Nutritional Secondary Hyperparathyroidism (NSHPT)

Outline

BASICS

Overview

NSHPT is a skeletal disorder of equids fed a diet with excess of phytates or oxalates, or a diet with a P:Ca ratio of >3:1. Phosphate, phytates, and oxalates bind calcium in the intestines, reducing Ca absorption. Low plasma ionized Ca stimulates secretion of PTH, leading to hyperparathyroidism
Also known as big head, bran disease, miller's disease, osteodystrophia fibrosa, osteitis fibrosa, equine osteoporosis
Systems affected—musculoskeletal, endocrine

Signalment

Signs

Physical Examination Findings

Causes and Risk Factors

Rations with a P:Ca ratio >3:1 even with adequate Ca
Access to high oxalate-containing plants, including Setaria grass, buffel grass, purple pigeon grass, kikuyu, dallis grass, panic grass, pangola, and pearl millet, soursob, shamrock, red-rooted pigweed, Halogeton, purslane, rhubarb, sorrel, others

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Differential Diagnosis

Primary hyperparathyroidism has increased PTH concentrations and increased calcium concentrations
Humoral hypercalcemia of malignancy results in hypercalcemia, hypophosphatemia, low to normal PTH, and increased PTH-related protein concentrations
Chronic renal failure may result in hypercalcemia. Renal secondary hyperparathyroidism has not been reported in horses

CBC/Biochemistry/Urinalysis

Other Laboratory Tests

Serum PTH may be normal or increased
Increased urinary fractional excretion of P (reference range 0–0.5%). Urinary excretion of Ca may be low but is often difficult to interpret due to excessive Ca content in equine urine
Analysis of dietary Ca and P
Plant oxalate content
Byproducts of bone resorption (CTX-1) may be increased in serum or urine

Imaging

Decreased bone density may be visualized in skull radiographs. A minimum decrease of 30% is necessary for detection
Loss of laminae durae of the mandible
Decreased cortical bone thickness and demineralization may be seen in chronic cases. Fractures may be detected

Pathologic Findings

Bone mineral is replaced by fibrous tissue
Increased bone volume but decreased bone density, primarily of the cancellous bone of the skull, ribs, and metaphyses of long bones
Parathyroid gland hypertrophy and hyperplasia may be evident

Treatment ⬆ ⬇

TREATMENT

Activity

Confine to a stall or small paddock until bone density normalizes
Remove oxalate-containing plants from the diet
Supplement Ca and P (CaCO₃ or CaHPO₄) 100–300 g/day at a ratio of 1 part CaCO₃ to 2 parts CaHPO₄ for horses grazing oxalate-rich pastures. For treatment, diet should have a Ca:P ratio of 3–4:1. Molasses may improve palatability
Feed alfalfa hay
Reduce grain intake

Medications ⬆ ⬇

MEDICATIONS

Use NSAIDs with caution—decreasing pain may lead to increased activity and skeletal trauma
Vitamin D may promote bone formation and reduce PTH secretion
The value of drugs that reduce osteoclast activity (e.g. bisphosphonates) is unknown

Follow-up ⬆ ⬇

Outline

FOLLOW-UP

Patient Monitoring

Radiography to assess bone density (ideally, compare with age-matched unaffected horses).

Prevention/Avoidance

Avoid a high-bran diet
Horses on high-grain diets should be supplemented with Ca to ensure a Ca:P ratio >1.5:1
Limit access to pastures containing oxalate-accumulating plants

Possible Complications

Horses may lose teeth, or develop fracture or periosteal avulsions.

Expected Course and Prognosis

Lameness usually resolves 4–6 weeks after diet correction, and before bone density normalizes
Recovery of bone strength may take 9–12 months. Severely affected horses may not recover
In most cases, enlarged skull bones do not resolve

Miscellaneous ⬆ ⬇

Outline