Dose–Response Studies for Pituitary and Testicular Function in Male Dogs Treated with the GnRH Superagonist, Deslorelin

We tested the effect of dose of GnRH superagonist on pituitary and testicular function in a study with four groups of four male dogs. The Controls received blank implants and the other three groups received implants containing 3, 6 or 12 mg deslorelin (d ‐Trp⁶‐Pro⁹‐des‐Gly¹⁰‐GnRH ethylamide). In all deslorelin‐treated groups, there was initially an acute increase in plasma concentrations of LH and testosterone, followed by declines such that both hormones became undetectable after approximately 12 days. There was a dose–response in some of these early aspects of the hormone profiles. With respect to long‐term effects of treatment, the 12‐mg dose had significantly greater effects than the smaller doses for the duration of minimum testicular volume [366 ± 77, mean ± SEM (3 mg), 472 ± 74 (6 mg), and 634 ± 59 (12 mg) days], absence of ejaculate [416 ± 88 (3 mg), 476 ± 83 (6 mg), and 644 ± 67 (12 mg) days], undetectable plasma concentrations of LH and testosterone [367 ± 64 (3 mg), 419 ± 72 (6 mg), and 607 ± 69 (12 mg) days], the delay until complete recovery of LH and testosterone secretion [394 ± 65 (3 mg), 484 ± 72 (6 mg) and 668 ± 47 (12 mg) days], and the delay until testes had regrown to normal volume [408 ± 77 (3 mg), 514 ± 74 (6 mg), 676 ± 59 (12 mg) days]. The time taken to restore full ejaculates was also longest for the 12‐mg dose: 716 ± 67 (12 mg) days vs 440 ± 66 (3 mg) and 538 ± 83 (6 mg) days after implantation. There was no correlation between delay to recovery of normal ejaculate quality and body mass. We conclude that the dose–response relationship with deslorelin implants is not expressed with respect to the degree of suppression of reproduction, but on the maximum duration of suppression and thus to delay until recovery.     

Severe calcinosis cutis associated with treatment of hypoparathyroidism in a dog.

A 6-month-old, female border collie was referred for evaluation of hypocalcemia, hyperphosphatemia, fever, and painful ventral abdominal skin. She had recently been treated intravenously and subcutaneously (SC) with a diluted 10% calcium gluconate solution. The medical evaluation supported the diagnosis of primary hypoparathyroidism, but the subsequent hospital course was complicated by severe calcinosis cutis, which caused extensive skin necrosis and marked debilitation. This patient illustrates that administration of a calcium gluconate solution SC can be associated with extensive morbidity when administered to hyperphosphatemic patients.     

QUANTITATIVE HEPATOBILIARY SCINTIGRAPHY IN NORMAL CATS AND IN CATS WITH EXPERIMENTAL CHOLANGIOHEPATITIS

Quantitative hepatobiliary scintigraphy using 99mTc-mebrofenin was performed on eight normal cats and on the same cats after induction of experimental cholangiohepatitis by infection with the liver fluke Platynosomum concinnum. Hepatobiliary scintigraphy was performed 3 times at 10 weeks, 4 months and 6 months after infection. In addition, routine biochemical tests, hepatic ultrasound and ultrasound guided hepatic biopsy samples were obtained at the same time points, and the results compared with hepatobiliary scintigraphy. The normal hepatic extraction fraction was determined to be 85%, and the normal hepatic excretion half time (T 1/2) was 14 minutes. There was no significant change in scintigraphic parameters compared to pre-infection values at any time following infection with the liver fluke. No correlation between scintigraphic parameters and histologic scores was found; however, significant correlation was identified between parasite burden and histologic scores 6 months following infection. Despite the presence of severe multifocal histologic abnormalities, minimal clinical, biochemical and scintigraphic derangements were identified using this model of cholangiohepatitis. Based on this study, hepatobiliary scintigraphy appears to be an insensitive test for structural hepatobiliary abnormalities. The role of hepatobiliary scintigraphy in functional hepatobiliary abnormalities of the feline liver has not been determined.