Hypocalcemia and Primary Hypoparathyroidism

Pelvic fracture triggering symptoms of an underlying primary hypoparathyroidism in an adult spayed bitch: A case report

“…In fact, on differential diagnosis, primary hypoparathyroidism may be due to the absence or destruction of the parathyroid glands (following surgical removal or immune‐mediated disease, for instance). However, transient hypoparathyroidism may occur after correction of long‐standing hypercalcemia (hypercalcemia causing temporary atrophy of the gland), with similar symptoms to those occurring from surgical removal or ablation of a parathyroid adenoma, responsible for primary hyperparathyroidism (Chew & Nagode, 2000; Feldman & Nelson, 2004). Thyroid surgery in either dogs or cats may result in the accidental damage or ablation of the parathyroid glands.…”

“…Thyroid surgery in either dogs or cats may result in the accidental damage or ablation of the parathyroid glands. Thyroidectomy is reported to be the most common cause of hypoparathyroidism in cats, where parathyroid glands can follow the resection of the thyroid (Feldman, 2005; Feldman & Nelson, 2004). However, the surgical ablation of parathyroid glands was not the cause of the clinical symptoms of this clinical case.…”

“…In the pseudo‐hypoparathyroidism, clinical symptoms are due to the failure of PTH receptors, which are hyporesponsive to its stimulation. Such a hyporesponsiveness of PTH receptors may occur during pharmacological treatments (chemotherapeutic agents), sepsis, primary or metastatic bone tumours, hypercalcitoninism or radiation‐induced damage (Bruyette & Feldman, 1988; Chew & Nagode, 2000 and Feldman & Nelson, 2004). Nevertheless, many of these causes have not yet been identified in veterinary medicine.…”

“…The onset of action of dihydrotachysterol is 1–7 days, displaying to be more rapidly eliminated after discontinuation, usually in four to 14 days (although it may last 30 days). For these reasons, dihydrotachysterol appeared safer and easier to handle when dosages needed to be adjusted in a more flexible way than ergocalciferol might have offered to (Feldman, 2005; Feldman & Nelson, 2004). In fact, the slow re‐establishment of circulating iCa levels highlighted the need to develop an individual protocol on the basis of the response to calcium and dihydrotachysterol administration, as a desirable effect, in association with the lifelong assessment of the nutritional status.…”

“…An additional causal factor of primary hypoparathyroidism is related to parathyroid agenesis. The parathyroid agenesis is, however, a very rare case, which has been reported in a dog (Feldman & Nelson, 2004) and was suspected in a cat (Bassett, 1998). Despite, in general, primary hypoparathyroidism is an uncommon clinical finding in the veterinary medicine, it is undoubtedful that both dogs and cats can suffer from primary hypoparathyroidism (Barber, 2004;Russell, Bond, Robertson, Parry, & Irwin, 2006;Sherding, Meuten, Chew, Knaack, & Haupt, 1980;Torrance &Nachreiner, 1989 andWaters &Scott-Moncrieff, 1992).…”