No full-text available
To read the full-text of this research,
you can request a copy directly from the authors.
Perioperative characteristics, histological diagnosis, and outcome in cats undergoing surgical treatment of primary hyperparathyroidism
Abstract
Objective
To report perioperative characteristics, complications, histopathologic diagnosis and outcome in cats undergoing surgical treatment for primary hyperparathyroidism (PHPT).
Study design
Multi‐institutional, retrospective case series.
Animals
Thirty‐two client‐owned cats.
Methods
Medical records of cats treated with surgical removal of 1 or more parathyroid gland(s) with confirmed histopathologic evaluation were reviewed. Cats were divided into preoperative ionized calcium (iCa) groups corresponding to the 33rd, 67th, and 100th percentiles of the preoperative iCa results of the study population. Follow‐up consisted of phone conversation with owners or primary veterinarian.
Results
Ionized calcium was above reference range in all cats (median 1.8 mmol/L [interquartile range, 1.5–1.9]). Abnormal tissue was excised after cervical exploration in all cats. The most common histopathologic diagnoses were parathyroid adenoma in 20 of 32 (62.5%) cats and parathyroid carcinoma in 7 of 32 (21.9%) cats. At discharge, 6 of 32 (18.8%) cats had hypercalcemia, 5 of 32 (15.6%) had hypocalcemia, and 21 of 32 (65.6%) were normocalcemic. Preoperative iCa did not correlate with postoperative iCa. The median follow‐up time was 332 days (range, 7–3156). Overall median survival time was 1109 days (95% CI, 856–1332). Survival time was not associated with preoperative iCa group, hypocalcemia at discharge, hypercalcemia at discharge, or diagnosis of carcinoma.
Conclusion
In this cohort of cats, parathyroid adenoma was the most common cause of PHPT, and surgical treatment resulted in very good median survival time. Preoperative iCa was not predictive of postoperative hypocalcemia.
Clinical significance
Surgical parathyroidectomy for treatment of PHPT in cats provides a favorable prognosis.
... Primary hyperparathyroidism is rarely reported in cats. [1][2][3][4][5][6][7] It is caused by overproduction of PTH due to parathyroid gland hyperplasia or an autonomously functioning parathyroid adenoma, cystadenoma or carcinoma, with adenoma being the most common and carcinoma the rarest form. 1,3-6,8-10 To our knowledge, this is the first case report of a bilateral parathyroid cystic carcinoma in a cat. ...
... No specific breed predispositions have been described. 1 Clinical signs include lethargy, anorexia, vomiting and weight loss, 1,3,6,7,11 and 37.5% of affected cats have a palpable mass in the cervical region. 1 Despite the bilateral and malignant presentation of the disease in this case, the only reported sign was chronic vomiting. ...
... 1 Clinical signs include lethargy, anorexia, vomiting and weight loss, 1,3,6,7,11 and 37.5% of affected cats have a palpable mass in the cervical region. 1 Despite the bilateral and malignant presentation of the disease in this case, the only reported sign was chronic vomiting. ...
Case summary
A 16-year-old neutered female Korat cat presented with chronic vomiting, mild azotaemia and mild hypercalcaemia. Physical examination revealed bilateral palpable masses on each side of the trachea. Laboratory results were consistent with primary hyperparathyroidism, diagnostic imaging findings with cystic thyroid or parathyroid masses, and fine-needle aspiration cytology with thyroid hyperplasia or adenoma. In order to confirm whether one or two of the masses were the cause of the hyperparathyroidism, cystic fluid was aspirated from both for parathyroid hormone concentration measurement. The concentration was shown to exceed that of the serum manyfold in both samples, confirming both masses to be functional and of parathyroid origin. A total parathyroidectomy and thyroidectomy were performed on the right side, and a subtotal thyroidectomy and a subtotal to total parathyroidectomy on the left, without any major postoperative complications. Histopathology was consistent with bilateral parathyroid carcinoma.
Relevance and novel information
To our knowledge, this report is the first to describe a rare case of bilateral parathyroid cystic carcinoma in a cat. It highlights the usefulness of determining parathyroid hormone concentration in the cystic fluid of a suspected neoplastic parathyroid mass preoperatively. It also demonstrates that it may be possible to remove most of the cervical parathyroid and thyroid tissue of a cat without causing any clinically relevant hypocalcaemia or iatrogenic hypothyroidism. However, serum concentrations of ionised calcium, thyroxine and creatinine should be closely monitored in the postoperative period in order to detect and control possible complications.
Primary hyperparathyroidism is rare, comprising 0.5% cases referred to one large academic institution. All clinical signs associated with primary hyperparathyroidism are related to the hypercalcemia secondary to the elevation in parathyroid hormone. Primary hyperparathyroidism is rare in cats, with few cases described to date. Since most hyperfunctioning parathyroid tissue occurs in the normal location of the parathyroid glands, cervical ultrasound is economical and readily available, and so is commonly the first line of imaging modality. Chronic renal failure is commonly associated with hyperparathyroidism through parathyroid gland hyperplasia. Exploratory surgery with parathyroidectomy in dogs with primary hyperparathyroidism serves as both a diagnostic test and definitive therapy. Preoperative treatment of hypercalcemia is contentious and there are no published standards. The greatest postoperative concern, reportedly occurring in 8–63% dogs, is hypocalcemia due to chronic suppression of the remaining parathyroid glands through negative feedback from the hypersecretory tumor.
This article provides a review with a focus on clinical updates in treating patients with surgical parathyroid or thyroid disease. Primary hyperparathyroidism is a common cause of hypercalcemia. Patients are older and often asymptomatic, and urinary stones and urinary tract infection are common. Surgical treatment is recommended with an excellent prognosis. Thyroid tumors in dogs are the most common endocrine neoplasm. Functional thyroid testing, laryngeal examinations, and regional lymphadenectomy should be considered during surgery, along with use of vessel-sealing devices to mitigate hemorrhage. Long-term outcomes for dogs with advanced disease can be reached, so surgical resection should be an option.
Pituitary tumors are recognized clinically either because the dog has clinical signs of hyperadrenocorticism or is having neurological signs. Several studies have found that the vast majority of dogs will have a return to normal or nearnormal neurologic status during or within several months after radiation treatment. Dogs with functional adrenal tumors require medical management perioperatively to help reduce the likelihood of complications. The majority of cats have a benign thyroid tumor described as multinodular adenomatous goiter, adenomatous hyperplasia, or adenoma. In dogs with a thyroid adenocarcinoma in the normal location, the thyroid gland appears abnormal in size, shape, or amount of uptake on scintigraphy compared with the normal gland, whereas in dogs with masses of non‐thyroid origin, the thyroid glands appear normal. The most common endocrine tumor of the pancreas in small animals is insulinoma, but it remains an uncommon tumor in dogs, rare in cats and common in ferrets.
A 16-year-old castrated male mixed breed cat was presented for anorexia and weight loss. On physical examination, the cat had a palpable mass in the left ventral cervical region. Blood test revealed hypercalcemia, increased ionized calcium. Intact parathyroid hormone (PTH) was higher than the reported range in healthy cats with experimentally induced hypercalcemia, suggesting that PTH suppression corresponding to serum ionized calcium concentration had been disrupted. The cervical mass was removed surgically and diagnosed as a parathyroid chief cell adenoma on histopathological examination. After surgical treatment, serum total calcium and ionized calcium decreased to within normal immediately and there was no recurrence after 2 years.
This chapter focuses on some of the most common disturbances in body fluid volume and composition, their etiologies, and the impact of their change on clinical management of patients before, during, and immediately after anesthesia. In general, perturbations in a patient's hydration, intravascular fluid volume, electrolyte composition, and/or acid–base status may be a manifestation of a disorder that has overwhelmed the body's ability to compensate for losses or additions in its content, or it may be indicative of a failure in regulatory mechanisms responsible for maintaining fluid and electrolyte balance. Normal respiratory and kidney functions are essential to maintain acid—base homeostasis in the body. There are two different methods used to describe and characterize a patient's acid—base status, the traditional and the Fencl—Stewart approaches.
Background:
Prophylactic administration of calcitriol has been suggested to mitigate the risk of hypocalcemia after parathyroidectomy. The effect of calcitriol on postoperative serum ionized calcium concentrations has not been evaluated in dogs after parathyroidectomy.
Hypothesis/objectives:
To determine the effect of prophylactic calcitriol administration on postoperative serum ionized calcium (iCa) concentrations in dogs with primary hyperthyroidism (PHPTH) treated by parathyroidectomy.
Animals:
Seventy-eight dogs with primary hyperparathyroidism treated surgically.
Methods:
Multi-institutional retrospective case study. Medical records from 2005 to 2015 were evaluated. Dogs were included if they had a diagnosis of PHPTH and had surgery to remove parathyroid tissue. Serum iCa concentrations were monitored for a minimum of 2 days postoperatively. Two study groups were evaluated: calcitriol administration and no calcitriol administration.
Results:
Serial postoperative iCa concentrations measured at 12-hour time intervals for 2 days postoperatively were positively associated with preoperative iCa concentrations. This association was evident at each time interval, and the effect of preoperative iCa concentrations on postoperative iCa concentrations decreased as time elapsed (12 hours, P < 0.0001; 24 hours, P < 0.0001; 36 hours, P < 0.04; and 48 hours, P = 0.01). Prophylactic calcitriol administration was not found to be significantly associated with postoperative iCa concentrations or its rate of decrease after parathyroidectomy.
Conclusion and clinical importance:
We found no protective value in administering calcitriol prophylactically to prevent hypocalcemia in the immediate postoperative period (48 hours) after parathyroidectomy. Preoperative iCa concentrations had a significant positive association with postoperative iCa concentrations throughout the monitoring period.
Background:
Development of hypocalcemia after treatment of hyperparathyroidism results in increased costs and risk of poorer outcomes. Previous studies have shown conflicting data about predictors of hypocalcemia after these procedures.
Hypothesis/objectives:
The objective of this study was to investigate whether ionized calcium (iCa) concentrations before treatment are predictive of hypocalcemia or its clinical signs after surgical removal or heat ablation in dogs with primary hyperparathyroidism.
Animals:
Fifty-four dogs with primary hyperparathyroidism (29 female, 25 male; 49 retrospective, 5 prospective).
Methods:
Dogs were enrolled if they met the inclusion criteria: persistent hypercalcemia (iCa >1.41 mmol/L) due to primary hyperparathyroidism and absence of preemptive calcitriol treatment. All dogs were treated with parathyroidectomy (n = 37) or percutaneous ultrasound-guided heat ablation (n = 17). After treatment, iCa was monitored twice daily until plateau or intervention.
Results:
There was a moderate correlation between before-treatment hypercalcemia and after-treatment hypocalcemia. The prospective study was terminated due to ethical concerns given findings in the retrospective section. All dogs were placed into groups according to their pretreatment iCa: 1.46-1.61 mmol/L, 1.62-1.71 mmol/L, iCa 1.72-1.81 mmol/L, or >1.81 mmol/L. After treatment, the mean lowest iCa for each group, respectively, was 1.19, 1.18, 1.13, and 1.01 mmol/L. There was a significant association between higher group and proportion of dogs with iCa <1.00 mmol/L (P = .014).
Conclusions and clinical importance:
This study demonstrates a moderate correlation between iCa concentration before treatment and hypocalcemia after treatment. Dogs with higher initial iCa concentrations should be treated to prevent rapid decline and development of clinical hypocalcemia.
Background
Chronic kidney disease ( CKD ) is a common comorbidity in cats with hypercalcemia, but whether CKD is a risk factor for hypercalcemia is unclear. Hypercalcemia often is diagnosed based on total calcium concentration ( tC a), which tends to underestimate the ionized calcium concentration ( iC a) in cats.
Objectives
Assessment of the performance of tC a for the diagnosis of ionized hypercalcemia, and exploration of factors influencing the relationship between iC a and tC a. Determination of risk factors for incident total hypercalcemia (ie, the development of hypercalcemia based on tC a during follow‐up).
Animals
Records of a cross‐section (n = 477) and observational cohort (n = 367) of client‐owned cats with and without azotemic CKD from first opinion practice.
Methods
Retrospective cross‐sectional and retrospective cohort study. The diagnostic accuracy of tC a as an index test for ionized hypercalcemia was evaluated, and risk factors for underestimation were explored by binary logistic and linear regression in a cross‐section of cats with and without azotemic CKD . Chronic kidney disease and clinicopathological variables were assessed as predictors of incident total hypercalcemia by both time‐invariant and time‐dependent Cox regression in a cohort of cats.
Results
Specificity of tC a for identification of ionized hypercalcemia was high (100%), but sensitivity was low. Underestimation was associated with lower venous bicarbonate concentrations. Cats with CKD had increased risk for incident total hypercalcemia (hazard ratio, 4.29; 95% confidence interval, 1.96–9.37; P < .001). Higher tC a predicted incident total hypercalcemia in both azotemic and nonazotemic cats ( P < .001).
Conclusions and Clinical Importance
Chronic kidney disease is a risk factor for incident total hypercalcemia, and most cats with increased tC a had concurrent ionized hypercalcemia. Higher baseline tC a predicts incident total hypercalcemia. Prospective studies assessing changes in iC a are warranted.
Hyperparathyroidism exists in primary and secondary forms. Primary hyperparathyroidism has typically been considered a disease that uncommonly affects cats, but this condition is more prevalent than previous diagnoses would suggest. Secondary hyperparathyroidism may be caused by either nutritional influences (ie, nutritional secondary hyperparathyroidism) or chronic kidney disease (ie, renal secondary hyperparathyroidism). Tertiary hyperparathyroidism has yet to be documented in veterinary medicine, but it is possible that this condition occurs in some cats following longstanding renal secondary hyperparathyroidism.
Diagnosis of this group of calcium metabolic disorders presents a number of challenges for the clinician. For example, clinical signs can be non-specific and, especially in the case of primary hyperparathyroidism, there is often a low index of suspicion for the disease; careful sample handling is required for testing of parathyroid hormone (PTH) and ionized calcium levels; and there is currently no feline-specific assay for PTH, which has implications for test sensitivity and interpretation of results.
This article briefly outlines PTH and calcium physiology by way of introduction to a review of PTH measurement and interpretation. Various forms of feline hyperparathyroidism are then described, encompassing diagnosis and treatment options.
© ISFM and AAFP 2015.
To review the inter-relationships between calcium, phosphorus, parathyroid hormone (PTH), parent and activated vitamin D metabolites (vitamin D, 25(OH)-vitamin D, 1,25(OH)2 -vitamin D, 24,25(OH)2 -vitamin D), and fibroblast growth factor-23 (FGF-23) during chronic kidney disease (CKD) in dogs and cats.
Human and veterinary literature.
Beneficial effects of calcitriol treatment during CKD have traditionally been attributed to regulation of PTH but new perspectives emphasize direct renoprotective actions independent of PTH and calcium. It is now apparent that calcitriol exerts an important effect on renal tubular reclamation of filtered 25(OH)-vitamin D, which may be important in maintaining adequate circulating 25(OH)-vitamin D. This in turn may be vital for important pleiotropic actions in peripheral tissues through autocrine/paracrine mechanisms that impact the health of those local tissues.
Limited information is available reporting the benefit of calcitriol treatment in dogs and cats with CKD.
A survival benefit has been shown for dogs with CKD treated with calcitriol compared to placebo. The concentrations of circulating 25(OH)-vitamin D have recently been shown to be low in people and dogs with CKD and are related to survival in people with CKD. Combination therapy for people with CKD using both parental and activated vitamin D compounds is common in human nephrology and there is a developing emphasis using combination treatment with activated vitamin D and renin-angiotensin-aldosterone-system (RAAS) inhibitors.
To determine whether preoperative serum ionized calcium (iCa) or parathyroid hormone (PTH) concentrations help predict postoperative hypocalcemia following parathyroidectomy in dogs with primary hyperparathyroidism.
Retrospective case series.
17 dogs with primary hyperparathyroidism treated with parathyroidectomy.
Medical records were evaluated from years 2001 to 2009. Data evaluated included age, breed, sex, clinical signs, diagnostic tests performed, preoperative and postoperative iCa concentrations, preoperative PTH concentrations, and whether calcium supplementation was provided following surgery. Two groups were identified on the basis of whether dogs became hypocalcemic (iCa < 1.2 mmol/L) following parathyroidectomy.
12 dogs developed hypocalcemia after surgery. Preoperative (within 24 hours before surgery) iCa concentrations for the hypocalcemic group (mean ± SD, 1.82 ± 0.22 mmol/L) and the nonhypocalcemic group (1.83 ± 0.29 mmol/L) were not significantly different. Calcium concentrations decreased in a linear fashion during the 24 hours following parathyroidectomy, and the slopes of the decrease over that time were not significantly different between the 2 groups. Preoperative PTH concentrations were not significantly different between the hypocalcemic and nonhypocalcemic groups.
Preoperative iCa and PTH concentrations were not predictive of postoperative hypocalcemia in dogs undergoing parathyroidectomy for primary hyperparathyroidism. Future studies to evaluate whether calcium supplementation should be provided on an individual basis with perhaps more emphasis on clinical signs than iCa concentrations after surgery may be warranted.
Corticosteroid-induced osteoporosis is the most common secondary cause of osteoporosis. We conducted a 12-mo, randomized clinical trial of human parathyroid hormone 1-34 (hPTH 1-34) in postmenopausal women (mean age was 63 yr) with osteoporosis who were taking corticosteroids and hormone replacement therapy. Response to the treatment was assessed with bone mineral density (BMD) measurements of the lumbar spine by quantitative computed tomography (QCT); BMD measurements of the lumbar spine, hip, and forearm by dual-energy x-ray absorptiometry (DXA); and biochemical markers of bone turnover. The mean (+/-SE) changes in BMD of the lumbar spine by QCT and DXA in the PTH group were 35+/-5.5% and 11+/-1.4%, respectively, compared with a relatively small change of 1.7+/-1.8% and 0+/-0.9% in the estrogen-only group. The differences in mean percentage between the groups at 1 yr were 33.5% for the lumbar spine by QCT (P < 0.001) and 9.8% for the lumbar spine by DXA (P < 0.001). The changes in the hip and forearm were not significantly different between or within the groups. During the first 3 mo of PTH treatment, markers of bone formation increased to nearly 150%, whereas markers of bone resorption increased only 100%, suggesting an early uncoupling of bone turnover in favor of formation. These results suggest that parathyroid hormone dramatically increases bone mass in the central skeleton of postmenopausal women with corticosteroid- induced osteoporosis who are taking hormone replacement.
Background:
Following parathyroidectomy for primary hyperparathyroidism (pHPT), serum calcium levels typically normalize relatively quickly. The purpose of this study was to identify potential factors associated with delayed normalization of calcium levels despite meeting intraoperative parathyroid hormone (IOPTH) criteria and to determine whether this phenomenon is associated with higher rates of persistent pHPT.
Methods:
This was a retrospective review of 554 patients who underwent parathyroidectomy for sporadic pHPT from January 2009 to July 2013. Patients who underwent presumed curative parathyroidectomy and had elevated POD0 calcium levels (>10.2 mg/dL) were matched 1:2 for age and gender to control patients with normal POD0 calcium levels.
Results:
Of the 554 patients, 52 (9 %) had an elevated POD0 Ca (median 10.7, range 10.3-12.2). Compared with the control group, these patients had higher preoperative calcium (12 vs. 11.1, p < 0.001) and PTH (144 vs. 110 pg/mL, p = 0.004) levels and lower 25OH vitamin D levels (26 vs. 31 pg/mL; p = 0.024). Calcium normalization occurred in 64, 90, and 96 % of patients by postoperative days (POD) 1, 14, and 30, respectively. There was no difference in rates of single-gland disease or cure rates between the groups.
Conclusions:
After presumed curative parathyroidectomy, nearly 10 % of patients had transiently persistent hypercalcemia. Most of these patients had normal serum calcium levels within the first 2 weeks and did not have increased rates of persistent pHPT. Immediate postoperative calcium levels do not predict the presence of persistent pHPT, and these patients may not require more stringent follow-up.
No other title offers such dedication to the depth, experience, and focus of endocrinology as Canine and Feline Endocrinology, 4th Edition. Comprehensive coverage includes virtually every common and uncommon condition in endocrinology, plus the most updated information on nutrition, geriatric care, pathophysiology, testing procedures, and cost-effective and expedient diagnostic protocols. With its logical, step-by-step guidance for decision making, diagnosis, and prescribing, you will be well-equipped to care for the wide spectrum of endocrine and metabolic disorders in dogs and cats. © 2015 by Saunders, an imprint of Elsevier Inc. All rights reserved.
Objective:
To describe outcomes for dogs with primary hyperparathyroidism following treatment with percutaneous ultrasound-guided ethanol ablation of presumed functional parathyroid nodules.
Design:
Retrospective case series.
Animals:
24 dogs with primary hyperparathyroidism that underwent 27 ultrasound-guided ethanol ablation procedures of presumed functional parathyroid nodules identified by cervical ultrasonography.
Procedures:
Dogs were anesthetized for each procedure. For each nodule, 95% ethanol was injected into the center with ultrasound guidance (volume injected calculated on the basis of ultrasonographic measurements). The interval from treatment to resolution of hypercalcemia, complications, and follow-up clinicopathologic data were recorded.
Results:
5 procedures involved simultaneous treatment of 2 nodules. Three dogs underwent a second treatment because of initial treatment failure or development of another nodule. Hypercalcemia resolved after 23 of 27 (85%) procedures. In those 23 treatments, 22 (96%) had resolution of hypercalcemia within 72 hours after treatment. Hypocalcemia was detected in 6 different dogs at 2 (1 dog), 7 (3 dogs), 14 (1 dog), and 21 (1 dog) days after treatment; 5 of these dogs had mild transient hypocalcemia and 1 developed clinical signs requiring calcium supplementation. Although there were no periprocedural adverse effects, 2 dogs had delayed adverse effects; the overall rate of complications (including delayed adverse events and clinical hypocalcemia) was 11.1%. Long-term follow-up data indicated sustained normocalcemia in 17 of 19 dogs.
Conclusions and clinical relevance:
Results suggested that percutaneous ultrasound-guided ethanol ablation of functional parathyroid nodules may be an effective treatment for primary hyperparathyroidism of dogs, with short duration of anesthesia, minimal complications, and low risk for hypocalcemia.
Objective:
To identify preoperative variables associated with postoperative hypocalcemia in dogs with primary hyperparathyroidism undergoing parathyroidectomy.
Design:
Retrospective case series.
Animals:
62 dogs.
Procedures:
Medical records of dogs undergoing parathyroidectomy for treatment of primary hyperparathyroidism between January 2004 and January 2009 at 4 institutions were reviewed; data regarding various preoperative variables and postoperative serum total and ionized calcium concentrations were recorded. Preoperative ultrasonographic and surgical findings were compared regarding laterality (right, left, or bilateral) of parathyroid gland lesions. Data were analyzed via ANOVA, simple linear regression, and multiple linear regression to identify associations between preoperative variables and postoperative serum total and ionized calcium nadir concentrations.
Results:
Preoperative variables significantly associated with low postoperative serum total calcium nadir concentrations included old age, history of weakness, lack of gastrointestinal tract signs, high serum parathyroid hormone concentration, and low serum calcium-phosphorus concentration product value. Preoperative variables significantly associated with low postoperative serum ionized calcium nadir concentrations included sexually intact status, low body weight, high serum urea nitrogen concentration, and lack of polyuria and polydipsia in the history. Age, body weight, serum calcium-phosphorus concentration product, and serum concentrations of parathyroid hormone and urea nitrogen were included in the final multiple linear regression model for prediction of postoperative serum calcium concentrations. Ultrasonography was performed in 58 dogs; results for 44 (75.9%) dogs agreed with surgical findings regarding laterality of parathyroid gland lesions.
Conclusions and clinical relevance:
Prediction of postoperative hypocalcemia in dogs in this study with primary hyperparathyroidism that underwent parathyroidectomy was difficult and depended on multiple (history, physical examination, and clinicopathologic) factors.
Two parathyroid masses were identified using ultrasound in two hypercalcemic cats. The masses were identified as parathyroid adenomas on surgical biopsy. Both parathyroid masses contained hypoechoic regions with distal acoustic enhancement, Both masses were greater than 1.0 cm in diameter.
To determine (1) whether the intraoperative parathyroid hormone concentration ([PTH]) during parathyroidectomy (PTX) can be used to indicate cure in dogs with primary hyperparathyroidism and (2) the time taken for postoperative serum calcium concentration to normalise.
Retrospective study (2005-10) from a private referral hospital in Sydney, New South Wales, Australia.
Nine client-owned dogs underwent surgical PTX for naturally occurring primary hyperparathyroidism. [PTH] was measured from serum samples taken immediately post-induction (pre-PTX]) and at least 20 min after adenoma removal (post-PTX) for all dogs, and during parathyroid gland manipulation (intra-PTX) for six dogs. The concentration of ionised calcium (iCa) was measured at various time points postoperatively until it normalised, then stabilised or decreased below reference ranges. Statistical analysis compared the mean pre-, intra- and post-PTX [PTH] and the average rate of decline of iCa concentration postoperatively.
All dogs demonstrated a significant decrease from mean pre-PTX [PTH] (168.51 pg/mL) to mean post-PTX [PTH] (29.20 pg/mL). There was a significant increase in mean intra-PTX [PTH] (279.78 pg/mL). The average rate of decline of iCa concentration postoperatively to within the reference range (1.12-1.40 mmol/L) occurred after 24 h.
Intraoperative measurements of [PTH] can be used clinically to determine cure of primary hyperparathyroidism. Parathyroid hormone increases significantly during parathyroid gland manipulation. Plasma iCa concentration returns to within the reference range on average 24 h after successful PTX. Not all dogs require vitamin D or calcium supplementation pre- or postoperatively.
Parathyroid carcinoma (PTC) is rare in dogs and there is little information documenting its treatment and prognosis. The objective of this study was to describe the outcome of dogs with PTC treated with surgical excision. Medical records of 19 dogs undergoing surgical excision of PTC between 1990 and 2010 were reviewed retrospectively. Dogs were presented for clinical hypercalcaemia or incidental hypercalcaemia noted by referring veterinarians on routine serum chemistry profiles. A parathyroid nodule was identified with cervical ultrasound in 17/17 dogs. Hypercalcaemia resolved in 18/19 dogs within 4 days postoperatively. Nine developed hypocalcaemia. None were confirmed to develop recurrent or metastatic PTC. The only death associated with PTC was a dog that was euthanized for intractable hypocalcaemia 9 days after surgery. Estimated 1-, 2- and 3-year survival rates were 72, 37 and 30%, respectively. Excision of PTC results in resolution of hypercalcaemia and excellent tumour control.
To (1) validate a rapid chemiluminescent parathyroid hormone (PTH) assay, (2) determine it's usefulness locating a parathyroid nodule(s), and (3) determine if >50% decrease in PTH corresponds with excision of autonomously functioning parathyroid tissue.
Prospective cohort study.
Dogs (n=12) with naturally occurring primary hyperparathyroidism and 25 healthy dogs.
The assay was validated with linearity, precision, and intermethod comparison. Preoperative and postoperative systemic plasma PTH concentrations, measured from saphenous venous blood, were compared. Intraoperative local PTH concentrations were measured in right and left jugular venous blood before and after surgical excision of the grossly abnormal parathyroid gland(s).
Within run and day-to-day precisions were acceptable (coefficient of variation <15%). Dilutional parallelism was used to demonstrate high correlation between measured and calculated PTH concentrations (R(2)=0.99). The assay methods had good correlation but numerical results of the rapid assay were usually lower than the immunoradiometric assay. Seven of 12 dogs had uniglandular disease and five had multiglandular disease. Systemic and local PTH concentrations decreased >50% in all the dogs after excision of the parathyroid gland(s). Mean preoperative systemic plasma PTH concentrations were significantly higher than mean postoperative systemic concentrations. Local PTH concentrations could not be used reliably to differentiate the side of the autonomously functioning gland(s). Hypercalcemia resolved postoperatively in all the dogs.
This assay measures PTH in dogs. Rapid PTH measurement provided documentation of decreased PTH concentration after removal of autonomously functioning parathyroid tissue.
Use of this assay allows documentation of a significant decrease in PTH concentration after excision of autonomously functioning parathyroid tissue.
Anorexia, severe skeletal demineralization, and muscular weaknesss developed in a 9 year-old Collie. Hypercalcemia, hypophosphatemia, and nephrocalcinosis were found on clinical evaluation. The surgical removal of a parathyroid adenoma was followed by profound hypocalcemia that was unresponsive to calcium therapy, and the dog died. The persistent hypocalcemia was attributed to increased deposition of calcium in mineral-deficient bone.
The medical records of 7 hypercalcemic cats with primary hyperparathyroidism were evaluated. Mean age was 12.9 years, with ages ranging from 8 to 15 years; 5 were female; 5 were Siamese, and 2 were of mixed breed. The most common clinical signs detected by owners were anorexia and lethargy. A cervical mass was palpable in 4 cats. Serum calcium concentrations were 11.1 to 22.8 mg/dl, with a mean of 15.8 mg/dl calculated from each cat's highest preoperative value. The serum phosphorus concentration was low in 2 cats, within reference limits in 4, and slightly high in 1 cat. The BUN concentration was greater than 60 mg/dl in 2 cats, 31 to 35 mg/dl in 2 cats, and less than 30 mg/dl in 3 cats. Abnormalities were detected in serum alanine transaminase, aspartate transaminase, and alkaline phosphatase activities from 2 or 3 cats. Parathormone (PTH) concentrations were measured in 2 cats before and after surgery. The preoperative PTH concentration was within reference limits in 1 cat and was high in 1 cat. The PTH concentrations were lower after surgery in both cats tested. A solitary parathyroid adenoma was surgically removed from 5 cats, bilateral parathyroid cystadenomas were surgically resected in 1 cat, and a parathyroid carcinoma was diagnosed at necropsy in 1 cat. None of the cats had clinical problems with hypocalcemia after surgery, although 2 cats developed hypocalcemia without tetany, one of which was controlled with oral administration of dihydrotachysterol and the other with oral administration of 1,25 dihydroxyvitamin D. All 5 of the cta that underwent removal of an adenoma were alive at least 240 days after surgery.(ABSTRACT TRUNCATED AT 250 WORDS)
Case records from 21 dogs with hypercalcemia and hyperparathyroidism were evaluated. The dogs were greater than or equal to 7 years old, and 6 were Keeshonds. The most common clinical signs were polydipsia/polyuria, listlessness, and muscle weakness. The serum calcium concentrations were 12.1 to 19.6 mg/dl. Serum phosphorus concentrations were low in 5 dogs, within the reference range in 13 dogs, and high in 3 dogs that also had high concentrations of BUN. Twenty dogs had a parathyroid adenoma, and 1 had a parathyroid carcinoma. Nineteen dogs had their parathyroid tumor surgically removed. Within 5 days of tumor removal, 11 of the 19 dogs became hypocalcemic and the remaining 8, normocalcemic. Nine of the 11 hypocalcemic dogs developed clinical signs. Iatrogenic hypercalcemia was induced in 7 of 16 dogs treated orally with calcium carbonate plus vitamin D. Only 1 of 19 dogs that had their parathyroid tumor excised died in hypocalcemic tetany. Two additional dogs died within 2 weeks of surgery, one because of pancreatitis, the other due to renal failure. Eight dogs died 9 to 37 months after surgery of unrelated problems. Eight dogs were alive for at least 7 to 28 months after surgery.
An adult Keeshond had clinical signs associated with hypercalcemia, including inappetence, polyuria, polydipsia, and vomiting. Blood biochemical findings and urinary clearance studies were consistent with a diagnosis of primary hyperparathyroidism. Histomorphometric analysis of trabecular bone in an iliac crest biopsy indicated increased bone remodeling activity. Surgical exploration of the neck revealed an oval mass, which was removed by blunt dissection. Histologic diagnosis was parathyroid gland adenoma. The dog died because of renal failure on the eighth postoperative day. This report defines primary hyperparathyroidism in the dog, thus facilitating diagnosis for the veterinary clinician.
A retrospective study was conducted to characterize the diseases, clinical findings, and clinicopathologic and ultrasonographic findings associated with hypercalcemia (serum calcium concentration >11 mg/dL) in 71 cats presented to North Carolina State University Veterinary Teaching Hospital. The 3 most common diagnoses were neoplasia (n = 21), renal failure (n = 18), and urolithiasis (n = 11). Primary hyperparathyroidism was diagnosed in 4 cats. Lymphoma and squamous cell carcinoma were the most frequently diagnosed tumors. Calcium oxalate uroliths were diagnosed in 8 of 11 cats with urolithiasis. Cats with neoplasia had a higher serum calcium concentration (13.5 +/- 2.5 mg/dL) than cats with renal failure or urolithiasis and renal failure (11.5 +/- 0.4 mg/dL; P < .03). Serum phosphorus concentration was higher in cats with renal failure than in cats with neoplasia (P < .004). Despite the fact that the majority of cats with uroliths were azotemic, their serum urea nitrogen and creatinine concentrations and urine specific gravity differed from that of cats with renal failure. Additional studies are warranted to determine the underlying disease mechanism in the cats we identified with hypercalcemia and urolithiasis. We also identified a small number of cats with diseases that are not commonly reported with hypercalcemia. Further studies are needed to determine whether an association exists between these diseases and hypercalcemia, as well as to characterize the underlying pathophysiologic mechanism for each disease process.
Two parathyroid masses were identified using ultrasound in two hypercalcemic cats. The masses were identified as parathyroid adenomas on surgical biopsy. Both parathyroid masses contained hypoechoic regions with distal acoustic enhancement. Both masses were greater than 1.0 cm in diameter.
In primary hyperparathyroidism, calcium homeostasis is disrupted by excessive synthesis and secretion of parathyroid hormone (PTH), which is usually caused by a solitary adenoma, or less often by nodular hyperplasia or carcinoma of the parathyroid glands. So far, the distinction between these forms of primary hyperparathyroidism has been made by histological examination. In this report clinical and histological findings, including PTH immunohistochemistry, are described in five dogs with primary hyperparathyroidism, three dogs with secondary hyperparathyroidism due to chronic renal failure, and eight control dogs. In the dogs with primary hyperparathyroidism, nodular adenomatous hyperplasia was found in two animals and parathyroid adenoma in three. The dogs with chronic renal failure had diffuse parathyroid gland hyperplasia. The parathyroid glands of the control dogs and the inactive cells surrounding the hyperplastic nodules showed slight to moderate, localized, paranuclear PTH immunolabelling. In the primary nodular and secondary diffuse hyperplasia, all parathyroid cells had a diffuse cytoplasmic PTH labelling pattern, sometimes in combination with localized paranuclear labelling. In parathyroid adenoma, areas with either paranuclear labelling or diffuse cytoplasmic labelling were observed. As both parathyroid adenoma and primary nodular parathyroid gland hyperplasia have characteristics of intrinsic autonomy (i.e., suppression of the remaining endocrine tissue), there would seem to be no functional difference between the two abnormalities. It is argued that primary (multi)nodular hyperplasia is a multiple form of parathyroid adenoma.
Reports of cystic thyroid and parathyroid masses in cats are uncommon. Herein, the authors describe a series of four cats with cystic ventral cervical lesions, among them thyroid cyst (n=1), thyroid cystadenoma (n=2), and parathyroid adenocarcinoma (n=1). Presentations ranged from completely asymptomatic cervical swellings to signs related to local compression of adjacent structures (e.g., trachea). Ultrasonographic evaluation was helpful in localization of the mass in two cases. Hormone analysis and concentration of cystic fluid were performed in one cat. Surgical excision was performed successfully in three cases. Histopathological examination was performed in all four cases. Long-term prognosis was excellent for those cases in which follow-up was available.
To review the records of 29 dogs diagnosed with primary hyperparathyroidism and see if any factors correlate with renal failure.
Dogs were selected retrospectively from case files from the QVSH and the QMH.
The majority of dogs were middle-aged and four were keeshonds. The primary presenting complaints were polyuria and polydipsia. All dogs had an elevated total and ionised plasma calcium concentration. Plasma phosphate concentrations were variable. Ultrasonography of the parathyroid gland revealed nodular enlargement which was found to correlate well with surgical findings. The majority of dogs underwent surgical parathyroidectomy. Five cases were treated by ultrasound-guided chemical ablation of the parathyroid gland, of which only two cases showed a partial response. Three dogs were euthanased within a week of presentation. Seven other dogs had renal failure diagnosed either at presentation or up to six months after parathyroidectomy. The development of renal failure was correlated with total calcium concentration but did not correlate with any other factor, including the calcium phosphate product. Thirteen treated dogs were known to be alive at the time of writing, which was six months to 3.5 years after parathyroidectomy.
Primary hyperparathyroidism cases with high total calcium were more likely to develop renal failure in this group of dogs; however, the calcium phosphate product did not seem to be a useful predictor. Ultrasound-guided chemical ablation seemed to have limited advantage over surgery.
To evaluate pretreatment clinical and laboratory findings in dogs with naturally occurring primary hyperparathyroidism.
Retrospective study.
210 dogs with primary hyperparathyroidism and 200 randomly selected, age-matched control dogs that did not have primary hyperparathyroidism.
Medical records for dogs with primary hyperparathyroidism were reviewed for signalment; clinical features; and results of clinicopathologic testing, serum parathyroid hormone assays, and diagnostic imaging.
Mean age of the dogs with primary hyperparathyroidism was 11.2 years (range, 6 to 17 years). The most common clinical signs were attributable to urolithiasis or urinary tract infection (ie, straining to urinate, increased frequency of urination, and hematuria). Most dogs (149 [71%]) did not have any observable abnormalities on physical examination. All dogs had hypercalcemia, and most (136 [65%]) had hypophosphatemia. Overall, 200 of the 210 (95%) dogs had BUN and serum creatinine concentrations within or less than the reference range, and serum parathyroid hormone concentration was within reference limits in 135 of 185 (73%) dogs in which it was measured. Urolithiasis was identified in 65 (31 %) dogs, and urinary tract infection was diagnosed in 61 (29%). Mean serum total calcium concentration for the control dogs-was significantly lower than mean concentration for the dogs with primary hyperparathyroidism, but mean BUN and serum creatinine concentrations for the control dogs were both significantly higher than concentrations for the dogs with primary hyperparathyroidism.
Results suggest that urolithiasis and urinary tract infection may be associated with hypercalcemia in dogs-with primary hyperparathyroidism, but that development of renal insufficiency is uncommon.
The medical records of 110 dogs treated for primary hyperparathyroidism were reviewed. Dogs were treated via parathyroidectomy (n=47), percutaneous ultrasound-guided ethanol ablation (n=15), or percutaneous ultrasound-guided heat ablation (n=48). Forty-five of 48 (94%) parathyroidectomies resulted in control of hypercalcemia for a median of 561 days. Thirteen of 18 (72%) ethanol ablation procedures resulted in control of hypercalcemia for a median of 540 days. Forty-four of 49 (90%) heat-ablation treatments resulted in control of hypercalcemia for a median of 581 days.
Fluoroscopic guided differential venous sampling of parathyroid hormone for diagnosis of persistent hyperparathyroidism following parathyroidectomy
- J Howard
- K Ham
- S Jones
Howard J, Ham K, Jones S. Fluoroscopic guided differential venous sampling of parathyroid hormone for diagnosis of persistent hyperparathyroidism following parathyroidectomy. In: Proceedings of the Society of Soft
Tissue Veterinary Surgery Annual Conference; June 15-17, 2017; Whitefish, MT.
Feline hyperparathyroidism: pathophysiology, diagnosis, and treatment of primary and secondary disease
- V Parker
- C Gilor
- DJ Chew
Parker V, Gilor C, Chew DJ. Feline hyperparathyroidism: pathophysiology,
diagnosis, and treatment of primary and secondary disease. J Feline Med
Surg. 2015;17(5):427-439.
Fluoroscopic guided differential venous sampling of parathyroid hormone for diagnosis of persistent hyperparathyroidism following parathyroidectomy
- Joness Howardj Hamk