Gout is seen in all orders of reptiles; visceral and articular forms have been reported. Radiographs often reveal mineralized or radiolucent tophi in affected organs and joints. Primary visceral gout is the accumulation of urate microcrystals in organs secondary to a chronic hyperuricemia and is generally caused by excessive protein in the diet. Secondary visceral gout is due to chronic hyperuricemia from such causes as dehydration and renal insufficiency. Gout can be very debilitating, causing discomfort to the point that some reptiles refuse to move, eat, or drink.
Primary visceral gout is treated by correcting the diet. Secondary visceral gout is treated by attempting to correct the underlying problem, be it dehydration or renal disease. The prognosis is typically poor in advanced cases. Allopurinol is effective at reducing blood uric acid levels. Drug administration usually must be longterm, because signs typically recur if treatment is discontinued. Euthanasia must be considered in reptiles in which movement is painful and appetite becomes suppressed.
Secondary nutritional hyperparathyroidism is the most common bone disease seen in reptile practice. It is caused by poor diet (low calcium to phosphorus ratio, vitamin D3 deficiency) or poor husbandry (lack of UVB light, inadequate thermal provision). Affected reptiles are generally rapidly growing herbivorous and insectivorous lizards and chelonians. Signs include anorexia; lethargy; an inability to walk normally; swollen/distorted mandible, maxilla, and/or long bones; limb and spinal pathologic fractures; cloacal prolapse; muscle fasciculations; and tetany. Diagnosis requires radiography to document generalized demineralization of the skeleton and low plasma levels of 25-dihydroxycholecalciferol. Findings in the late stages include hyperphosphatemia and low total and ionized calcium. Treatment of critical cases requires fluid therapy, nutritional support, parenteral calcium therapy if hypocalcemic, and phosphate binders if hyperphosphatemic. Correction of the diet and husbandry are the mainstays of successful therapy, and prognosis is favorable, particularly if the animal is still eating.
Secondary renal hyperparathyroidism occurs in adult reptiles and is associated with hyperphosphatemia, soft-tissue calcification, osteodystrophy, and hypocalcemia secondary to a primary nephrosis. Provisional diagnosis generally rests on history, radiography, and plasma biochemistry, although a definitive diagnosis requires demonstration of reduced renal function (eg, iohexol clearance) and renal pathology (eg, renal biopsy).
Reports of hypertrophic osteopathy are uncommon and currently appear to be limited to lizards with extensive periosteal proliferation beginning in the distal long bones and progressing proximally. The pathogenesis is unknown, but theories include chronic anoxia, toxins, and vagal neurologic pathways. Many cases appear to be chronic bacterial infections of the spine.
Endocrine diseases are not often documented in reptiles. Diabetes mellitus has been reported in chelonians; glucosuria and hyperglycemia are the primary findings, and polyphagia may or may not be apparent. The etiology is often undetermined but has been associated with gastric neuroendocrine carcinomas in bearded dragons. Pancreatectomy in lizards may result in hypoglycemia, implying that other hormones, such as glucagon or somatotropin, may play a role in the pathogenesis of diabetes mellitus in reptiles.
Hyperthyroidism has been reported in a female green iguana that presented with polyphagia, loss of the dorsal spines, hyperactivity, increased aggression, tachycardia, and a bilobate mass palpable anterior to the thoracic inlet. Surgical thyroidectomy returned the lizard to a euthyroid state.