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Cobalamin is a member of the B-group of vitamins and a cofactor for metabolic processes like nucleic acid synthesis, amino acid synthesis, and the citric acid cycle. Mammals are unable to synthesize cobalamin and therefore rely on adequate food intake. Cobalamin absorption is a complex process in the stomach, duodenum, and ileum, requiring a functional exocrine pancreas. Thus, a great number of gastrointestinal diseases like chronic enteropathies, intestinal lymphoma, or exocrine pancreatic insufficiency can lead to hypocobalaminemia. Furthermore, some dog breeds (Giant Schnauzer, Border Collie, Australian Sheperd Dog, and Beagle) can have a primary, hereditary cobalamin deficiency (Imerslund-Gräsbeck syndrome). Clinical signs of cobalamin deficiency comprise anorexia, vomiting, diarrhoea, failure to thrive, and neuropathies. Laboratory findings like non-regenerative anemia, leukopenia, hypoglycemia, and hyperammonaemia have also been described. When hypocobalaminemia is suspected usually in dogs and cats, the cobalamin concentration is usually measured by immunoassay. Because the concentrations of cobalamin in blood and cells can differ the sole measurement of the vitamin concentration is of limited informative value. Treatment depends on the underlying disease aiming at eliminating the cause of hypocobalaminemia. However, successful therapy of gastrointestinal diseases often requires an additional oral or parenteral cobalamin supplementation. In patients with Imerslund-Gräsbeck syndrome, a regular and lifelong cobalamin supplementation is essential., Competing Interests: Die Autoren bestätigen, dass kein Interessenkonflikt besteht., (Georg Thieme Verlag KG Stuttgart · New York.)

Aim of this study was to record the clinical findings in bitches with ovarian cyst syndrome (OCS) and to interpret them in connection with the endocrine status in peripheral blood and in cyst liquid. For our investigation 16 bitches of different breeds with an average age of 9.7 years were used. They have been presented to the clinic due to different gynecological symptoms. The leading symptom was in 87.5 % of the cases a chronic vaginal secretion. In addition to a detailed anamnesis a clinical examination was performed including vaginalcytologic, sonographic, hematologic and hormonal findings (progesterone P4, 17β estradiol E2). As basic diagnoses could be made: Cycle aberrations (n = 8), pyometra endometritis complex (n = 4), vaginal tumor (n = 4). In addition 3 patients were presented with alopecia. All patients were ovariohysterectomized without prior conservative treatment and the ovaries histologically examined and classified. Based on sonographic findings before and macroscopic evaluation the ovaries after surgery, the OCS could be divided into an oligocystic and polycystic syndrome. There were predominating (94 %) follicle theca cysts. The formation of cysts on the ovary was in the vast majority (66.7 %) combined with corpora lutea. The endometrium showed mainly (50 %) a glandular cystic hyperplasia (CHE) and the hematologic examination revealed in 31.2 % of the patients a combination of advanced erythropenia and thrombocytopenia. Generally there was no direct relationship between increased P4 and E2 values in the pooled cyst fluid and in the peripheral blood when the oestrous phase was considered. Based on present data the diagnosis of OCS of the bitch by means of peripheral P4 and E2 values is not possible.

Hypernatremia due to different pathophysiological mechanisms results in a rise in plasma osmolality. Dependent on its severity and on the speed of its development hyperosmolality can be life-threatening. This article describes 2 dogs and 1 cat with central nervous system disorders (adenoma of the pituitary gland, cerebral trauma). All patients developed normovolemic hypernatremia due to pituitary gland and hypothalamus dysfunction, respectively. Plasma sodium concentrations ranged from 163 to 185 mmol/l. Neurological examinations revealed lethargy, disturbances of consciousness, and ataxia, respectively. The dogs had to be euthanased due to the grave prognosis, the cat with cerebral trauma survived.

Peter Stewart criticized the traditional theory of the acid-base status by Henderson-Hasselbalch as too simple and incomplete. He developed a new model with 3 independent variables: (1) pCO2, (2) SID (strong ion difference) and (3) Atot (Acid total). In healthy and ill dogs the diagnostic usefulness of both acid-base models were compared. This study included n=58 healthy dogs and 3 clinical cases of sick dogs. The age of the healthy dogs was 5.0 (2.0-7.0) years (= median (1.-3. quartil)). The 3 clinical cases included (1) a dog with septic shock, (2) with acute renal insufficiency, and (3) with hypovolaemic shock due to gastric torsion. Venous blood was taken of all dogs and the acid-base parameters were determined within < or =30 minutes. Electrolytes and albumin were determined in blood serum and used for calculation of the Stewart variables. Limits of reference intervals (x+/-1.96 - s) were determined for the healthy dogs yielding pCO2 = 3.6-6.5 kPa, [SID3] = 33.1-50.9 mmol/l resp. [SID4] = 31.8-49.6 mmol/l and [Al = 8.5-13.1 mmol/l. In Case 1 the Henderson-Hasselbalch parameters demonstrated the presence of a strong metabolic acidosis with mild respiratory influence (pH, [HCO3-], [BE] and PCO2 at upper range of normal). Analysis of the Stewart variables [SID3] resp. [SID4] revealed an electrolyte imbalance with [Cl-] and [lactate-] as the reason for metabolic acidosis. Case 2 showed a metabolic acidosis with respiratory compensation (pH, [HCO3-], [BE] and PCO2). Analysis of the Stewart variables with [SID3] resp. [SID4 caused by [K+], [Na+] and [lactate-]demonstrated the acidotic metabolism due to a renal malfunction. Case 3 had a metabolic acidosis (pH-value in the lower range) caused by electrolyte imbalances ([SID4]. The Stewart variables allow a better understanding of the causes of acid-base-disturbances in animals with implications for successful therapy via infusion.

Elevated Creatine kinase-activitiy (CK) indicates disturbances of the muscle cell integrity. In addition to primary muscle disease, like trauma, inflammation or dystrophy, diseases of other organs can lead to secondary muscle involvement, which will be indicated by increased serum activities of the CK. The mechanisms of muscle cell disturbance are still unknown. An elevated protein catabolism in the muscle cell is suspected. In the present study we investigated, if dogs and cats with metabolic diseases have increased CK-activity in the serum. From 34 dogs and cats in a group with different metabolic diseases without metabolic acidosis 19% of the dogs and 50% of the cats had increased CK-activity in the serum. From 33 dogs and cats with different metabolic diseases connected with metabolic acidosis 86% of the dogs and 95% of the cats had simultaneously increased CK-activity in the serum. In comparison to healthy dogs and cats animals with metabolic diseases have significant and in cases of metabolic di-seases with metabolic acidosis cats have high significant elevation (dogs significant) of CK-activity in the serum. There was no significant correlation between the groups of patients. In conclusion we think that our results show that metabolic diseases often induce secondary myopathy, measured by CK-activity in the serum, but metabolic acidosis has no direct influence on elevated CK activity in dogs and cats.

The pilot study included serum analysis of ionized calcium, copper, zinc, various hormones and amino acid profiles from dogs affected with panosteitis, as well as protein electrophoresis performed on bone biopsies. Results of these analyses are as follows: ionized calcium, copper, zinc and hormones (parathyroid hormone, IGF-1, T3 and T4) were within reference ranges. Eleven of 23 serum amino acids from panosteitis-affected dogs were found to be significantly increased (P = 0.05). SDS-polyacrylamide gel electrophoresis performed on bone biopsies, which were pretreated with SDS, resulted in a double band of 39,000 D molecular weight in all panosteitis-affected dogs. Similar studies in control dogs resulted in a single band in this region. Attempts at amino acid sequencing from the N-terminal of the proteins in this double band region were unsuccessful. A chemical interference at the N-terminal end of these proteins was suspected. The composition of this double band is as yet unknown. The etiology of panosteitis could therefore not be definitively verified. However, it does appear that protein- or amino acid metabolism is affected in dogs with panosteitis.

This article shows the possibilities of liver diagnosis in dogs. After a short introduction about metabolism with some aspects in pathophysiology follows the way of investigation from anamnesis, clinical examination, blood work and urinalysis to ultrasound, x-ray and biopsy.

The determination of the intracellular acid-base state is reported in this paper, using erythrocytic haemolysate in dogs as an example. Reference values are given for 217 clinically healthy dogs. The effects of various selected stages of illness and additional stresses on the erythrocytic acid-base equilibrium are reported and compared with acid-base changes in the blood. The metabolic acidosis observed may occur earlier and be stronger in the intracellular space than in the blood. There seems to be a closer correlation between a disturbed intraerythrocytic acid-base equilibrium and the degree of clinical symptoms than between the (commonly investigated) acid-base changes in the blood and the clinical presentations. The investigation of the blood alone does not provide a satisfactory indication of the patient's acid-base state and of the necessity for treatment.

It was the aim of the investigation to evaluate the influence of marginal (60-30 micrograms/kg BW/d) or adequate (680-360 micrograms/kg BW/d) Cu-intake on the development of growing beagles (n = 10) and the incidence of skeletal diseases. Low Cu-intake (6 dogs) reduced Cu-concentrations in plasma (1.4 vs. 9.7 mumol/l), hair (3.3-4.5 vs. 12.6-14.5 mg/kg DM), liver (19 vs. 246 mg/kg fat free DM), bile (0.28 vs. 7.04 mg/l), and other samples significantly. Hemoglobin and packed cell volume decreased after 4 months of depletion (normochromic anemia). First clinical signs of Cu-deficiency were depigmentation and greying of hair, followed by hyperextensions in the distal forelegs. After necropsy deformations of the long bones were seen more frequently in the depleted animals, without distinct alterations of the microstructure or chemical composition of bones or tendons.

In three young fox terriers a lipid storage disease is reported. This thesaurosis is almost identical to Wolman's disease in children. Clinically and pathologically hepatosplenomegaly is the most striking feature. Morphologically the disease is characterized by extensive lipid deposition mainly in liver, spleen, lymphnodes, intestinal mucosa, and bone marrow. Circular corneal lipid deposit (Arcus lipoides corneae) is of diagnostic significance. Some of the material has the typical structure of cholesterol crystals. Under polarized light the deposits consist of birefringent and non-birefringent lipids. All three dogs with lipid storage disease have one common ancestor. In addition their pedigrees reveal close relationship amongst the nearer forefathers and the affected animals themselves. From analogy with human Wolman's disease it is concluded, that in the Foxterrier, too, this lipid storage disease is caused by an inheritable deficiency of acid esterase. The mode of inheritance of this inborn lysosomal disease is probably autosomal recessive.