Insulinoma in a dog with pre-existing insulin-dependent diabetes mellitus

A 10-year-old golden retriever with a 3-year history of insulin-dependent diabetes mellitus was presented with recurring episodes of hypoglycemia and seizures. A presumptive diagnosis of an insulinoma was made based on hypoglycemia with concurrent endogenous hyperinsulinemia and unremarkable radiographic and ultrasonographic images of the chest and abdomen. A beta cell carcinoma of the pancreas with metastasis to the liver and a mesenteric lymph node was confirmed by surgery and histopathology.     

Insulinoma in a normoglycaemic dog with low serum fructosamine

An insulinoma was diagnosed in an eight-year-old, male golden retriever. Four fasted serum glucose concentrations were within the reference values over a seven-week period. Two serum fructosamine values over the same seven-week period were both low. An exploratory laparotomy and histopathology of an excised pancreatic nodule confirmed the diagnosis of insulinoma. This report demonstrates that a dog with a histologically confirmed insulinoma can have normal fasting serum glucose concentrations on multiple assays. It also demonstrates that fructosamine assays may be helpful in the diagnostic evaluation of normoglycaemic dogs with clinical signs suggestive of insulinoma.     

Insulinoma in a ferret

Insulinoma was diagnosed in a 7-year-old female ferret examined because of generalized seizures, intermittent paraplegia, and abnormal behavior. Low serum glucose, high serum insulin, and infinite amended insulin/glucose ratio values in this ferret supported the clinical diagnosis of insulinoma. Histologic examination of the pancreas confirmed the diagnosis of insulinoma. The clinical signs and laboratory evaluations in this case and in a previously reported case of insulinoma in a ferret were consistent with variations reported in dogs with insulinoma.     

Insulinoma in a cat

A 14-year-old domestic shorthair cat was presented with hypoglycaemia and seizures of several weeks duration. Bloodwork revealed hypoglycaemia (1.83 mmol/l; reference range 4.22-8.05 mmol/l) with concurrent normal insulin levels (171 pmol/l; reference range 72-583 pmol/l). An insulinoma was suspected and medical and dietary management were attempted with minimal success. An exploratory laparotomy was performed and a single, well-defined mass was found within the left lobe of the pancreas. The mass was removed and histologically classified as an islet cell carcinoma, consistent with an insulinoma. The cat had an episode of presumed postoperative pancreatitits, but recovered with appropriate treatment. The cat has had no clinical signs of recurrence of greater than 32 months postsurgery. There are only four cases of insulinoma in cats reported in the literature. All prior insulionomas reported were in older cats and were malignant in character, which is similar to the reports in the dog. This case is unique because of the apparent lack of local recurrence and development of metastatic disease, leading to the prolonged survival.     

Insulinoma in dogs: a review

Insulinomas are rare malignant functional pancreatic tumors of the β cells that retain the ability to produce and secrete insulin. Insulinomas are the most common pancreatic neuroendocrine tumor in dogs that can induce a variety of clinical signs that result from hypoglycemia and secondary neuroglycopenic and adrenergic effects. Diagnosis and treatment is considered challenging, and the prognosis can be extremely variable depending on the therapeutic choices. This review aims to summarize and update classic knowledge with current trends in the diagnosis, treatment, and prognosis of insulinomas.     

Glycogenosis in the dog.

Four cases of a generalized form of glycogenosis occurring in German Shepherd dogs, all females, are described. Symptoms could be noticed as early as the age of two months and progressed slowly for months. They appeared as dizziness, muscular weakness, and in two of the cases as poor nutritional state. The abdomen became gradually distended. The main lesion seen at postmortem was a greatly increased liver size with some moderate liver fibrosis. Heavy deposits of a granular substance behaving as glycogen in histochemical tests and at electron microscopy were found in the hepatic cells, muscle fibres of the heart, skeletal and smooth muscles, and in nerve and glial cells of the central nervous system. The substance was lying freely dispersed in the cell cytoplasm without any indication of lysosomal storage. The disease of dogs does not seem to be fully comparable with any of the types observed in man, but is probably much related to Type III or Cori''s Disease. Structure analysis of the deposits and enzyme investigations have been done and are published (Čeh et al. 1976).     

Bromocyclen poisoning in the dog.

An 18-week-old male German shepherd dog had a convulsion following the accidental ingestion of bromocyclen two hours previously. The dog then vomited and had a second convulsion. A pulse rate of 150 per minute and a respiratory rate of 54 per minute were recorded. The dog was treated with 2mg acepromazine and 0.6mg atropine administered intramuscularly (im) and repeated every four hours, 10ml of 20 per cent calcium borogluconate administered subcutaneously and 2ml penicillin and streptomycin im. Eighteen hours later, the respiratory rate was in excess of 60 per minute, and penicillin and streptomycin plus 2mg betamethasone were administered im. Only atropine was administered over the next 12 hours and then discontinued. Forty hours after the original convulsion, the respiratory rate had fallen to 30 per minute and the pulse rate to 84 per minute. A day later, the dog had fully recovered.     

Extraocular myositis in the dog.

Extraocular myositis is a rare condition in the dog and is poorly reported in the peer-reviewed veterinary literature. This case series and review are designed to be of value to those veterinary ophthalmologists seeking to investigate the disease further and also to veterinarians outside the specialty, for whom this may be their first introduction to the disease.     

Hypervitaminosis A in the dog.

Toxic effects of excessive vitamin A and of excessive vitamin ADE were studied in 9 mixed Labrador Retriever pups. Clinical signs were loss of body weight, dullness, emaciation, roughened coat, evident pain in limb joints, and retarded growth. Radiologic changes were decreases in overall length and thickness of long bones, development of osteophytes, periosteal reaction, and premature closure of epiphyses. Pathologic changes were degenerative epiphyseal plate, hemorrhage and exostotic proliferation of periosteum, fatty liver, and microcalculi in kidney. Toxic effects of excessive vitamin A did not appear to be so great when it was administered as vitamin ADE.     

Limb fractures in the dog and cat. VI. Complications of fractures in the dog

Abstract— A review is made of possible complications of fractures which may occur in the dog. The complications are classified and then the subject is dealt with under the headings of mal-union, delayed-union, non-union and prevention of complications. Emphasis is given to metallurgical problems and post operative care. Résumé— Un compte-rendu est établi sur les complications éventuelles des fractures qui pourraient arriver chez le chien. Les complications sont classifiées, le sujet est ensuite traîté sous le nom de mal-soudure, soudure-lente, non-soudure et prévention des complications. Les problème metallurgiques et les soins post-opérationnels sont soulignés. Zusammenfassung— Besprechung über mögliche Bruchkomplikationen, die bei Hunden und Katzen vorkommcn können. Die Komplikationen werden klassifiziert, wora ut die betreffenden Gegenstände unter den Titeln: schlech es Zusammenwachsen, verzögertes Zusammen wachsen, ausgebliebenes Zusammenwachsen und Komplikationsverhütung behandelt werden. Besonderes Gewicht wird auf metallurgische Probleme und postoperative Behandlung gelegt.     

Uremic gastropathy in the dog.

Stomachs of four dogs with uremia and four normal dogs were examined. Uremic stomachs represented four types of disease: atrophic, amyloidotic, ulcerative and necrotic gastropathy. Pathologic changes common to all uremic stomachs were expansion of the lamina propria, atrophy of gastric glands, and submucosal arteriopathy; lesions were limited to body and fundic zones. Lamina propria was markedly expanded by edema, mastocytosis, deposition of acidic mucosubstances, fibroplasia and mineralization. Capillaries in lamina propria had swollen endothelium and calcium salts were present extracellularly as amorphous granular laminae. Gastric glands were distorted and irregular and had fewer cells per unit of tissue. Parietal cells were swollen and had fragmentation of cytocavitary network and mitochondrial swelling with calcification. Chief cells were shrunken, agranular and atrophic with foci of glycogen and dilation of endoplasmic reticulum. Argentaffin cell content was diminished. Muscular arteries of submucosae had segmental degenerative lesions characterized by myocyte necrosis, calcification, and deposition of acidic mucosubstances and fibrin; thrombosis and obstructive arteriopathy were common. These studies suggest that uremic gastropathy is a disease of mucosal lamina propria and that lesions were due to anoxia caused by diffuse vascular injury and to altered parietal cell function.