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

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.

Insuffisances hormonales hypophysaires multiples chez un chaton : hyposomatotropisme, hypothyroïdie, diabète insipide central et hypogonadisme. En médecine humaine, l'hypopituitarisme post-traumatisme crânien (HPPT) est une complication fréquente après un trauma crânien. Les insuffisances hormonales les plus fréquemment rapportées sont l'hyposomatotropisme et l'hypogonadisme, suivis de l'hypothyroïdie, de l'hypocortisolisme et du diabète insipide central. À ce jour, l'HPPT a rarement été décrit chez le chat, et les cas publiés décrivent bien souvent une déficience hormonale unique. Dans le cas présent, un chat âgé d'environ 7 mois, avec un antécédent de trauma crânien suspecté à l'âge de 5 semaines, a été présenté avec un retard de croissance (1,53 kg) et un syndrome polyurie-polydipsique. Les examens d'endocrinologie complémentaires incluaient le dosage des hormones thyroïdiennes, la stimulation de l'hypophyse par la thyrolibérine, une scintigraphie thyroïdienne (Technetium-99), le dosage de l'IGF-1, du cortisol basal, de la concentration d'ACTH endogène, et un test de stimulation à l'ACTH. Le chat a été diagnostiqué de manière présomptive avec un HPPT causant de multiples insuffisances hormonales hypophysaires : hyposomatotropisme, hypothyroïdie, diabète insipide central et hypogonadisme. Chez ce chat, le traitement de l'hypothyroïdie et du diabète insipide central a été réussi. L'hyposomatotropisme et l'hypogonadisme n'ont pas été traités. Alors que les rapports de cas publiés sur l'HPPT félin décrivent souvent une seule déficience hormonale, ce chat a été diagnostiqué avec de multiples insuffisances hormonales hypophysaires. Les cliniciens doivent rester attentifs au développement potentiel d'un hypopituitarisme après un trauma crânien.Message clinique clé :L'hypopituitarisme post-traumatique chez le chat peut entraîner de multiples déficiences hormonales, entraînant un hyposomatotropisme, une hypothyroïdie, un diabète insipide central et un hypogonadisme.(Traduit par les auteurs).

Case report: Hypoadrenocorticism crisis complicated by non-cardiogenic pulmonary edema in a dog.

A 6-year-old castrated male Labradoodle was referred in uncompensated hypovolemic shock, with a 72-h history of lethargy, vomiting and diarrhea that had acutely worsened with subsequent development of profuse hemorrhagic diarrhea in the last 24 h after a visit to the groomer. In most respects this case was classic for a patient with a primary hypoadrenocortical crisis. After initial attempts to address hypovolemia and refractory hypotension, no clinical improvement was seen, and the respiratory rate had increased acutely to 80 bpm with crackles detected on thoracic auscultation and serosanguineous fluid began draining from the nose and mouth. An arterial blood gas sample while breathing room air revealed moderate hypoxemia (PaO2 59.9: RI 95-100 mmHg), an elevated alveolar-arterial (A-a) gradient at 54.7 (RI < 15 mmHg) and a PaO2:FiO2 ratio of 285 mmHg. Thoracic radiographs revealed severe bilateral alveolar lung pattern largely limited to the perihilar and caudodorsal lung fields. The radiographic findings, along with signs of ongoing hypovolemia, the lack of evidence of typical long-standing acquired cardiac disease, and the rapid resolution of the pulmonary edema without the need for diuretics or long-term cardiac medications supported non-cardiogenic pulmonary edema. The proposed cause of the non-cardiogenic pulmonary edema was speculated to be neurogenically mediated. Oxygen supplementation along with mineralocorticoid and glucocorticoid replacement therapy was sufficient for the management of the non-cardiogenic pulmonary edema in this case.

Online survey to determine client perceptions of feline chronic lower airway disease management: response to therapy, side effects and challenges encountered.

OBJECTIVES: The first aim of this survey was to report client experiences associated with the administration of common medications, particularly glucocorticoids and bronchodilators, in managing cats with feline lower airway disease (FLAD). The second aim was to ascertain client perception of response to treatment and level of satisfaction. METHODS: This was a prospective cross-sectional study. An online survey was distributed worldwide to cat owners caring for cats with a chronic cough. Only cats reported to have FLAD were included. RESULTS: A total of 153 complete responses describing cats with FLAD were analyzed. Glucocorticoids and bronchodilators were the predominantly prescribed therapeutics for 140/153 (92%) and 80/153 (52%) of FLAD cats, respectively. Oral and inhalant administration routes were reported most commonly: glucocorticoids (64% oral and 75% inhalant) and bronchodilators (21% oral and 88% inhalant). A review of how air quality could be improved was conducted for 54% of cats. Almost half (43%) of owners reported adverse effects secondary to glucocorticoid administration, the most frequent being polyphagia (26%) and polydipsia (21%). Only 10% of owners reported bronchodilator-associated side effects, with restlessness (9%) being the most common. Difficulties giving glucocorticoid or bronchodilator tablets orally were reported for 33% and 71% of owners, respectively. Glucocorticoid or bronchodilator inhalant therapies were difficult to administer for 28% and 31% of owners, respectively. Frequency and severity of coughing were significantly lower after at least 2 months of treatment, with median numerical input on a slider scale (0-100) of 48 and 42 before, and 10 and 7 after treatment, respectively (P <0.0001). Median numerical input of owner satisfaction was 83%. CONCLUSIONS AND RELEVANCE: Despite significant improvements in client-reported responses to treatment, challenges associated with the administration of medications and their adverse effects still exist. Promoting awareness of client experiences can facilitate appropriate follow-up, guidance and empathy to further optimize outcomes.

Association between hyperlipidemia and calcium oxalate lower urinary tract uroliths in dogs.

BACKGROUND: Metabolic syndrome is associated with formation of calcium oxalate (CaOx) uroliths in humans. OBJECTIVES: To investigate the association between obesity and hyperlipidemia with CaOx lower urinary tract uroliths in client-owned dogs. ANIMALS: Dogs with (n = 55, U [uroliths]-dogs) and without (n = 39, UF [uroliths-free]-dogs) CaOx lower urinary tract uroliths. METHODS: Case-control study. U-dogs were retrospectively enrolled and compared to UF-dogs. Body condition score (BCS; 1-9 scoring scale), serum triglyceride (TG) and total cholesterol (CH) concentrations and glycemia (after >12-hour food withholding) were recorded in both groups. RESULTS: On univariate logistic regression, when excluding Miniature Schnauzers, odds of having uroliths increased by a factor of 3.32 (95% CI 1.38-11.12) for each mmol/L of TG (P = .027), of 39 (95% CI 9.27-293.22) for each mmol/L of glycemia (P < .0001), and of 2.43 (95% CI 1.45-4.45) per unit of BCS (P = .002). In multivariable models, the effect of TG was retained when all breeds were included for analysis and odds of having uroliths increased by a factor of 4.34 per mmol/L of TG (95% CI 1.45-19.99; P = .02). CONCLUSIONS AND CLINICAL IMPORTANCE: Serum lipid screening in dogs diagnosed with CaOx uroliths might be recommended to improve their medical staging and management.

Histopathologic, phenotypic, and molecular criteria to discriminate low-grade intestinal T-cell lymphoma in cats from lymphoplasmacytic enteritis.

BACKGROUND: Differentiation of low-grade intestinal T-cell lymphoma (LGITL) from lymphoplasmacytic enteritis (LPE) in cats is a diagnostic challenge for pathologists. OBJECTIVE: Characterize histologic, immunohistochemical, and molecular features of LGITL and LPE. ANIMALS: Forty-four client-owned cats, 22 diagnosed with LGITL and 22 with LPE. METHODS: Prospective, cohort study. Clinical suspicion of LGITL or LPE was based on persistent gastrointestinal signs, unresponsive to empirical treatments. All cats underwent a standardized diagnostic evaluation, including biopsy (preferentially full-thickness), and were diagnosed with LGITL or LPE after review of clinical, laboratory, sonographic, histologic, immunohistochemical, and clonality results. RESULTS: A monomorphic lymphocytic population (22/22, 100%) and in-depth mucosal infiltration (15/22, 68%) were hallmarks of LGITL. Epithelial patterns (nests and plaques) were significantly more frequent in LGITL (11/22, 50%) than in LPE (1/22, 5%) cases (P = .001). A CD3+ lymphocytic apical-to-basal gradient was observed in 9/22 (41%) of LGITL vs 1/22 (5%) of LPE cases (P = .004). Most LPE cases (17/18, 94%) featured marked fibrosis in the superficial part of the lamina propria. The Ki-67 20%- and 30%-thresholds discriminated between LGITL and LPE within both the epithelium (specificity >95%) and lamina propria (specificity >95%), respectively. All LGITL cases were CD3+ pSTAT3- and pSTAT5+. T-cell receptor gamma chain gene rearrangements indicated monoclonality in 86% of LGITL cases. Surprisingly, 70% of LPE cases featured monoclonality (40%) or monoclonality on a polyclonal background (30%). CONCLUSIONS AND CLINICAL IMPORTANCE: We identified new histologic, immunohistochemical, and clonality criteria to distinguish LGITL from LPE.

Surgical treatment of a distal oesophageal stricture by mucosal radial incision and dilation in a kitten with secondary megaoesophagus.

CASE SUMMARY: A 7-month-old intact female Maine Coon cat was presented with a 2-month history of regurgitations. Contrast radiographic and endoscopic examinations revealed a diffuse megaoesophagus secondary to a severe lower oesophageal stricture. An epiphrenic diverticulum was noted. Endoscopic balloon dilation was unsuccessful. Gastrotomy was thus performed in order to incise the oesophageal wall radially along the stricture site, and then to dilate the stricture. A diameter of 20 mm was reached. With the aim of preventing stricture recurrence, submucosal injections of triamcinolone acetonide were performed. An 18 Fr oesophagogastric feeding tube was placed and a left gastropexy was performed in order to exert some traction on the gastroesophageal junction, with the aim of reducing the oesophageal diverticulum. Twelve months postoperatively, clinical signs had completely resolved and follow-up radiographs revealed marked improvement of the oesophageal dilatation. RELEVANCE AND NOVEL INFORMATION: Lower oesophageal strictures should be considered when evaluating regurgitations or megaoesophagus in a kitten. Surgical mucosal radial incision is a therapeutic option in cases of lower oesophageal stricture refractory to balloon dilation, and can lead to a marked improvement of clinical signs and of the oesophagus diameter leading to clinical success.

Feline low-grade alimentary lymphoma: an emerging entity and a potential animal model for human disease.

BACKGROUND: Low-grade alimentary lymphoma (LGAL) is characterised by the infiltration of neoplastic T-lymphocytes, typically in the small intestine. The incidence of LGAL has increased over the last ten years and it is now the most frequent digestive neoplasia in cats and comprises 60 to 75% of gastrointestinal lymphoma cases. Given that LGAL shares common clinical, paraclinical and ultrasonographic features with inflammatory bowel diseases, establishing a diagnosis is challenging. A review was designed to summarise current knowledge of the pathogenesis, diagnosis, prognosis and treatment of feline LGAL. Electronic searches of PubMed and Science Direct were carried out without date or language restrictions. RESULTS: A total of 176 peer-reviewed documents were identified and most of which were published in the last twenty years. 130 studies were found from the veterinary literature and 46 from the human medicine literature. Heterogeneity of study designs and outcome measures made meta-analysis inappropriate. The pathophysiology of feline LGAL still needs to be elucidated, not least the putative roles of infectious agents, environmental factors as well as genetic events. The most common therapeutic strategy is combination treatment with prednisolone and chlorambucil, and prolonged remission can often be achieved. Developments in immunohistochemical analysis and clonality testing have improved the confidence of clinicians in obtaining a correct diagnosis between LGAL and IBD. The condition shares similarities with some diseases in humans, especially human indolent T-cell lymphoproliferative disorder of the gastrointestinal tract. CONCLUSIONS: The pathophysiology of feline LGAL still needs to be elucidated and prospective studies as well as standardisation of therapeutic strategies are needed. A combination of conventional histopathology and immunohistochemistry remains the current gold-standard test, but clinicians should be cautious about reclassifying cats previously diagnosed with IBD to lymphoma on the basis of clonality testing. Importantly, feline LGAL could be considered to be a potential animal model for indolent digestive T-cell lymphoproliferative disorder, a rare condition in human medicine.