Skip to main content
NCBI home page
The Canadian Veterinary Journal logoLink to The Canadian Veterinary Journal
. 2023 Mar;64(3):245–251.

Multiple pituitary hormone deficiencies in a kitten: Hyposomatotropism, hypothyroidism, central diabetes insipidus and hypogonadism

Mathieu V Paulin 1,✉, Shauna Gleasure 1, Elisabeth C Snead 1
PMCID: PMC9979728  PMID: 36874542

Abstract

In humans, post-traumatic hypopituitarism (PTHP) is a common complication of traumatic brain injury, with the most frequently reported hormonal deficiencies resulting in hyposomatotropism and hypogonadism, followed by hypothyroidism, hypocortisolism, and central diabetes insipidus. To date, PTHP has rarely been reported in cats, and the reported cases often describe a single hormone deficiency. This report details an approximately 7-month-old cat with a history of suspected traumatic brain injury at 5 wk of age, that presented with growth retardation (1.53 kg) and polyuria-polydipsia. Thyroid panel, thyrotropin-releasing hormone stimulation test, thyroid scan with Technetium-99, repeat measurement of serum IGF-1, resting cortisol, endogenous ACTH concentration, and ACTH stimulation testing were performed. The cat was diagnosed with presumptive PTHP leading to hyposomatotropism, hypothyroidism, central diabetes insipidus, and hypogonadism. In this case, treatment of the hypothyroidism and central diabetes insipidus were successful. Hyposomatotropism and hypogonadism were not treated. Although reported feline PTHP cases have described a single hormone deficiency, this report details a cat with presumptive PTHP leading to hyposomatotropism, hypothyroidism, central diabetes insipidus, and hypogonadism. Attention should be paid to the potential for the development of PTHP in cats secondary to traumatic brain injury.

Key clinical message:

Post-traumatic hypopituitarism in cats can lead to multiple hormone deficiencies, leading to hyposomatotropism, hypothyroidism, central diabetes insipidus, and hypogonadism.

Altercations with animals, falls from a height, and traffic accidents are common causes of traumatic brain injury (TBI) in cats (1,2). There is minimal attention paid to the potential for the development of post-traumatic hypopituitarism (PTHP) in animals (1,2). To date, PTHP has rarely been reported in cats and the reported cases often have described only a single hormone deficiency (3–5). Conversely, PTHP is well-recognized in humans following TBI (6). This report details a cat with suspected PTHP leading to hyposomatotropism, hypothyroidism, central diabetes insipidus (CDI), and hypogonadism.

Case description

An approximately 5-week-old, 0.34 kg (body condition score of 4/9), intact female, domestic medium hair kitten was presented to the emergency department after being found by a good Samaritan (Figure 1 A). On admission, vital parameters were within normal limits. General physical examination revealed a moderate amount of dried blood around both nostrils, at the lip commissures, and on the right thoracic limb. A blood clot was also visualized in the oropharynx and was removed. A neurological examination was performed by a neurologist (ACVIM Diplomate). The cat was mentally depressed; posture and gait were normal. Postural reactions, spinal reflexes, and sensation were unremarkable. The kitten was also assessed by an ophthalmologist (ACVO Diplomate) and a visual deficit, more prominent in the left eye, was suspected based on rudimentary maze testing and lack of normal tracking with noiseless movement of a pen and cotton ball in front of her face. The kitten also had bilateral mydriasis, with preserved pupillary light reflexes. The cranial nerve examination was otherwise unremarkable and a fundic examination was normal. Based on the history and physical examination findings, TBI was suspected. Mentation and vision steadily improved over 5 d in hospital with basic supportive care. Over the course of the next 6 wk, the kitten was repeatedly dewormed, she received her routine vaccination series for feline viral rhinotracheitis, calicivirus, panleukopenia (FVRCP), and rabies and tested negative for feline immunodeficiency virus (FIV) and feline leukemia virus (FeLV) (FIV/FeLV snap tests; IDEXX Laboratories, Westbrook, Maine, USA).

Figure 1.

Figure 1

Open in a new tab

Photographs at different ages of the detailed cat with presumptive post-traumatic hypopituitarism. A — 5-weeks-old; B — 7-months-old; C — 2-years-old beside an 11-week-old kitten; D — 3-years-old beside a 7-year-old cat.

At approximately 7 months-of-age, the cat was seen for further evaluation of growth retardation (1.53 kg) and polyuriapolydipsia (PUPD). On physical examination, a proportionate growth failure was appreciated (Figure 1 B). The cat’s hair coat was soft and woolly with suspicion of retained secondary hairs. The kitten had persistent but less severe bilateral mydriasis at rest, with preserved pupillary light reflexes. Differential diagnoses for stunted growth in this case included congenital or acquired pituitary or hypothalamic dysfunction leading to hyposomatotropism and/or hypothyroidism, portosystemic shunt, congenital renal disease, or lysosomal storage diseases.

A complete blood (cell) count (CBC) was unremarkable other than a mild lymphocytosis [7.3 × 109/L; reference interval (RI): 1.0 to 6.9 × 109/L], suspected to be secondary to recent vaccination, but hypocortisolemia was also considered possible. Serum biochemical abnormalities were limited to a mild elevation in ALP (124 U/L; RI: 11 to 56 U/L). Urinalysis revealed a urine specific gravity (USG) of 1.012 and was otherwise unremarkable. Both serum pre- (1 μmol/L; RI: 0 to 10 μmol/L) and post-prandial (5 μmol/L; RI: 0 to 20 μmol/L) bile acids concentrations were within normal limits. A thyroid panel, measurement of serum insulin-like growth factor 1 (IGF-1), resting cortisol, and endogenous ACTH (eACTH) concentrations were performed at Michigan State University (MSU), Veterinary Diagnostic Laboratory (Lansing, Michigan, USA). Serum IGF-1 concentration was measured as a surrogate for growth hormone (GH) because it is less subject to fluctuation and the assay is more readily available (7). Samples from an apparently healthy 6-month-old intact male kitten, who weighed more than twice the affected kitten, were measured at the same time for comparison. Full body radiographs (2 orthogonal views) were performed to look for findings consistent with hypothyroidism such as non-clinical constipation, delayed closure of ossification centers in long bones, shortening and scalloping of the ventral borders of the vertebral bodies). The radiographs only revealed open physes of the axial and appendicular skeleton, considered appropriate for the kitten’s age, as well as moderate urinary bladder distension (Figure 2). There was no evidence of epiphyseal or metaphyseal dysplasia or osteopenia. A portosystemic shunt was not appreciated on abdominal ultrasound but there was evidence of mild bilateral pyelectasis consistent with the reported PUPD.

Figure 2.

Figure 2

Open in a new tab

Full body radiograph, right lateral, of the kitten at 7-months-old, revealing open physes of the axial and appendicular skeleton, considered appropriate for the patient’s age. There was no evidence of epiphyseal or metaphyseal dysplasia or osteopenia.

Hypothyroidism

Serum total thyroxine (TT4: 8 nmol/L; RI: 9 to 46 nmol/L), total triiodothyronine (TT3: 0.8 nmol/L; RI: 0.6 to 1.4 nmol/L), and free T4 by dialysis (13 pmol/L; RI: 10 to 53 pmol/L) concentrations were all low to borderline low with a physiologically inappropriate low normal serum thyroid stimulation hormone concentration (TSH: 0.11 ng/mL; RI: 0 to 0.38 ng/mL) indicating no pituitary compensation from the lack of negative feedback, especially for a growing kitten (Table 1). Therefore, primary consideration was given to suspected secondary hypothyroidism and the kitten was empirically started on levothyroxine (LEVENTA 1 mg/mL; Merck Animal Health, Kirkland, Quebec) at a standard dose of 0.01 mg/cat, PO, q12h. Two months later, TT4 (19 nmol/L; RI: 13 to 50 nmol/L) and TSH (0.03 ng/mL, in-house reference interval not available) concentrations 4 h after administration of the morning dose of levothyroxine, measured through a local laboratory (Prairie Diagnostic Services, Saskatoon, Saskatchewan), suggested an insufficient hormonal supplementation, especially given her growing state and our inability to supplement for the GH deficiency. The dose of levothyroxine was increased to 0.02 mg, PO, q12h. To try to definitively prove the cat had secondary hypothyroidism, 6 mo after initiating the levothyroxine supplementation when the consequences of a thyroid deficiency would have been less severe, levothyroxine was discontinued for 2 wk before performing a thyrotropin-releasing hormone (TRH) stimulation test and a thyroid scintigraphy scan with technetium as pertechnetate (99mTcO4-) (Ultra-Technekow V4 generator, Curium, Laval, Quebec). There are no published data on the duration of hypothalamic-pituitary-thyroid axis recovery in cats after oral levothyroxine administration. However, a study assessing thyroid function tests 1 wk after cessation of oral levothyroxine at 0.026 mg/kg, q24h for up to 16 wk, provided an accurate assessment of thyroid function in healthy euthyroid dogs (8). Based on these available results in dogs, the authors decided to discontinue oral levothyroxine supplementation for 2 wk before performing a TRH stimulation test and a thyroid scintigraphy scan. Unfortunately, there is a paucity of data regarding TSH and TRH stimulation tests in cats with hypothyroidism, likely due to the low prevalence of this disease in cats (9). The authors chose to perform a TRH stimulation test given the high suspicion of secondary hypothyroidism and the high cost of TSH. Acknowledging the lack of validation of TRH stimulation test for diagnosis of hypothyroidism in cats, a thyroid scintigraphy scan was also performed to further support the diagnosis of hypothyroidism and to also definitively rule out euthyroidism.

Table 1.

Endocrinologic testing performed at Michigan State University, Veterinary Diagnostic Laboratory (Lansing, Michigan, USA).

Parameters Patient Control Reference intervals
Age (mo) 7 8 6
Weight (kg) 1.53 1.55 3.1
TT4 (nmol/L) 8 (L) 22 9 to 46
TT3 (nmol/L) 0.8 1.2 0.6 to 1.4
FT4 (pmol/L) 13 25 10 to 53
TSH (ng/mL) 0.11 0.04 0 to 0.38
IGF-1 (nmol/L) 8 (L) 5 (L) 126 (H) 12 to 92
Resting cortisol (nmol/L) 10 (L) 24 109 (H) 15 to 97
Cortisol 30 min post-ACTH (nmol/L) 145 NA
Cortisol 1 h post-ACTH (nmol/L) 158 97 to 207
eACTH (pmol/L) 38.7 8.8 2 to 21
Open in a new tab

(L) — Low result; (H) — High result; NA — Not available; eACTH — Endogenous ACTH; FT4 — Free thyroxine; IGF-1 — Insulin-like growth factor 1; TSH — Thyroxine stimulating hormone; TT3 — Total triiodothyronine; TT4 — Total thyroxine.

Blood for serum TT4 determination was obtained before and 4 h after TRH administration at the dose of 0.1 mg/kg, and blood for serum TSH determination was obtained before and 30 min after TRH administration (Table 2) (MSU, Veterinary Diagnostic Laboratory). Unfortunately, there was not sufficient serum to determine the baseline TSH, and given the suspicion of secondary hypothyroidism, measurement of TSH at 30 min post-TRH administration was prioritized. Results showed a baseline TT4 sample of 3 nmol/L (RI: 9 to 46 nmol/L), a TSH sample at 30 min post-TRH stimulation of 0.25 ng/mL (RI: 0 to 0.38 ng/mL), and a follow-up T4 assay at 4 h post-TRH stimulation of 6 nmol/L (RI: 9 to 46 nmol/L). These results supported hypothyroidism of apparently central origin. A thyroid scintigraphy scan (Tc99,130 MBq SC) was performed under sedation (diluted dexmedetomidine 0.05 mg/mL, 5 μg/kg, IV, i.e., 0.15 mL, IV, Zoetis, Kirkland, Quebec) with images to 300 000 counts recorded at 20- and 60-min post-administration. The percentage Tc99 uptake was calculated using GE Xeleris workstation software. There was virtually no uptake of Tc99 by the thyroid glands at 20 and 60 min (Figure 3). Hypothyroidism was also supported clinically by a very slow recovery from sedation with requirement for passive rewarming to address hypothermia despite rapid reversal of the sedative with atipamezole (diluted atipamezole 0.5 mg/mL, i.e., 0.15 mL IV, Zoetis, Kirkland, Quebec), 50 μg/kg, IM.

Table 2.

Results of the thyrotropin-releasing hormone stimulation testing, performed at 14-months-old. Serum total thyroxin (TT4) and thyroxine stimulating hormone (TSH) were measured at Michigan State University, Veterinary Diagnostic Laboratory (Lansing, Michigan, USA). Oral levothyroxine supplementation was discontinued for 2 wk prior to performing the thyrotropin-releasing hormone stimulation test.

Parameters Baseline Reference intervals
T = 0 T = 30 min T = 4 h
TT4 (nmol/L) 3 (L) QNS 6 (L) 9 to 46
TSH (ng/mL) QNS 0.25 QNS 0.0 to 0.38
Open in a new tab

(L) — Low result; QNS — Quantity not sufficient.

Figure 3.

Figure 3

Open in a new tab

Thyroid scintigraphy scan with Technetium-99 (Tc99, 130 MBq SC). There was virtually no uptake of Tc99 by the thyroid glands at 60 min (Imaging Department, VMC-WCVM, University of Saskatchewan, Canada). For comparison, images of a thyroid scan with Technetium-99 in a euthyroid 13-year-old castrated male domestic long hair cat are also available (the thyroid scan was performed to rule out hyperthyroidism in this patient). Arrows indicate thyroid glands.

Hyposomatotropism

Serum IGF-1 concentration was low in the affected kitten (8 nmol/L; RI: 12 to 92 nmol/L). As exogenous forms of GH hormone are either very expensive (human recombinant) or not readily available, and since congenital hypothyroidism has been reported to suppress IGF-1 secretion (10), the decision was made to first treat hypothyroidism. The serum IGF-1 concentration remained low (5 nmol/L; RI: 12 to 92 nmol/L) when reassessed after adequate thyroid supplementation (10), leading to a presumptive diagnosis of hyposomatotropism suspected secondary to TBI (Table 1).

Central diabetes insipidus

Urinalysis revealed a USG of 1.012 and 1.008 at 5 and 9 months-of-age, respectively. Given the other documented pituitary hormone deficiencies, CDI was suspected as the cause of the PUPD. A trial using oral desmopressin acetate (DDAVP; Ferring, North York, Ontario) was initiated (0.05 mg, PO, q12h). A calculated serum osmolality was 337.6 mOsm/L based on the formula:

2([Na]+[K]) (mEq/L)+0.05 [glucose] (mg/dL)+0.33 [BUN] (mg/dL),

which also suggested primary polydipsia was less likely as serum osmolality is often < 280 mOsm/L with this condition (11). Three weeks after initiating oral desmopressin acetate, a marked reduction of the PUPD was reported and the USG was 1.020; the oral desmopressin acetate dose was increased to 0.05 mg, PO, q8h. Eight weeks later, the owners reported complete resolution of the PUPD, and the USG was 1.043. These findings strongly supported a diagnosis of CDI, again suspected secondary to TBI.

Hypogonadism

By 3 years-of-age (at the time of writing), the cat had never shown signs of estrus (behavior or vaginal discharge) or reproductive development. In addition, an abdominal ultrasound performed by an ACVR Board-certified radiologist when the cat was just over 1 year-of-age failed to demonstrate any ovaries or a uterus. However, resting and provocative testing were not performed to confirm hypogonadism. Given her small stature and increased likelihood of anesthetic complications, the kitten did not undergo exploratory laparotomy for potential ovariohysterectomy.

Adrenal function

At 7 months-of-age, serum resting cortisol concentration was low (10 nmol/L; RI: 15 to 97 nmol/L) with a compensatory increase in plasma eACTH concentration (39.7 pmol/L; RI: 2 to 21 pmol/L — provided by the MSU, Veterinary Diagnostic Laboratory) (Table 1). The ACTH assay was performed on the Immulite 2000 analyzer (Diagnostic Products Corporation, Los Angeles, California, USA). These results raised the suspicion for primary hypoadrenocorticism, but no immediate action was taken due to limited supportive clinical findings. Adrenal function was rechecked 1 mo later: serum concentrations of resting cortisol at 30 min and 60 min post-ACTH stimulation test (Cortrosyn 0.25 mg/vial; Amphastar Pharmaceuticals, Rancho Cucamonga, California, USA) conclusively ruled out hypocortisolism (Table 1). A recheck CBC also showed resolution of the lymphocytosis.

Long-term follow-up

At 3 years-of-age, the cat had a 10-second generalized tonicclonic seizure. Serial blood glucose measurements ruled out hypoglycemia as a cause of seizure activity. Brain MRI with contrast (gadobenate dimeglumine IV; MultiHance, Bracco, Italy) was performed at a private referral practice. There was a T2 hyperintense, T1 and FLAIR hypointense lined structure around the pituitary gland in the ventral 3rd ventricle, primarily on midline but bulging further to the right than the left, and which was non-contrast enhancing. The findings were consistent with a pituitary cyst. A cerebrospinal fluid tap was attempted, but unfortunately, only a limited sample was obtained; this was not enough for cytological analysis. Bacterial culture was negative. The seizure could have occurred secondary to post-trauma induced epileptogenic brain damage or idiopathic epilepsy. Given its localization, it was unlikely that the pituitary cyst was the cause of the seizure.

Discussion

Based on the initial clinical suspicion of external trauma, PTHP was primarily suspected in this cat, leading to hyposomatotropism, hypothyroidism, CDI, and hypogonadism. Although a congenital pituitary cyst resulting in hypopituitarism cannot be ruled out, the reported arachnoid cyst may have resulted from TBI. The visual deficits and the lack of findings on radiographs supportive of severe congenital hypothyroidism could have been because thyroid hormone was not deficient in the first few weeks of life making trauma more likely to be the underlying cause of the hormonal deficiencies rather than a congenital cyst. Also, the initial physical examination findings on admission (moderate amount of dried blood around both nostrils, at the lip commissures, and on the right thoracic limb, blood clot in the oropharynx, depressed mentation, visual deficit that resolved later, bilateral mydriasis) supported suspected head trauma. The authors acknowledge that trauma may have resulted from decreased mentation, secondary to a pituitary cyst, but this is considered less likely given the totality of the findings. Indeed, arachnoid cysts in humans often result from post-inflammatory accumulation of cerebrospinal fluid in the subarachnoid space in patients with TBI (12–14). In one case report of CDI associated with a possible congenital cyst of the sella turcica in a 1 year-old-cat, the owners also reported that the cat had fallen from a high window at 2 months-of-age (15). It is known that PTHP is a common complication of TBI in humans (6), including: hyposomatotropism, hypothyroidism, CDI, hypogonadism, and hypocortisolism (16,17), whereas congenital pituitary cysts are rare in cats (18), and have only been reported in cats with central diabetes insipidus (15,19), and the syndrome of inappropriate antidiuretic hormone secretion (20). However, in one of these cases with a congenital cyst leading to CDI (19), the cat was also described as being small in stature with proportional dwarfism, so it cannot be conclusively ruled out that the cause of the pituitary hormonal deficiencies in this case were not the result of a congenital cyst.

Traumatic brain injury can lead to temporary or permanent neurologic dysfunction and PTHP (16), which can result in hyposomatotropism, hypothyroidism, CDI, hypoadrenocorticism, and hypogonadism due to either injury to the hypothalamus, the pituitary gland, or both (6,16). The most frequently reported hormonal deficiencies in humans with PTHP are hyposomatotropism and hypogonadism, followed by hypothyroidism, hypocortisolism, and CDI (16,17). The precise pathophysiology of PTHP is poorly understood. Primary injury from the mechanical event (such as hypophyseal pituitary stalk transection, hemorrhage into the hypothalamus and pituitary gland, and infarction of vessels) and secondary insults (such as hypotension, hypoxia, increased intracranial pressure or neuroinflammation leading to autoantibodies directed against the pituitary or hypothalamus) have been hypothesized (6,16,17). In humans, screening tests for hormone deficiencies are typically the first step in supporting a diagnosis of PTHP. Testing involves measuring serum concentrations of morning cortisol, free T3, free T4, TSH, IGF-1, follicle-stimulating hormone (FSH), luteinizing hormone (LH), testosterone (males), estradiol (females), prolactin, urinary free cortisol on a 24-hour urine collection, and serum osmolarity if PUPD is reported (17). If equivocal results are obtained, or clinical signs are subtle, follow-up provocation testing is recommended (17).

Hyposomatotropism is a rare endocrinopathy in felines, with only a few cases featuring a history of TBI (4,21). If TBI occurs at an early age, then results of anterior pituitary deficiencies leading to growth retardation can be prominent (21), as in this case in which the signs manifested were similar to those seen in rare congenital cases of hyposomatotropism reported in this species (retention of secondary hair leading to a soft, woolly haircoat, and proportional dwarfism) (21,22). Animals with early onset hyposomatotropism may also show failure of reproductive development (testicular atrophy, unilateral or bilateral cryptorchidism, persistent anestrus) which may have contributed to hypogonadism in the reported cat. Screening tests for hyposomatotropism include screening for low basal IGF-1 and GH concentrations. Unfortunately, random serum GH and basal IGF-1 concentrations are not always reliable in the acute phase after injury so provocative testing may be required in the form of a GnRH, xylazine ghrelin, or clonidine stimulation tests (23). These tests have been used in dogs, however, their use has not been reported in cats (23). In humans, a glucagon stimulation test is often done to try to confirm hyposomatotropism, but there are no reports of this test in cats (6,24). This was not considered necessary in this case given the repeatedly very low serum IGF-1 concentrations. Since congenital hypothyroidism has been reported to decrease serum IGF-1 concentrations in a kitten, the fact that IGF-1 was still low after oral supplementation with levothyroxine was also helpful in further supporting a diagnosis of true hyposomatotropism in this case (10).

Central hypothyroidism secondary to TBI is rare in cats (25). Given the proportionate dwarfism, the effect of hyposomatotropism was more clinically dominant in this case since hypothyroidism growth failure is usually disproportionate (7).

Of the 3 endocrine deficiencies confirmed in this kitten, CDI is the most reported deficiency after TBI in cats (3–5,11). A water deprivation test, modified water deprivation test, or desmopressin acetate challenge are frequent methods used to diagnose CDI and to assist in distinguishing between nephrogenic diabetes insipidus and psychogenic polydipsia (26). In this case, the initial 2 phases of a water deprivation test were not pursued prior to an oral desmopressin acetate trial, as CDI seemed probable given the dwarfism from suspected PTHP. The complete response to an adequate dose of oral desmopressin acetate confirmed the diagnosis. We suspect this is a permanent condition in this cat but some cases of acute CDI from TBI in humans will resolve if there is no transection of the pituitary stalk or hypothalamic damage (6,16,17).

Although not discussed in the other papers describing trauma induced or congenital cases of pituitary dysfunction (3–5,21,25), by 3 years-of-age the cat had never shown signs of estrus (behavior or vaginal discharge) or reproductive development. Resting and provocative testing could have been considered to confirm hypogonadism but was not considered necessary.

Treatment for PTHP involves exogenous supplementation of deficient hormones (7). In humans, hormone replacement therapy is warranted for hypoadrenocorticism, hypothyroidism, and CDI; however, GH deficiency and hypogonadism have a high degree of spontaneous resolution and supplementation is usually recommended only after cortisol, thyroid, and vasopressin levels have been normalized and if the patient is showing clinical signs from GH or sexual hormone deficiencies (27). In this case, treatment of the hypothyroidism and CDI were successful. The hyposomatotropism was not treated specifically as exogenous forms of GH are either very expensive (human recombinant) or not readily available (7,28). Supplementation with progestins has been used to induce mammary gland secretion of GH in dogs with congenital hyposomatotropism (29), but failed to increase serum GH or IGF-1 concentrations in cats, despite the expression of feline GH genes in mammary tissue undergoing progestin-induced fibroadenomatous changes, so this was not recommended here (30,31).

The underlying cause of the adult onset of the single seizure in this cat cannot be definitively determined. The seizure could have occurred secondary to post-trauma induced epileptogenic brain damage or idiopathic epilepsy. Given its localization, it was unlikely that the pituitary cyst was the cause of the seizure. Although head trauma is an established cause of secondary epilepsy in humans and domestic small animals (32), in 1 study of 110 cats with a history of head trauma, none of them developed seizures during the follow-up period (≥ 2 y after head injury) (32). Also, it would be unusual for the seizure to occur almost 3 y after the suspected trauma.

Although reported feline PTHP cases often described a single hormone deficiency (3–5), this report details a cat with presumptive PTHP leading to hyposomatotropism, hypothyroidism, central diabetes insipidus, and hypogonadism. CVJ

Footnotes

Use of this article is limited to a single copy for personal study. Anyone interested in obtaining reprints should contact the CVMA office (hbroughton@cvma-acmv.org) for additional copies or permission to use this material elsewhere.

References

  • 1.Kuo KW, Bacek LM, Taylor AR. Head trauma. Vet Clin North Am Small Anim Pract. 2018;48:111–128. doi: 10.1016/j.cvsm.2017.08.005. [DOI] [PubMed] [Google Scholar]
  • 2.Adamantos S, Garosi L. Head trauma in the cat: 1. Assessment and management of craniofacial injury. J Feline Med Surg. 2011;13:806–814. doi: 10.1016/j.jfms.2011.09.002. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 3.Campbell FE, Bredhauer B. Trauma-induced central diabetes insipidus in a cat. Aust Vet J. 2008;86:102–105. doi: 10.1111/j.1751-0813.2007.00214.x. [DOI] [PubMed] [Google Scholar]
  • 4.Smith JR, Elwood CM. Traumatic partial hypopituitarism in a cat. J Small Anim Pract. 2004;45:405–409. doi: 10.1111/j.1748-5827.2004.tb00256.x. [DOI] [PubMed] [Google Scholar]
  • 5.Oliveira KM, Fukushima FB, Oliveira CM, et al. Head trauma as a possible cause of central diabetes insipidus in a cat. J Feline Med Surg. 2013;15:155–159. doi: 10.1177/1098612X12463162. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 6.Kgosidialwa O, Hakami O, Muhammad Zia-Ul-Hussnain H, Agha A. Growth hormone deficiency following traumatic brain injury. Int J Mol Sci. 2019;20:3323. doi: 10.3390/ijms20133323. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 7.Reusch CE. Disorders of growth hormone. In: Feldman EC, Nelson RW, Reusch CE, editors. Scott-Moncrieff, Behrend E Canine & Feline Endocrinology. 4th ed. St. Louis, Missouri: Elsevier; 2015. pp. 37–76. [Google Scholar]
  • 8.Ziglioli V, Panciera DL, Troy GC, Monroe WE, Boes KM, Refsal KR. Effects of levothyroxine administration and withdrawal on the hypothalamic-pituitary-thyroid axis in euthyroid dogs. J Vet Intern Med. 2017;31:705–710. doi: 10.1111/jvim.14711. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 9.Feldman EC, Nelson RW, Reusch CE, editors. Scott-Moncrieff, Behrend E Canine & Feline Endocrinology. 4th ed. St. Louis, Missouri: Elsevier; 2015. Scott-Moncrieff Hypothyroidism; p. 128. [Google Scholar]
  • 10.Quante S, Fracassi F, Gorgas D, et al. Congenital hypothyroidism in a kitten resulting in decreased IGF-I concentration and abnormal liver function tests. J Feline Med Surg. 2010;12:487–490. doi: 10.1016/j.jfms.2010.01.013. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 11.Aroch I, Mazaki-Tovi M, Shemesh O, Sarfaty H, Segev G. Central diabetes insipidus in five cats: Clinical presentation, diagnosis and oral desmopressin therapy. J Feline Med Surg. 2005;7:333–339. doi: 10.1016/j.jfms.2005.03.008. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 12.Orrison WW, Hanson EH, Alamo T, et al. Traumatic brain injury: A review and high-field MRI findings in 100 unarmed combatants using a literature-based checklist approach. J Neurotrauma. 2009;26:689–701. doi: 10.1089/neu.2008.0636. [DOI] [PubMed] [Google Scholar]
  • 13.Eskandary H, Sabba M, Khajehpour F, Eskandari M. Incidental findings in brain computed tomography scans of 3000 head trauma patients. Surg Neurol. 2005;63:550–553. doi: 10.1016/j.surneu.2004.07.049. [DOI] [PubMed] [Google Scholar]
  • 14.Gosalakkal JA. Intracranial arachnoid cysts in children: A review of pathogenesis, clinical features, and management. Pediatr Neurol. 2002;26:93–98. doi: 10.1016/s0887-8994(01)00329-0. [DOI] [PubMed] [Google Scholar]
  • 15.Cyril Duperrier MF, Lenaerts Hendrik. A case of central diabetes insipidus associated with a congenital cyst of the sella turcica in a young cat. JFMS Open Rep. 2020;6:2055116920935017. doi: 10.1177/2055116920935017. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 16.Sav A, Rotondo F, Syro LV, Serna CA, Kovacs K. Pituitary pathology in traumatic brain injury: A review. Pituitary. 2019;22:201–211. doi: 10.1007/s11102-019-00958-8. [DOI] [PubMed] [Google Scholar]
  • 17.Scranton RA, Baskin DS. Impaired pituitary axes following traumatic brain injury. J Clin Med. 2015;4:1463–1479. doi: 10.3390/jcm4071463. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 18.MacKillop E. Magnetic resonance imaging of intracranial malformations in dogs and cats. Vet Radiol Ultrasound. 2011;52:S42–S51. doi: 10.1111/j.1740-8261.2010.01784.x. [DOI] [PubMed] [Google Scholar]
  • 19.Evenhuis J, Epstein SE, Della-Maggiore A, Reagan KL. Congenital pituitary cyst resulting in adipsic central diabetes insipidus and secondary hypernatremia in a cat. JFMS Open Rep. 2021;7:2055116921990294. doi: 10.1177/2055116921990294. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 20.DeMonaco SM, Koch MW, Southard TL. Syndrome of inappropriate antidiuretic hormone secretion in a cat with a putative Rathke’s cleft cyst. J Feline Med Surg. 2014;16:1010–1015. doi: 10.1177/1098612X14528192. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 21.Konig ML, Henke D, Adamik K, Perez Vera C. Juvenile hyposomatotropism in a Somali cat presenting with seizures due to intermittent hypoglycaemia. JFMS Open Rep. 2018;4:2055116918761441. doi: 10.1177/2055116918761441. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 22.Donaldson D, Billson FM, Scase TJ, et al. Congenital hyposomatotropism in a domestic shorthair cat presenting with congenital corneal oedema. J Small Anim Pract. 2008;49:306–309. doi: 10.1111/j.1748-5827.2007.00517.x. [DOI] [PubMed] [Google Scholar]
  • 23.Reed N, Gunn-Moore D. Hyposomatotropism in cats. In: Rand J, editor. Clinical Endocrinology of Companion Animals. Ames, Iowa: John Wiley & Sons; 2013. p. 418. [Google Scholar]
  • 24.Reusch CE. Disorders of growth hormone. In: Feldman EC, Nelson RW, Reusch CE, Scott-Moncrieff, Behrend E, editors. Canine & Feline Endocrinology. 4th ed. St. Louis, Missouri: Elsevier; 2015. pp. 49–50. [Google Scholar]
  • 25.Mellanby RJ, Jeffery ND, Gopal MS, Herrtage ME. Secondary hypothyroidism following head trauma in a cat. J Feline Med Surg. 2005;7:135–139. doi: 10.1016/j.jfms.2004.08.002. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 26.Nelson RW. Water metabolism and diabetes insipidus. In: Feldman EC, Nelson RW, Reusch CE, Scott-Moncrieff, Behrend E, editors. Canine & Feline Endocrinology. 4th ed. St. Louis, Missouri: Elsevier; 2015. pp. 1–36. [Google Scholar]
  • 27.Greco DS. Pituitary deficiencies. Top Companion Anim Med. 2012;27:2–7. doi: 10.1053/j.tcam.2012.04.002. [DOI] [PubMed] [Google Scholar]
  • 28.Naceradska M, Navojova Horackova K, Fridrichova M. Case report: Human recombinant growth hormone therapy in a DSH cat presented with dwarfism. Front Vet Sci. 2021;8:773355. doi: 10.3389/fvets.2021.773355. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 29.Knottenbelt CM, Herrtage ME. Use of proligestone in the management of three German shepherd dogs with pituitary dwarfism. J Small Anim Pract. 2002;43:164–170. doi: 10.1111/j.1748-5827.2002.tb00051.x. [DOI] [PubMed] [Google Scholar]
  • 30.Church DB, Watson AD, Emslie DR, Middleton DJ, Tan K, Wong D. Effects of proligestone and megestrol on plasma adrenocorticotrophic hormone, insulin and insulin-like growth factor-1 concentrations in cats. Res Vet Sci. 1994;56:175–178. doi: 10.1016/0034-5288(94)90101-5. [DOI] [PubMed] [Google Scholar]
  • 31.Peterson ME. Effects of megestrol acetate on glucose tolerance and growth hormone secretion in the cat. Res Vet Sci. 1987;42:354–357. [PubMed] [Google Scholar]
  • 32.Grohmann KS, Schmidt MJ, Moritz A, Kramer M. Prevalence of seizures in cats after head trauma. J Am Vet Med Assoc. 2012;241:1467–1470. doi: 10.2460/javma.241.11.1467. [DOI] [PubMed] [Google Scholar]

Articles from The Canadian Veterinary Journal are provided here courtesy of Canadian Veterinary Medical Association

RESOURCES