma. IAPP from human insulinoma contained 37 amino acid residues and had a theoretical molecular mass of 3850 Da. The amino acid sequence is unique but has >40% identity with the human calcitonin gelie-related peptide. A partial amino acid sequence of cat islet IAPP corresponding to positions 1-27 of human insulinoma IAPP was identical to the human IAPP except for substitutions in three positions. An antiserum raised to a synthetic human insulinoma IAPP-(7-17) undecapeptide showed specific immunohistochemical reactivity with human and cat islet amyloid and with islet B cells.

Serum and seminal plasma concentrations or activities of acid phosphatase (AP), prostate specific antigen (PSA), and canine prostate specific esterase (CPSE) were measured in normal dogs, dogs with benign prostatic hyperplasia (BPH), dogs with bacterial prostatitis, and dogs with prostatic carcinoma t o determine if these assays would be of value in differentiating dogs with prostatic carcinoma from normal dogs, and dogs with other prostatic disorders. In addition, tissue sections of prostatic adenocarcinomas were stained with antiprostatic AP, anti-CPSE, and anti-PSA antibodies t o determine if these would be suitable immunohistochemical markers of prostatic carcinoma. Prostate-specific antigen was not detected in canine serum or seminal plasma. Serum and seminal AP activities did not differ significantly between normal dogs and those with prostatic diseases, or among dogs with different prostatic disorders. Serum CPSE activities were significantly higher in dogs with BPH than in normal dogs. Mean serum enign prostatic hyperplasia (BPH), prostatic carci-B noma, and bacterial prostatitis can be difficult to differentiate in dogs because of similarities in clinical presentation, and laboratory and radiographic findings. A definitive diagnosis often requires prostatic biopsy, which is complicated by the relative inaccessibility of the prostate gland. In patients with prostatic carcinoma, inability to rapidly confirm the diagnosis may contribute to the poor prognosis typically associated with thisIn men with prostatic carcinoma, the use of serum markers such as acid phosphatase (AP) and prostate-specific antigen (PSA) has facilitated diagnosis, determination of the extent of disease, evaluation of therapeutic response, and detection of relapse after the rap^.^.^ Prostate-specific antigen is a proteolytic glycoprotein found in normal, hyperplastic, and malignant human prostatic tissue. Increases in serum PSA concentrations have been reported in human patients with BPH, prostatitis, and prostatic carcinomx8 In human patients with prostatic carcinoma, PSA concentrations correlate with the stage ofdisease, and serum activities of PSA are considered more sensitive than serum acid phosphatase activities for monitoring the disease.6 Acid phosphatase and PSA have been identified in normal, neoplastic, and hyperplastic canine prostatic epithelial cells. ' Canine prostate specific esterase (CPSE), the major secretory product of the canine prostate gland, is similar to human PSA and, like PSA, is a serine protease. Although the proteins are closely related, they are clearly distinct from one another." Both CPSE and PSA are under hormonal regulation, and decreases in serum testosterone activities result in reduction in the serum and seminal plasma concentrations or activities.' ' 3 ' ' Canine prostate specific esterase has been identified in normal canine prostatic cells, in canine seminal fluid,I2-I5 and in hyperplastic and neoplastic prostatic tissue.' The esterase is predominantly localized to the apical portions of canin...

Diagnosis of malignant histiocytosis (MH), a disorder characterized by systemic proliferation of morphologically atypical histiocytes and their precursors, in an 8-year-old neutered female Golden Retriever was based on light and electron microscopic and immunohistochemical findings. Clinically, the dog presented with unilateral forelimb lameness. Eight days after surgical exploration of a swollen brachium, the dog developed sudden onset of posterior paresis, fecal and urinary incontinence, and a flaccid tail. Necropsy revealed infiltrative and nodular lesions in the right forelimb and regional lymph nodes, thoracic and abdominal cavities, and lumbar epidural space. Gross lesions were not found in the lungs or integument. Histopathologic examination showed infiltrates of atypical histiocytes in skeletal muscle, joint, and regional lymph nodes of the right forelimb; intercostal muscle; lung; liver; spleen; pancreas; kidneys; and spinal dura. Most tumor infiltrates were nodular and composed of loosely aggregated cells that were 10-30 μm in diameter with abundant eosinophilic to foamy cytoplasm, had central or eccentric nuclei, and were periodic acid-Schiff negative. Many binucleated cells, multinucleated giant cells, and mitotic figures were seen. Tumor cells contained phagocytosed erythrocytes, mononuclear cells, and some leukocytes. Ultrastructural features of tumor cells included cytoplasmic lipid droplets, lysosomes, and phagolysosomes. Immunohistochemical studies on paraffin-embedded sections showed positive reactivity to human T-cell Ag (clone UCHL-1) and for lysozyme, α-1-antitrypsin, and cathespin B. Polyclonal intracellular immunoglobulin reactivity and lectin binding (peanut, soybean, and wheat germ agglutinins and concanavalin A) were also demonstrated. Criteria for diagnosis of malignant histiocytic tumors and differential diagnosis are discussed.

Five horses were examined because of signs of muscle stiffness, colic, or both. All 5 had been exposed to Streptococcus equi within 3 weeks prior to examination or had high serum titers of antibodies against the M protein of S equi. Horses had signs of unrelenting colic-like pain and focal areas of muscle swelling. Four horses were euthanatized. The fifth responded to treatment with penicillin and dexamethasone; after 3 weeks of treatment with dexamethasone, prednisolone was administered for an additional 10 weeks. Common hematologic and serum biochemical abnormalities included neutrophilia with a left shift and toxic changes, hyperproteinemia, hypoalbuminemia, and high serum creatine kinase and aspartate transferase activities. Necropsy revealed extensive infarction of the skeletal musculature, skin, gastrointestinal tract, pancreas, and lungs. Histologic lesions included leukocytoclastic vasculitis in numerous tissues and acute coagulative necrosis resembling infarction. These horses appeared to have a severe form of purpura hemorrhagica resembling Henoch-Schönlein purpura in humans and characterized by infarction of skeletal muscles. Early recognition of focal muscle swelling, abdominal discomfort, neutrophilia, hypoalbuminemia, and high serum creatine kinase activity combined with antimicrobial and corticosteroid treatment may enhance the likelihood of a successful outcome.

A 2.5-year-old female Thoroughbred was examined because of lethargy, anorexia, and weight loss. Analysis of a CBC revealed erythrocytosis and an increase in PCV. Serum biochemical analysis revealed increases in activities of several hepatic enzymes. Ultrasonography revealed hepatomegaly and a heterogeneous appearance of the hepatic parenchyma. The horse did not improve despite supportive care, and it was euthanatized. Necropsy revealed numerous raised white to gray foci in the liver. Histologically, these foci consisted of neoplastic cells that resembled fetal hepatocytes, embryonal-type cells, and cells with features intermediate between those 2 cell types. Immunohistochemical staining revealed that hepatocytes stained strongly with anti-alpha-fetoprotein. On the basis of these results, hepatoblastoma was diagnosed. Diagnosis of hepatoblastoma is difficult, because it can appear histologically similar to other hepatic tumors, such as hepatocellular carcinomas. Definitive diagnosis requires histologic evaluation of tumor architecture and cell morphology. Immunohistochemical staining for alpha-fetoprotein in tumor cells may serve as a tumor marker but is not pathognomonic of hepatoblastoma. Paraneoplastic syndromes, such as erythrocytosis, can accompany hepatoblastoma. The prognosis for horses with hepatoblastoma is grave.