Hyperparathyroidism in dogs with hyperadrenocorticism

Ramsey, Ian; Tebb, A.J.; Harris, Emily; Evans, Helen; Herrtage, M. E.

doi:10.1111/j.1748-5827.2005.tb00282.x

Cited by 44 publications

(60 citation statements)

References 29 publications

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“…The observations in this study support previous studies that have suggested that PTH concentrations are increased in dogs with HAC (Sturgeon and others 1995, Ramsey and Herrtage 2001, Ramsey and others 2005. There may be three reasons for this.…”

Section: Discussionsupporting

confidence: 92%

“…However, it has been previously demonstrated that dogs with HAC have normal total calcium, normal ionised calcium, increased serum phosphate (Ramsey and others 2005) and increased parathyroid hormone (PTH) concentrations -so-called adrenal secondary hyperparathyroidism (Sturgeon and others 1995, Ramsey and Herrtage 2001, Ramsey and others 2005 -when compared with age-and weight-matched dogs without HAC.…”

Section: Introductionmentioning

confidence: 99%

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Canine hyperadrenocorticism: effects of trilostane on parathyroid hormone, calcium and phosphate concentrations

Tebb

Arteaga

Evans³

et al. 2005

J of Small Animal Practice

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Objectives: To determine the effects of treating canine hyperadrenocorticism (HAC) on parathyroid hormone (PTH), calcium and phosphate concentrations in dogs. Methods: Serum calcium, phosphate and PTH concentrations were analysed in 22 dogs with HAC before treatment with trilostane and at a median of 210 days after commencing treatment. Pretreatment data were compared with data from an age‐ and weight‐matched group of hospitalised patients, and post‐treatment data were compared with pretreatment data. Results: PTH and phosphate concentrations were significantly higher in dogs with HAC compared with control dogs. PTH concentrations reduced significantly with treatment, such that there was no longer difference between the HAC and control groups. Phosphate concentrations also reduced significantly with treatment but there was still a significant difference between those in dogs with HAC and control dogs. Despite no significant difference between calcium concentrations in the pretreatment HAC and control groups, calcium concentrations increased significantly with treatment. Clinical Significance: These results show that adrenal secondary hyperparathyroidism resolves with treatment and suggest that increased calcium and phosphate levels have a role in its pathogenesis.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Canine hyperadrenocorticism: effects of trilostane on parathyroid hormone, calcium and phosphate concentrations

Tebb

Arteaga

Evans³

et al. 2005

J of Small Animal Practice

Self Cite

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“…Surprisingly, the only hypercalcémie animal detected (case 5) was the most hypekalemic. Although 10 out of 40 hypercalcémie dogs were diagnosed to suffer from hypoadrenocorticism in one study (Elliot et al 1991), the pathogenesis of hypercalcemia is poorly understood at the moment (Ramsey et al 2005, Gow et al 2007.…”

Section: Discussionmentioning

confidence: 99%

Οξύς Υποφλοιοεπινεφριδισμος (Αδισσώνια Κρίση) Στο Σκύλο: Αναφορά Σε Έξι Περιστατικά

Kasabalis

Soubasis

Pardali

et al. 2017

J Hellenic Vet Med Soc

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Medical records of six dogs admitted with acute hypoadrenocorticism were reviewed. All 6 animals were bradycardic and had prolonged capillary refilling time. Hypothermia was detected in 5/6 animals. Clinicopathological evaluation on admission revealed anemia (3/6 dogs), increased (2/6) and normal (2/6) lymphocyte and eosinophil counts, azotemia and hyperkalemia (6/6), hyponatremia, in 5/6 dogs in which sodium was measured with a sodium (Na) : potassium (K) ratio lower than 24, hypoglycemia (2/6) and hypercalcemia, hypocholosterolemia, increased serum alkaline phosphatase and alaninoaminotransferase activities, one dog each. Urine specific gravity was lower than 1025 in 4 dogs. Thoracic radiographs and abdominal ultrasonography disclosed microcardia (2/6), pleural effusion (2/6) and ascites (1/6). Two dogs (2/6), also, presented atrial standstill or atrioventricular block, detected on electrocardiograms. In all 6 animals emergency treatment included the use of intravenous normal saline and glucocorticoids (dexamethasone) immediately after the completion of an ACTH stimulation test with tetracosactide. Two dogs died, one during the 1st day and the other on the 4th day of hospitalization, the latter after the sudden appearance of severe hemorrhagic gastroenteritis. Hospitalization time in the remaining 4 dogs ranged from 3 to 10 days. Prolongation of hospitalization was associated with worsening of anemia, hypoalbuminemia, neurologic complications and non-responsive azotemia. Four dogs (4/6) were discharged on oral prednisolone and fluodrocortisone, but one died after a week for unknown reasons. Acute hypoadrenocorticism is a life threatening condition requiring emergency treatment for a successful outcome. Its inclusion in the differential diagnosis of canine emergencies, presented with acute weakness and gastrointestinal signs, is mandatory, but for its confirmation a complete laboratory and, most importantly, an ACTH stimulation test are always required.

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“…Despite hypercalciuria, plasma ionized calcium was normal in people and dogs with hypercortisolism compared with control subjects (Faggiano et al, 1982;Ramsey et al, 2005). On the other hand, hyperphosphaturia is a common observation following GC therapy or in Cushing's disease (Vrtovsnik et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

Niacin Ameliorates Hypercalciuria and Hyperphosphaturia Due to Glucocorticoid Administration in Rats

Shomali¹

2013

American Journal of Pharmacology and Toxicology

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Hypercalciuria and hyperphosphaturia are present in long term and high dose regimens of glucocorticoid therapy. This study aims to evaluate the effect of niacin at its pharmacological dose on calcium and phosphate disturbances due to methylprednisolone administration in growing rats. Twenty one rats were randomly divided into three equal groups and treated as follows for 4 weeks: 1-Normal saline (Control); 2-Methyl Prednisolone (MP) acetate, 3.5 mg kg −1 five days a week, SC and 3-MP acetate, 3.5 mg kg −1 five days a week, SC + niacin 200 mg kg −1 daily by oral gavages. At the end of the experiment, serum and urinary calcium and phosphate assays were performed and calcium content of forth lumbar vertebrate and tibia-fibula bone was determined by atomic absorption method. No significant difference observed in serum calcium or phosphate levels among different groups (p>0.05), however an obvious hypercalciuria associated with hyperphosphaturia was present in MP group as compared to control (p<0.001). Niacin significantly decreased urinary calcium (p<0.001) and phosphate (p = 0.005) concentrations as compared to MP group. Calcium level was still significantly higher than control (p<0.001), while phosphate decreased even to a lower level than control (p = 0.005). Calcium content of forth lumbar vertebrate or tibia-fibula bone of rats remained statistically the same among different groups (p>0.05). Niacin at its pharmacological dose can ameliorate hypercalciuria and hyperphosphaturia due to long term and high dose glucocorticoid administration in growing rats without affecting bone calcium content. The possible clinical importance of this effect needs to be clarified in future studies.

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Hyperparathyroidism in dogs with hyperadrenocorticism

Cited by 44 publications

References 29 publications

Canine hyperadrenocorticism: effects of trilostane on parathyroid hormone, calcium and phosphate concentrations

Canine hyperadrenocorticism: effects of trilostane on parathyroid hormone, calcium and phosphate concentrations

Οξύς Υποφλοιοεπινεφριδισμος (Αδισσώνια Κρίση) Στο Σκύλο: Αναφορά Σε Έξι Περιστατικά

Niacin Ameliorates Hypercalciuria and Hyperphosphaturia Due to Glucocorticoid Administration in Rats

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