Congenital Lobar Emphysema in a Kitten with Concomitant Hiatal Hernia and Nutritional Secondary Hyperparathyroidism.

A 2 mo old domestic shorthair kitten was presented for acute respiratory distress and severe ambulatory difficulties. Thoracic radiography revealed hyperinflation of the left cranial lung lobe and a mass with soft-tissue/gas opacity in the caudal mediastinum, leading to the suspicion of congenital lung lobe emphysema and hiatal hernia. Decreased bone radiopacity and suspected pathological fractures were also present. Complete clinicopathological analyses showed significant ionized hypocalcemia and suspicion of secondary hyperparathyroidism related to an inadequate diet. Lung lobectomy and reduction of the hiatal hernia following a median sternotomy and a cranial laparotomy were performed. IV and oral supplementation of calcium led to a full recovery and improvement in the kitten's walking. A histopathological analysis revealed pulmonary emphysema associated with hypoplastic and irregular bronchial cartilage. Congenital lobar emphysema is a rare disease in both humans and animals. This is the first veterinary report describing a kitten affected by congenital lobar emphysema combined with a hiatal hernia and additionally complicated by secondary nutritional hyperparathyroidism with a good long-term outcome.

Renal Osteodystrophy due to Secondary Hyperparathyroidism in a Cat.

A 6 yr old neutered male mixed-breed cat presented for renal transplantation (RTx) for chronic kidney disease. Severe periodontal disease was identified, and before initiation of immunosuppressive therapy, a comprehensive oral health assessment and treatment procedure was performed to reduce the burden of existing oral infection. Dental radiography revealed diffuse, severe bone demineralization across the mandible and maxilla, with thinning of the cortices. Nasal turbinates were easily visualized owing to the decreased opacity of maxillary bone. Generalized bone resorption left teeth to appear minimally attached. A Vitamin D panel revealed a severely elevated parathyroid hormone level. Full mouth extractions were performed. Seven days following this procedure, RTx was performed. Serum creatinine concentration was within normal limits by 48 hr after surgery and remained normal until discharge 12 days after RTx. At 3.5 mo after RTx, the cat was mildly azotemic, and the parathyroid hormone level was elevated but significantly decreased from the original measurement. Secondary hyperparathyroidism is a common abnormality in cats with chronic kidney disease. However, clinical manifestations of hyperparathyroidism are rare in this species. This is a novel presentation of a cat demonstrating bone loss in the oral cavity as a result of renal secondary hyperparathyroidism.

Dietary imbalances in a large breed puppy, leading to compression fractures, vitamin D deficiency, and suspected nutritional secondary hyperparathyroidism.

A 6-month-old intact female giant schnauzer dog fed a nutritionally unbalanced homemade diet was evaluated because of a 1-month history of lameness and difficulty walking. Abnormalities identified on ancillary tests, in conjunction with the dog's clinical improvement following diet change, suggested a diagnosis of vitamin D deficiency and nutritional secondary hyperparathyroidism. This report underlines the importance of appropriate feeding management, especially during the vulnerable growth phase.

Déséquilibres alimentaires chez un chiot de grande race causant des fractures de compression, une carence en vitamine D et de l'hyperparathyroïdisme soupçonné secondaire à la nutrition. Une chienne Schnauzer géante intacte âgée de 6 mois qui consommait une diète maison qui n'était pas équilibrée sur le plan nutritionnel a été évaluée en raison d'une anamnèse de 1 mois de boiterie et de difficultés ambulatoires. Les anomalies identifiées sur des tests ancillaires, de concert avec l'amélioration clinique du chien après le changement de diète, suggéraient un diagnostic de carence en vitamine D et d'hyperparathyroïdisme nutritionnel secondaire. Ce rapport souligne l'importance d'une gestion appropriée de l'alimentation, particulièrement durant la phase de croissance vulnérable.(Traduit par Isabelle Vallières).

Nutritional secondary hyperparathyroidism in a kitten, supported by immunoenzymatic measurement of feline intact parathyroid hormone.

A 6-mo-old, intact male, domestic shorthair cat was referred with a history of poor growth, reluctance to move, and deformation of the nasal profile. The kitten had been fed a diet composed almost exclusively of a complementary pet food and tuna, which was similar to an all-meat diet. We detected osteopenia and hypocalcemia associated with severe parathyroid hormone (PTH) and calcitriol increases; we measured PTH concentrations with an immunoenzymatic method that has been validated in cats. Dietary correction, consisting of a complete and balanced wet pet food formulated for growth, resulted in normalization of calcium and PTH concentrations within 2 mo.

Clinical and computed tomography features of secondary renal hyperparathyroidism.

An atypical case of secondary renal hyperparathyroidism was diagnosed in a 9-year-old miniature schnauzer after a skull computed tomography (CT) showed the presence of 2 bilateral and symmetrical soft tissue maxillary masses, and osteopenia of the skull.

Nutritional Secondary Hyperparathyroidism and Fibrous Osteodystrophy in a Captive African Penguin (Spheniscus demersus) Similar to Osteomalacia in Poultry.

A 9-yr-old female black-footed African penguin (Spheniscus demersus) was presented for necropsy after a history of reproductive abnormalities, paresis of limbs, weakness, and sudden death. Postmortem examination revealed soft keel, collapsed rib cage with beading of the ribs, and bilateral parathyroid enlargement. Classic histologic lesions of fibrous osteodystrophy with osteomalacia were observed in the ribs, vertebrae, and to a lesser extent in the femur and tibiotarsus associated with hyperplasia of parathyroid glands. This represents the first report of nutritional secondary hyperparathyroidism in birds of the order Spheniciformes, most likely caused by low levels of calcium supplementation during egg laying. The reproductive abnormalities observed in this penguin and others from the same group (asynchronous egg-laying cycles, abnormal breeding behavior) were most likely exacerbated by the lack of an adequate photoperiod mimicking the natural daylight pattern.

Reporte de caso­Hiperparatiroidismo secundario nutricional y osteodistrofia fibrosa en un pingüino africano (Spheniscus demersus) en cautiverio similar a la osteomalacia observada en de aves de corral. Una hembra de pingüino africano de patas negras (Spheniscus demersus) de nueve años fue sometida a necropsia después de un historial de anomalías reproductivas, paresia de extremidades, debilidad y muerte súbita. El examen post mortem reveló que la quilla del esternón estaba blanda, la caja torácica colapsada, se observaron "perlas raquíticas" en las costillas y agrandamiento bilateral de las paratiroides. Se observaron lesiones histológicas clásicas de osteodistrofia fibrosa con osteomalacia en las costillas, vértebras y en menor medida, en el fémur y tibiotarsus asociadas con hiperplasia de glándulas paratiroides. Esto representa el primer informe de hiperparatiroidismo secundario nutricional en un ave del orden Spheniciformes, muy probablemente causado por un bajo nivel de suplementos de calcio durante la producción de huevos. Las anomalías reproductivas observadas en este pingüino y otros del mismo grupo (ciclos de puesta de huevos asincrónicos, comportamiento de reproducción anormal) probablemente se vieron exacerbadas por la falta de un fotoperíodo adecuado que imitara el patrón de luz natural.

Severe calcification of systemic blood vessel walls caused by continuous hypercalcemia in a cat with congenital hypothyroidism.

A 97-day-old male Japanese domestic cat was diagnosed as congenital hypothyroidism. During the treatment, continuous hypercalcemia was detected. Although fluid therapy was performed, the cat died at the age of 1785 days. At autopsy, both parathyroid glands were enlarged, and elastic arterial walls were increased in thickness and hardness. Histopathological examination revealed hyperplasia of both parathyroid glands and interstitial fibrosis of bilateral kidneys. Severe calcification of the tunica media and tunica externa in systemic elastic and muscular arteries were also observed. These calcifications were considered to be due to renal secondary hyperparathyroidism. In the present case, hypothyroidism might have caused hyperparathyroidism through renal failure. In veterinary medicine, this is the first reported case of hypothyroidism accompanied with hyperparathyroidism.

Primary Hyperparathyroidism Associated With Atypical Headshaking Behavior in a Warmblood Gelding.

A 14-year-old Zweibrücker Warmblood gelding was presented for evaluation of lethargy and headshaking. The horse had a history of bouts of lameness in different limbs and back problems. It also had many mild colic episodes in the past. Results of repeat laboratory tests had shown persistent hypercalcemia (4.8 mmol/L; reference interval [RI]: 2.0-3.2 mmol/L) for 1.5 years and later on hypophosphatemia (0.4 mmol/L; RI: 0.5-1.3 mmol/L) and mild hypermagnesemia (1.0 mmol/L; RI: 0.5-0.9 mmol/L). Parathyroid hormone (PTH) concentration was within the RI. Other causes of hypercalcemia, such as renal failure, vitamin D toxicosis, and granulomatous disease, and nutritional secondary hyperparathyroidism were ruled out. Furthermore, there was no evidence of neoplastic disease. Parathyroid hormone-related protein was measured but inconclusive. A diagnosis of primary hyperparathyroidism was established on the basis of hypercalcemia, hypophosphatemia, low fractional excretion of calcium, and high fractional excretion of phosphorus in combination with a PTH secretion refractory to high calcium levels. Because of the bad prognosis, the owner decided to euthanize the horse. Results of postmortem examination were unremarkable. Hypercalcemia should always be considered abnormal, and further examinations need to be performed to proof hypercalcemia and subsequently find the cause. The main differential diagnoses are renal insufficiency and humoral hypercalcemia of malignancy, but also rare diseases, such as hyperparathyroidism, have to be taken into account.

Diffuse osteopenia and myelopathy in a puppy fed a diet composed of an organic premix and raw ground beef.

CASE DESCRIPTION: An 8-month-old Shetland Sheepdog was evaluated because of the sudden onset of signs of neck pain, collapse, and inability to rise. A cursory diet history indicated that the dog had been fed a raw meat-based diet. CLINICAL FINDINGS: Initial evaluation of the dog revealed small physical stature, thin body condition, and signs of cranial cervical myelopathy. Radiographically, diffuse osteopenia of all skeletal regions was identified; polyostotic deformities associated with fracture remodeling were observed in weight-bearing bones, along with an apparent floating dental arcade. Hypocalcemia and hypophosphatemia were detected via serum biochemical analyses. The dog's diet was imbalanced in macronutrients and macrominerals. TREATMENT AND OUTCOME: The dog received supportive care and treatment of medical complications; neurologic abnormalities improved rapidly without intervention. Dietary changes were implemented during hospitalization, and a long-term feeding regimen was established. Following discharge from the hospital, exercise restriction was continued at home. Serial follow-up evaluations, including quantitative bone density measurements, revealed that dietary changes were effective. After 7 months, the dog was clinically normal. CLINICAL RELEVANCE: In the dog of this report, vitamin D-dependent rickets type I and suspected nutritional secondary hyperparathyroidism developed following intake of a nutritionally incomplete and unbalanced diet. The raw meat-based, home-prepared diet fed to the dog was not feed-trial tested for any life stage by the Association of American Feed Control Officials, and its gross nutrient imbalance induced severe metabolic, orthopedic, and neurologic abnormalities. Inadvertent malnutrition can be avoided through proper diet assessment and by matching nutrient profiles with patients' nutritional needs.

Paradise lost: Evidence for a devastating metabolic bone disease in an insular Pleistocene deer.

PURPOSE: This communication reports skeletal pathology in a Pleistocene endemic deer from the Mavromouri caves of Crete. MATERIALS: 287 bones and bone fragments from Mavromouri caves are compared to 2986 bones from Liko Cave. METHODS: Bones were evaluated macroscopically, and measurements were made of morphometric characteristics of limb long bones. Representative bone specimens were examined radiographically and histologically. RESULTS: Macroscopic hallmarks were loss of bone mass and increased porosity. The long bones were brittle, some of them having thin cortices, and others reduction of medullary cavities that contain dense Haversian tissue. The flat bones were spongy and fragile. Erosions of the metaphyses and articular surfaces were noted. Histological findings included: sub-periosteal resorption; loss of lamellar bone; enlargement of vascular canals; and remodeling of cortical bone. Two types of fibrous osteodystrophy were recognized in skeletal remains, subostotic and hyperostotic. CONCLUSIONS: The deer of Mavromouri caves were affected by severe metabolic bone disease, likely nutritional secondary hyperparathyroidism. We hypothesize a multifactorial cause, including overgrazing, flora senescence, soil mineral deficiencies, and a prolonged period of climate extremes, degrading the Cretan deer habitat. VALUE: This is the first evidence of a metabolic bone disease causing this level of destructive pathology in an insular fossil deer. LIMITATIONS: The lack of absolute chronometric dates for the site limits potential linking with the prevailing environmental conditions. SUGGESTIONS FOR FURTHER RESEARCH: Investigation of similar skeletal pathologies at other islands or isolated habitats is advised.

Unusual case of osteopenia associated with nutritional calcium and vitamin D deficiency in an adult dog.

A 6-year-old, spayed female rottweiler was presented for facial enlargement from swelling of the maxilla and mandible. The dog was fed a homemade diet deficient in calcium and vitamin D, suggesting that rubber jaw syndrome was a secondary nutritional disorder. Radiographic and tomodensitometric examinations revealed diffuse bone resorption in the skull. The plasma parathormone concentration was high, and serum 25-hydroxycholecalciferol concentration was low. Based on these findings, nutritional calcium and vitamin D deficiency associated with secondary hyperparathyroidism was diagnosed. Dietary correction resulted in clinical and biological improvement, with an increase in skull mineralization.

[Mandibular fracture in a Lhasa Apso with secondary renal hyperparathyroidism]. / Fracture mandibulaire chez un Lhassa Apso avec hyperparathyroïdie secondaire rénale.

A Lhassa Apso is presented in emergency after having been injured by another dog. It was suffering from a mandibular fracture. The clinical exam revealed generalized and excessive mobility of the whole dentition. Radiographs showed generalized jaw bone demineralisation. A blood sample was analysed and revealed chronic renal disease. We came to the conclusion that this dog was suffering from secondary renal hyperparathyroidism. The hypocalcified bone was so thin that a slight trauma induced the mandibular fracture.

Comparison of the effects of daily and intermittent-dose calcitriol on serum parathyroid hormone and ionized calcium concentrations in normal cats and cats with chronic renal failure.

BACKGROUND: Chronic renal failure is complicated by secondary hyperparathyroidism, which traditionally has been controlled by dietary restriction of phosphorus and administration of phosphorus binders. Early treatment of patients with chronic renal failure with calcitriol may be indicated because once established, parathyroid gland hyperplasia does not readily resolve with therapy. HYPOTHESIS: Daily and intermittent dosing of calcitriol will decrease plasma parathyroid hormone concentration in normal cats and cats with chronic renal failure without causing ionized hypercalcemia. ANIMALS: Ten normal cats; 10 cats with chronic renal failure. METHODS: Phase 1 was daily calcitriol administration (2.5 ng/kg PO q24h) for 14 days. Phase 2 was intermittent calcitriol administration (8.75 ng/kg PO q84h) for 14 days. A 7-day washout period separated phases 1 and 2. Before each phase, calcitriol, parathyroid hormone, and ionized calcium concentrations were measured. On days 1, 2, and 3 of both phases, serum ionized calcium concentrations were measured. On the last day of both phases, calcitriol, parathyroid hormone, and ionized calcium concentrations were measured 0, 2, 4, and 6 hours after calcitriol administration. RESULTS: Overall, serum parathyroid hormone concentrations were significantly higher in cats with chronic renal failure than in normal cats (P = .022), but serum parathyroid hormone concentrations for both normal cats and cats with chronic renal failure were not significantly different before and after 14 days of treatment with calcitriol, regardless of whether calcitriol was administered daily or intermittently. Adverse effects of calcitriol administration (specifically ionized hypercalcemia) were not seen in either feline group during either phase of the study over the 3-day evaluation after calcitriol administration was initiated. CONCLUSIONS AND CLINICAL IMPORTANCE: At the dosages used, calcitriol treatment did not result in significant differences in serum parathyroid hormone concentrations before and after treatment in both normal cats and cats with chronic renal failure. With these dosages, adverse affects of calcitriol administration were not seen. Potential reasons for lack of apparent effect include small sample size, insufficient duration of study, insufficient dosage of calcitriol, problems with formulation or administration of calcitriol, and variable gastrointestinal absorption of calcitriol.

Comparison between different sources of minerals in horses with nutritional secondary hyperparathyroidism / [Comparação entre diferentes fontes de minerais em cavalos com hiperparatireoidismo secundário nutricional]

Minerals perform several functions in the body, such as coagulation actions, muscle contraction, enzymatic and hormonal production, among others. This study aims to evaluate the effect of a 150 days chelated and not chelated mineral supplementation with and without potassium oxalate on serological parameters and bone mineral density of horses. Twenty-four crossbred yearlings (12 females and 12 males) with an average age of 21±3 months and body weight of 330.8±37.9kg were divided into four groups containing six equines in each (three females and three males) in a completely randomized design with repeated measurements in a 2x2 factorial arrangement. Treatments were: 1 - chelated minerals compound; 2 - chelated minerals compound and potassium oxalate; 3 - not chelated minerals compound; and 4 - not chelated minerals compound and potassium oxalate. Clinical signs of nutritional secondary hyperparathyroidism (NSH) were observed only in treatment 4. Results showed no treatment effect in bone biopsy for calcium, phosphorus and bone density. There were significant reductions of parathyroid hormone (PTH) means concentrations in treatments 2 and 4 during supplementation. Animals supplemented with chelated minerals compounds avoided mineral imbalances and NSH even when in dietary potassium oxalate challenged.(AU)

Os minerais desempenham diversas funções no organismo, como ações de coagulação, contração muscular, produção enzimática e hormonal, entre outras. O objetivo deste estudo foi avaliar o efeito da suplementação de minerais quelatados e não quelatados, por 150 dias, com e sem oxalato de potássio, sobre parâmetros sorológicos e densidade mineral óssea em equinos. Vinte e quatro filhotes mestiços (12 fêmeas e 12 machos), com idade média de 21±3 meses e peso corporal de 330,8±37,9kg, foram divididos em quatro grupos contendo seis equinos cada (três fêmeas e três machos), em delineamento inteiramente ao acaso, com repetição medida em arranjo fatorial 2x2. Os tratamentos foram: 1 - composto mineral quelatado; 2 - composto mineral quelatado e oxalato de potássio; 3 - composto mineral não quelatado; e 4 - composto mineral não quelatado e oxalato de potássio. Os sinais clínicos do hiperparatireoidismo secundário nutricional (NSH) foram observados apenas no tratamento 4. Os resultados não mostraram efeito de tratamento na biópsia óssea para cálcio, fósforo e densidade óssea. Houve redução significativa do hormônio da paratireoide (PTH) em concentrações médias nos tratamentos 2 e 4 durante a suplementação. Os animais suplementados com compostos minerais quelatados evitaram desequilíbrios minerais e NSH, mesmo quando desafiados no oxalato de potássio na dieta.(AU)

Nutritional secondary hyperparathyroidism in rabbits.

The present study was designed to document the effect of a low (0.6%) calcium-high (1.2%) phosphorus (LCaHP) diet on the development of parathyroid gland hyperplasia in rabbits and to describe the dynamics of parathyroid function (PTH-Ca2+ curves) in rabbits with nutritional secondary hyperparathyroidism (N2HPT). Parathyroid gland weight, parathyroid cell proliferation (measured as percentage of cells in S-phase), and parathyroid calcium (CaRmRNA) and Vitamin D (VDRmRNA) receptor expression were measured in normal rabbits and in rabbits with N2HPT. The PTH-Ca2+ curve was studied in normal rabbits (Group I) and in rabbits with N2HPT at two stages: 2-3 weeks (Group IIA) and 5-6 weeks (Group IIB) after being fed LCaHP diet. An increase in parathyroid gland weight and percentage of cells in S-phase was detected in the course of N2HPT. After receiving a LCaHP diet for 6 weeks rabbits had decreased levels of CaRmRNA but VDRmRNA remained unchanged. A progressive increase in the concentrations of plasma PTH (Group IIA=167+/-14 pg/ml and Group IIB=377+/-54 pg/ml, P<0.05 versus Group I=27+/-3 pg/ml) was detected in the rabbits fed a LCaHP diet. This was accompanied by an increase in maximal and minimal PTH, reductions in plasma Ca2+ and calcitriol and elevations in plasma phosphate and creatinine. In conclusion, feeding a LCaHPD results in a rapid induction of N2HPT in rabbits. After 6 weeks on the LCaHPD rabbits develop parathyroid hyperplasia characterized by increases in PTH secretion, glandular weight and proliferation and by a decrease in CaRmRNA.

Vitamin D-dependent rickets type 2 with characteristic radiographic changes in a 4-month-old kitten.

This report describes the presenting signs, biochemical abnormalities, and radiographic changes in a 4-month-old kitten with vitamin D-dependent rickets type 2. Details of therapy are described and possible reasons for treatment failure are discussed.

Hyperparathyroidism in dogs with hyperadrenocorticism.

OBJECTIVES: To assess the effect of canine hyperadrenocorticism (HAC) on parathyroid hormone (PTH), phosphate and calcium concentrations. METHODS: PTH concentrations and routine biochemical parameters were measured in 68 dogs with HAC. Ionised calcium was measured in 28 of these dogs. The results obtained were compared with an age- and weight-matched group of 20 hospital patients that did not show signs of HAC. RESULTS: There were significant differences between the PTH, phosphate, alkaline phosphatase, creatinine and albumin concentrations between the two groups. Total and ionised calcium concentrations were not significantly different. Most of the dogs (92 per cent) with HAC had PTH concentrations that were greater than the reference range (10 to 60 pg/ml), and in 23 dogs they were greater than 180 pg/ml. There were significant positive correlations between the PTH and basal cortisol, post-adrenocorticotropic hormone (ACTH) cortisol and alkaline phosphatase concentrations, and also the phosphate and post-ACTH cortisol concentrations. CLINICAL SIGNIFICANCE: Adrenal secondary hyperparathyroidism is a cause of increased PTH concentrations and may be associated with abnormalities in calcium and phosphate metabolism in dogs with HAC. The findings of this study could explain why canine HAC may cause clinical signs such as calcinosis cutis that are associated with altered calcium metabolism.

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

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 a 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.

Feline hyperparathyroidism: pathophysiology, diagnosis and treatment of primary and secondary disease.

PRACTICAL RELEVANCE: 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. CLINICAL CHALLENGES: 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. AIMS: 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.

Oxyphil cells in a red-tailed hawk (Buteo jamaicensis) with nutritional secondary hyperparathyroidism.

A captive, immature red-tailed hawk (Buteo jamaicensis) was presented with multiple long-bone fractures, a serum calcium of 7.9 mg/dl, and a history of being fed an all-meat diet. Gross and microscopic examinations of the parathyroid glands revealed marked glandular hypertrophy and the presence of interlacing cords and clusters of light chief cells and oxyphil cells in approximately equal numbers. Bone sections showed severe fibrous osteodystrophy. These findings support the observation that the oxyphil cell is a product of continued stimulation, and they suggest that hypocalcemia may be a stimulating factor.