BACKGROUND:The survival of dogs with pheochromocytoma (PCC) treated with adrenoreceptor antagonists has not been described or compared to surgically managed cases. HYPOTHESIS/OBJECTIVES:The objective of this study is to evaluate the survival of medically and surgically managed dogs with PCC and investigate factors associated with survival. ANIMALS:Two hundred fifty-five dogs with PCC, treated with alpha-adrenoreceptor antagonists (AA) without adrenalectomy (Group 1, n = 75), adrenalectomy +/- AA (Group 2, n = 128), or neither treatment (Group 3, n = 52). METHODS:Retrospective, multicenter review of medical records. Median overall survival time (OST) for Groups 1 and 2 combined was calculated using Kaplan-Meier estimates, and then compared between Group 1 and Group 2 using Log-Rank testing. Cox proportional hazard analysis identified factors associated with survival in Groups 1 and 2 individually and combined. RESULTS:Median OST for all cases was 854 (95% CI: 572-1136) days. Median OST was lower in Group 1 (247 days, 95% CI: 76-418 days) than in Group 2 (927 days, 95% CI: 587-1267 days; p < 0.001). In Group 2, 88/92 dogs (97.8%) that received presurgical AA treatment survived to discharge compared to 23/27 (85.2%) that did not receive AA pretreatment (p = 0.03). Lack of clinical signs at presentation was associated with increased survival in both groups combined (HR 0.5; 95% CI 0.3-0.9; p = 0.02) and in Group 2 alone (HR 0.3; 95% CI 0.1-0.7; p = 0.01). CONCLUSIONS AND CLINICAL IMPORTANCE:Dogs with PCC treated with adrenalectomy have longer survival compared to those managed with AA without adrenalectomy.

Pituitary-dependent hypersomatotropism is rarely diagnosed in dogs and surgical treatment is not reported. A 6-year-10-month male neutered Patterdale Terrier presented with polyuria, polydipsia, progressive pharyngeal stertor, excessive hair growth and widened facial features and paws. Serum insulin-like growth factor-1 concentration via radioimmunoassay was consistent with hypersomatotropism (1783 ng/mL). A pituitary mass was identified on magnetic resonance and computed tomography imaging. Six weeks later, glucosuria, starved hyperglycemia and serum fructosamine above the reference range (467.6 μmol/L, RI 177-314) were documented, consistent with diabetes mellitus. Transsphenoidal hypophysectomy was performed under general anesthesia without complications. Pituitary histopathology identified an acidophil neoplasm, with positive immunostaining for growth hormone. Postoperatively, there was rapid resolution of clinical, biochemical and morphologic changes of hypersomatotropism with persistence of diabetes mellitus. This case demonstrates successful resolution of hypersomatotropism with ongoing diabetes mellitus in a dog after surgical treatment by transsphenoidal hypophysectomy.

PRACTICAL RELEVANCE:Diabetes mellitus is the second-most common feline endocrinopathy, affecting an estimated 1/200 cats. While the underlying causes vary, around 15-25% of cats with diabetes mellitus develop the condition secondarily to progressive growth hormone (GH)-induced insulin resistance. This typically results in a form of diabetes that is challenging to manage, whereby the response to insulin is very variable or high doses are required to achieve even minimal diabetic control. CLINICAL CHALLENGES:Although uncontrolled chronic excessive GH may result in phenotypic changes that raise suspicion for acromegaly, many cats with hypersomatotropism (HST) do not have these changes. In these situations, a clinician's index of suspicion may be increased by the presence of less dramatic changes such as marked polyphagia, stertor or uncontrolled diabetes mellitus. The current diagnostic test of choice is demonstration of a markedly increased serum insulin-like growth factor 1 (IGF1) concentration, but some affected cats will have only a marginal increase; additionally, chronic insulin administration in cats results in an increase in serum IGF1, making the diagnosis less clear cut and requiring additional confirmatory tests. EVIDENCE BASE:Over the past two decades, HST has increasingly been recognised as an underlying cause of diabetes mellitus in cats. This review, which focuses on diagnosis and treatment, utilises data from observational studies, clinical trials and case series, as well as drawing on the experience of the authors in managing this condition.

Clinical abstract presented at BSAVA Congress 2023. See full text for abstract and see clinical abstract sessions for a recording of the presentation. Abstracts are presented as supplied and have not been edited.

Insulinomas are the most common pancreatic tumours in dogs. Diagnosis of insulinoma requires the concurrent presence of hypoglycaemia and serum insulin levels within or above the upper limit of the reference range. The diagnostic imaging modality of choice is triple-phase contrast enhanced tomography. Surgical resection is generally the most effective treatment option, leading to prolonged survival; however, medical management becomes necessary for many dogs at some point. After surgery, dogs can live for a few years without clinical signs of hypoglycaemia, but eventually clinical hypoglycaemia frequently recurs due to the outgrowth of micrometastases that were undetected at the time of surgery. This review consolidates and provides updated recommendations from the veterinary literature on the diagnosis and management of canine insulinomas.

A 9-year-old male neutered Cockerpoo dog was presented with pyrexia and was diagnosed with sterile idiopathic panniculitis. During initial investigations, advanced imaging revealed a suspected left-sided cervical paraganglioma and bilateral adrenal masses. The dog underwent immunosuppression and achieved remission of the sterile idiopathic panniculitis. Bilateral adrenalectomy and paraganglioma excision were then performed. Histopathology identified bilateral adrenocortical carcinoma and cervical neuroendocrine carcinoma. Three months later, the dog was diagnosed with primary hyperparathyroidism. Despite left total thyroidectomy and parathyroidectomy, mild hypercalcaemia persisted for several months. Eight months later the dog became persistently hypokalaemic refractory to potassium supplementation, had metabolic alkalosis and systemic hypertension. The dog was euthanised 5 months later due to clinical deterioration. On post-mortem examination, right parathyroid hyperplasia and metastatic neuroendocrine carcinoma involving liver, jejunum, pancreas and tracheobronchial lymph node were identified. This is the first report describing the concurrent presence of these types of endocrine neoplasms in a dog.

Patients harbouring mutations in genes encoding C-type natriuretic peptide (CNP; NPPC) or its receptor guanylyl cyclase B (GC-B, NPR2) suffer from severe growth phenotypes; loss-of-function mutations cause achondroplasia, whereas gain-of-function mutations cause skeletal overgrowth. Although most of the effects of CNP/GC-B on growth are mediated directly on bone, evidence suggests the natriuretic peptides may also affect anterior pituitary control of growth. Our previous studies described the expression of NPPC and NPR2 in a range of human pituitary tumours, normal human pituitary, and normal fetal human pituitary. However, the natriuretic peptide system in somatotropes has not been extensively explored. Here, we examine the expression and function of the CNP/GC-B system in rat GH3 somatolactotrope cell line and pituitary tumours from a cohort of feline hypersomatotropism (HST; acromegaly) patients. Using multiplex RT-qPCR, all three natriuretic peptides and their receptors were detected in GH3 cells. The expression of Nppc was significantly enhanced following treatment with either 100 nM TRH or 10 µM forskolin, yet only Npr1 expression was sensitive to forskolin stimulation; the effects of forskolin and TRH on Nppc expression were PKA- and MAPK-dependent, respectively. CNP stimulation of GH3 somatolactotropes significantly inhibited Esr1, Insr and Lepr expression, but dramatically enhanced cFos expression at the same time point. Oestrogen treatment significantly enhanced expression of Nppa, Nppc, Npr1, and Npr2 in GH3 somatolactotropes, but inhibited CNP-stimulated cGMP accumulation. Finally, transcripts for all three natriuretic peptides and receptors were expressed in feline pituitary tumours from patients with HST. NPPC expression was negatively correlated with pituitary tumour volume and SSTR5 expression, but positively correlated with D2R and GHR expression. Collectively, these data provide mechanisms that control expression and function of CNP in somatolactotrope cells, and identify putative transcriptional targets for CNP action in somatotropes.

C-type natriuretic peptide (CNP) is the major natriuretic peptide of the central nervous system and acts via its selective guanylyl cyclase-B (GC-B) receptor to regulate cGMP production in neurons, astrocytes and endothelial cells. CNP is implicated in the regulation of neurogenesis, axonal bifurcation, as well as learning and memory. Several neurological disorders result in toxic concentrations of ammonia (hyperammonaemia), which can adversely affect astrocyte function. However, the relationship between CNP and hyperammonaemia is poorly understood. Here, we examine the molecular and pharmacological control of CNP in rat C6 glioma cells and rat GPNT brain endothelial cells, under conditions of hyperammonaemia. Concentration-dependent inhibition of C6 glioma cell proliferation by hyperammonaemia was unaffected by CNP co-treatment. Furthermore, hyperammonaemia pre-treatment (for 1 h and 24 h) caused a significant inhibition in subsequent CNP-stimulated cGMP accumulation in both C6 and GPNT cells, whereas nitric-oxide-dependent cGMP accumulation was not affected. CNP-stimulated cGMP efflux from C6 glioma cells was significantly reduced under conditions of hyperammonaemia, potentially via a mechanism involving changed in phosphodiesterase expression. Hyperammonaemia-stimulated ROS production was unaffected by CNP but enhanced by a nitric oxide donor in C6 cells. Extracellular vesicle production from C6 cells was enhanced by hyperammonaemia, and these vesicles caused impaired CNP-stimulated cGMP signalling in GPNT cells. Collectively, these data demonstrate functional interaction between CNP signalling and hyperammonaemia in C6 glioma and GPNT cells, but the exact mechanisms remain to be established.

Case records of two dogs diagnosed with carotid body tumour (CBT) treated with radiotherapy were reviewed. Clinical signs of a unilateral space-occupying lesion were identified. Cytology or histopathology and CT imaging confirmed CBT. Metastatic lymphadenopathy was identified in one dog. The tumour was surgically unresectable in one dog. Radiotherapy was administered with 38Gy in 10 and 48Gy in 12 fractions, respectively. VRTOG grade I cutaneous radiotoxicity was recognised in both dogs upon completing the treatment protocol. One dog was diagnosed with primary hypothyroidism 16 months later. One dog has ongoing partial response at 13 months post-radiotherapy, the other dog had complete response with no recurrence at 40 months post-radiotherapy. The results of this study suggest that for non-resectable carotid body paraganglioma radiation therapy provided excellent disease control with mild permanent side effects not affecting the dog's quality of life. Careful monitoring of the thyroid function is recommended post-treatment.

Objectives An affordable and effective treatment is needed to manage feline hypersomatotropism. The aim of this study was to assess whether treatment with oral cabergoline for 90 days in cats with hypersomatotropism and diabetes mellitus improved diabetic and insulin-like growth factor 1 (IGF-1) control. Methods This was a prospective cohort non-blinded pilot study enrolling client-owned cats with spontaneously occurring diabetes mellitus and hypersomatotropism. Cats received oral cabergoline (5–10 µg/kg q24h) for 90 consecutive days. Serum IGF-1 and fructosamine concentrations were measured on days 1, 30 and 90. Quality of life was determined using the DIAQoL-pet questionnaire on days 1 and 90. Results Nine cats were enrolled and eight completed the study. There was no significant change in the following: IGF-1 (day 1 median 2001 ng/ml [range 890–2001 ng/ml]; day 30 median 2001 ng/ml [range 929–2001 ng/ml]; day 90 median 1828 ng/ml [range 1035–2001 ng/ml]; χ 2 (2) = 0.667, P = 0.805); fructosamine (day 1 median 499 µmol/l [range 330–887 µmol/l], day 30 median 551 µmol/l [range 288–722 µmol/l], day 90 median 503 [range 315–851 µmol/l]; χ 2 (2) = 0.581, P = 0.764); or DIAQoL-pet score (median on day 1 –2.79 [range –4.62 to –0.28], median on day 90 –3.24 [range –4.41 to –0.28]; P = 0.715). There was a significant change of insulin dose (χ 2 (2) = 8.667, P = 0.008) with cats receiving higher insulin doses at day 90 compared with day 1 (median on day 1 was 0.98 [range 0.63–1.49] and median on day 90 was 1.56 [range 0.49–2.55] units/kg q12h; P = 0.026). Conclusions and relevance Cabergoline did not improve diabetic control or normalise insulin-like growth factor concentration, or improve patient quality of life.

Hypersomatotropism (HST) is an increasingly recognized endocrinopathy in cats and is mostly described associated with diabetes mellitus (DM). To evaluate the efficacy and safety of transsphenoidal hypophysectomy in treating HST and DM in cats. Sixty-eight client-owned cats with HST and DM treated by transsphenoidal hypophysectomy. Retrospective cohort study. Medical records were reviewed for glycemic control and serum insulin-like growth factor-1 (IGF-1) concentrations. Postoperative complications, death within 4 weeks, and proportion achieving diabetic remission were recorded. Survival times and DM-free intervals were calculated. Fifty-eight cats (85.3%) were alive 4 weeks postoperatively with 10 (15%) postoperative deaths. Complications included hypoglycemia (n = 9), electrolyte imbalance (n = 9), and transient congestive heart failure (n = 5). Fifty-five cats (95% of 58 surviving cats [81% of all cats undergoing surgery]) had improved control of diabetes. Diabetic remission occurred in 41 cats (71% of 58 surviving cats [60% of all cats]) with insulin administration discontinued after a median of 9 days (range, 2-120). Postoperative 4-week serum IGF-1 concentration nadir was significantly lower in cats achieving diabetic remission (median 20 ng/mL [15-708] than those that did not (324 ng/mL [15-1955]; P = .03). All cats received long-term levothyroxine and hydrocortisone PO, alongside desmopressin (conjunctival) in 38 of 53 cats (72%). Recurrence of DM occurred in 5 of 41 cats (12%) after a median of 248 days (range, 84-1232). Median survival time of all cats was 853 days (range, 1-1740). Transsphenoidal hypophysectomy is an effective treatment for cats with HST and DM, with a long-term outcome that compares favorably to existing options.

Abstract Background Hypersomatotropism (HST) is an increasingly recognized endocrinopathy in cats and is mostly described associated with diabetes mellitus (DM). Objectives To evaluate the efficacy and safety of transsphenoidal hypophysectomy in treating HST and DM in cats. Animals Sixty‐eight client‐owned cats with HST and DM treated by transsphenoidal hypophysectomy. Methods Retrospective cohort study. Medical records were reviewed for glycemic control and serum insulin‐like growth factor‐1 (IGF‐1) concentrations. Postoperative complications, death within 4 weeks, and proportion achieving diabetic remission were recorded. Survival times and DM‐free intervals were calculated. Results Fifty‐eight cats (85.3%) were alive 4 weeks postoperatively with 10 (15%) postoperative deaths. Complications included hypoglycemia (n = 9), electrolyte imbalance (n = 9), and transient congestive heart failure (n = 5). Fifty‐five cats (95% of 58 surviving cats [81% of all cats undergoing surgery]) had improved control of diabetes. Diabetic remission occurred in 41 cats (71% of 58 surviving cats [60% of all cats]) with insulin administration discontinued after a median of 9 days (range, 2‐120). Postoperative 4‐week serum IGF‐1 concentration nadir was significantly lower in cats achieving diabetic remission (median 20 ng/mL [15‐708] than those that did not (324 ng/mL [15‐1955]; P = .03). All cats received long‐term levothyroxine and hydrocortisone PO, alongside desmopressin (conjunctival) in 38 of 53 cats (72%). Recurrence of DM occurred in 5 of 41 cats (12%) after a median of 248 days (range, 84‐1232). Median survival time of all cats was 853 days (range, 1‐1740). Conclusions and Clinical Importance Transsphenoidal hypophysectomy is an effective treatment for cats with HST and DM, with a long‐term outcome that compares favorably to existing options.

ObjectivesTo develop a protocol for safe pre-medication of patients undergoing general anaesthesia for radiotherapy.

Abstract A 3‐month‐old male intact Shiba Inu dog was evaluated for a seizure disorder initially deemed idiopathic in origin. Seizure frequency remained unchanged despite therapeutic serum phenobarbital concentration and use of levetiracetam. The dog was documented to be markedly hypoglycemic during a seizure episode on reevaluation at 6 months of age. Serum insulin concentrations during hypoglycemia were 41 U/μL (reference range, 10‐29 U/μL). The dog was transitioned to 4 times per day feeding, diazoxide was started at 3.5 mg/kg PO q8h, and antiepileptic drugs were discontinued. No clinically relevant abnormalities were identified on bicavitary arterial and venous phase contrast computed tomographic imaging. The dog remained seizure‐free and clinically normal at 3 years of age while receiving 5.5 mg/kg diazoxide PO q12h and twice daily feeding. Seizures later occurred approximately twice per year and after exertion, with or without vomiting of a diazoxide dose. Blood glucose curves and interstitial glucose monitoring were used to titrate diazoxide dose and dosing interval. Congenital hyperinsulinism is well recognized in people but has not been reported in veterinary medicine.

Abstract Endocrine Disrupting Chemicals (EDCs) are substances that have been increasingly implicated in many serious pathologies, such as tumor formation, metabolic, growth and reproductive disorders. The economic and health burden of exposure to these compounds has an annual predicted cost in excess of €150 billion, across the EU regions alone. Of the growing list of compounds that act as EDCs, the organohalogenated compounds (OHCs), polybrominated diphenyl ethers (PBDEs) and polychlorinated biphenyls (PCBs) have been associated with an increased risk of pituitary disease. We have previously reported that feline patients with hypersomatotropism (acromegaly) are exposed to elevated levels of PBDEs and PCBs in their environment. However, the mechanisms by which these compounds might directly influence somatotroph function have yet to be established. In this study, we use the GH3 rat somatolactotrope cell line to investigate how two PCB congeners - 138 and 153 - influence cell proliferation (using a Crystal Violet assay) and somatotrope gene expression (using a multiplex RT-qPCR approach to examine expression of Esr1, Esr2, Sstr1, Sstr2, Sstr3, Sstr4, Sstr5, Insr, Tshr, Pou1f1, Ghrhr2, Gh). GH3 cells were treated with Phenol Red-free media in the absence or presence of either PCB138 or 153 (-10 to -6 M), or in combination (-10 to -6M) for up to 72h. Treatment with either PCB alone, or in combination, caused significant concentration-dependent, biphasic changes in cell proliferation at each time point, but with a different profile of response on each day (significantly increased at high pM/low nM concentrations); there was no evidence of toxicity at maximum concentrations (-6M). Gene expression changes were determined in GH3 cells treated in the absence or presence of either -8M or -6M PCB138 or 153 for 24h. Differential effects of these compounds were seen on the expression of Sstr3, Sstr4, Sstr5 and Insr; all other gene transcripts were unaffected. These findings reveal that GH3 cells exposed to physiologically relevant concentrations of PCB138 and 153, alone or in combination, show concentration-dependent increases in cell proliferation; furthermore, the expression of genes associated with therapeutic targets for the treatment of acromegaly (i.e. SSTRs) are differentially affected by exposure to PCB138 and 153. Our data indicate a potential mechanism for EDCs in the onset of acromegaly, that require further, in vivo, investigations.

Correspondence Simon Cook, Queen Mother Hospital for Animals, Hawkshead Lane AL9 7TA, United Kingdom. Email: sdcook@rvc.ac.uk Abstract A 3-month-old male intact Shiba Inu dog was evaluated for a seizure disorder initially deemed idiopathic in origin. Seizure frequency remained unchanged despite therapeutic serum phenobarbital concentration and use of levetiracetam. The dog was documented to be markedly hypoglycemic during a seizure episode on reevaluation at 6 months of age. Serum insulin concentrations during hypoglycemia were 41 U/μL (reference range, 10-29 U/μL). The dog was transitioned to 4 times per day feeding, diazoxide was started at 3.5 mg/kg PO q8h, and antiepileptic drugs were discontinued. No clinically relevant abnormalities were identified on bicavitary arterial and venous phase contrast computed tomographic imaging. The dog remained seizurefree and clinically normal at 3 years of age while receiving 5.5 mg/kg diazoxide PO q12h and twice daily feeding. Seizures later occurred approximately twice per year and after exertion, with or without vomiting of a diazoxide dose. Blood glucose curves and interstitial glucose monitoring were used to titrate diazoxide dose and dosing interval. Congenital hyperinsulinism is well recognized in people but has not been reported in veterinary medicine.

C-type natriuretic peptide (CNP) is the most conserved member of the mammalian natriuretic peptide family, and is implicated in the endocrine regulation of growth, metabolism and reproduction. CNP is expressed throughout the body, but is particularly abundant in the central nervous system and anterior pituitary gland. Pituitary gonadotropes are regulated by pulsatile release of gonadotropin releasing hormone (GnRH) from the hypothalamus, to control reproductive function. GnRH and CNP reciprocally regulate their respective signalling pathways in αT3-1 gonadotrope cells, but effects of pulsatile GnRH stimulation on CNP expression has not been explored. Here, we examine the sensitivity of the natriuretic peptide system in LβT2 and αT3-1 gonadotrope cell lines to continuous and pulsatile GnRH stimulation, and investigate putative CNP target genes in gonadotropes. Multiplex RT-qPCR assays confirmed that primary mouse pituitary tissue express Nppc,Npr2 (encoding CNP and guanylyl cyclase B (GC-B), respectively) and Furin (a CNP processing enzyme), but failed to express transcripts for Nppa or Nppb (encoding ANP and BNP, respectively). Pulsatile, but not continuous, GnRH stimulation of LβT2 cells caused significant increases in Nppc and Npr2 expression within 4 h, but failed to alter natriuretic peptide gene expression in αT3-1 cells. CNP enhanced expression of cJun, Egr1, Nr5a1 and Nr0b1, within 8 h in LβT2 cells, but inhibited Nr5a1 expression in αT3-1 cells. Collectively, these data show the gonadotrope natriuretic peptide system is sensitive to pulsatile GnRH signalling, and gonadotrope transcription factors are putative CNP-target genes. Such findings represent additional mechanisms by which CNP may regulate reproductive function.

Veterinary RecordVolume 184, Issue 26 p. 805-806 Letters and notices Call for coordinated antimicrobial approach at veterinary diagnostic laboratories Fergus Allerton, Corresponding Author Fergus Allerton Chairman fergus.allerton@willows.uk.net SAMSoc, c/o Willows Veterinary Centre and Referral Service, Highlands Road, Shirley, Solihull, West Midlands, B90 4NHemail: fergus.allerton@willows.uk.netSearch for more papers by this authorJohn Fishwick, John Fishwick Senior Vice President BVA, 7 Mansfield Street, London, W1G 9NQSearch for more papers by this authorSusan Paterson, Susan Paterson President BSAVA, Woodrow House, 1 Telford Way, Quedgeley, Gloucester, GL2 2ABSearch for more papers by this authorRenate Weller, Renate Weller President BEVA, Mulberry House, 31 Market St, Fordham, Ely, Cambridgeshire, CB7 5LQSearch for more papers by this authorIan Battersby, Ian Battersby Davies Veterinary SpecialistsSearch for more papers by this authorRonan Doyle, Ronan Doyle MRC Laboratory of Molecular BiologySearch for more papers by this authorDavid Gould, David Gould MRC Laboratory of Molecular BiologySearch for more papers by this authorSarah Caddy, Sarah Caddy MRC Laboratory of Molecular BiologySearch for more papers by this authorMark Dunning, Mark Dunning School of Veterinary Medicine and Science, University of NottinghamSearch for more papers by this authorHeidi J. Featherstone, Heidi J. Featherstone The Ralph Veterinary Referral CentreSearch for more papers by this authorJon Hardy, Jon Hardy Willows Veterinary Centre and Referral ServiceSearch for more papers by this authorAndrew Kent, Andrew Kent Willows Veterinary Centre and Referral ServiceSearch for more papers by this authorBrigite Pedro, Brigite Pedro Willows Veterinary Centre and Referral ServiceSearch for more papers by this authorKinley Smith, Kinley Smith Willows Veterinary Centre and Referral ServiceSearch for more papers by this authorFaye Swinbourne, Faye Swinbourne Willows Veterinary Centre and Referral ServiceSearch for more papers by this authorJames Harris, James Harris White Cross VetsSearch for more papers by this authorChristine Heinrich, Christine Heinrich Eye Veterinary ClinicSearch for more papers by this authorPeri Lau-Gillard, Peri Lau-Gillard Vale ReferralsSearch for more papers by this authorAnette Loeffler, Anette Loeffler RVCSearch for more papers by this authorRebecca Maddinson, Rebecca Maddinson Dragon Veterinary CentreSearch for more papers by this authorCarly Mason, Carly Mason SurreySearch for more papers by this authorIan Ramsey, Ian Ramsey University of Glasgow Small Animal HospitalSearch for more papers by this authorAlison Ridyard, Alison Ridyard University of Glasgow Small Animal HospitalSearch for more papers by this authorLouise Robin, Louise Robin Camlas Petcare VetsSearch for more papers by this authorChristopher Scudder, Christopher Scudder Southfields Veterinary SpecialistsSearch for more papers by this authorMayank Seth, Mayank Seth Dick White ReferralsSearch for more papers by this authorSimon Tappin, Simon Tappin Dick White ReferralsSearch for more papers by this authorDavid Singleton, David Singleton Small Animal Veterinary Surveillance Network, University of LiverpoolSearch for more papers by this authorHeather Smith, Heather Smith Woodcroft ReferralsSearch for more papers by this authorPeter Southerden, Peter Southerden Eastcott Veterinary Clinic and HospitalSearch for more papers by this authorJames Warland, James Warland University of CambridgeSearch for more papers by this authorMartin Whitehead, Martin Whitehead Chipping Norton Veterinary HospitalSearch for more papers by this authorJohn Williams, John Williams Vets Now 24/7 Emergency and Specialty Hospital, ManchesterSearch for more papers by this author Fergus Allerton, Corresponding Author Fergus Allerton Chairman fergus.allerton@willows.uk.net SAMSoc, c/o Willows Veterinary Centre and Referral Service, Highlands Road, Shirley, Solihull, West Midlands, B90 4NHemail: fergus.allerton@willows.uk.netSearch for more papers by this authorJohn Fishwick, John Fishwick Senior Vice President BVA, 7 Mansfield Street, London, W1G 9NQSearch for more papers by this authorSusan Paterson, Susan Paterson President BSAVA, Woodrow House, 1 Telford Way, Quedgeley, Gloucester, GL2 2ABSearch for more papers by this authorRenate Weller, Renate Weller President BEVA, Mulberry House, 31 Market St, Fordham, Ely, Cambridgeshire, CB7 5LQSearch for more papers by this authorIan Battersby, Ian Battersby Davies Veterinary SpecialistsSearch for more papers by this authorRonan Doyle, Ronan Doyle MRC Laboratory of Molecular BiologySearch for more papers by this authorDavid Gould, David Gould MRC Laboratory of Molecular BiologySearch for more papers by this authorSarah Caddy, Sarah Caddy MRC Laboratory of Molecular BiologySearch for more papers by this authorMark Dunning, Mark Dunning School of Veterinary Medicine and Science, University of NottinghamSearch for more papers by this authorHeidi J. Featherstone, Heidi J. Featherstone The Ralph Veterinary Referral CentreSearch for more papers by this authorJon Hardy, Jon Hardy Willows Veterinary Centre and Referral ServiceSearch for more papers by this authorAndrew Kent, Andrew Kent Willows Veterinary Centre and Referral ServiceSearch for more papers by this authorBrigite Pedro, Brigite Pedro Willows Veterinary Centre and Referral ServiceSearch for more papers by this authorKinley Smith, Kinley Smith Willows Veterinary Centre and Referral ServiceSearch for more papers by this authorFaye Swinbourne, Faye Swinbourne Willows Veterinary Centre and Referral ServiceSearch for more papers by this authorJames Harris, James Harris White Cross VetsSearch for more papers by this authorChristine Heinrich, Christine Heinrich Eye Veterinary ClinicSearch for more papers by this authorPeri Lau-Gillard, Peri Lau-Gillard Vale ReferralsSearch for more papers by this authorAnette Loeffler, Anette Loeffler RVCSearch for more papers by this authorRebecca Maddinson, Rebecca Maddinson Dragon Veterinary CentreSearch for more papers by this authorCarly Mason, Carly Mason SurreySearch for more papers by this authorIan Ramsey, Ian Ramsey University of Glasgow Small Animal HospitalSearch for more papers by this authorAlison Ridyard, Alison Ridyard University of Glasgow Small Animal HospitalSearch for more papers by this authorLouise Robin, Louise Robin Camlas Petcare VetsSearch for more papers by this authorChristopher Scudder, Christopher Scudder Southfields Veterinary SpecialistsSearch for more papers by this authorMayank Seth, Mayank Seth Dick White ReferralsSearch for more papers by this authorSimon Tappin, Simon Tappin Dick White ReferralsSearch for more papers by this authorDavid Singleton, David Singleton Small Animal Veterinary Surveillance Network, University of LiverpoolSearch for more papers by this authorHeather Smith, Heather Smith Woodcroft ReferralsSearch for more papers by this authorPeter Southerden, Peter Southerden Eastcott Veterinary Clinic and HospitalSearch for more papers by this authorJames Warland, James Warland University of CambridgeSearch for more papers by this authorMartin Whitehead, Martin Whitehead Chipping Norton Veterinary HospitalSearch for more papers by this authorJohn Williams, John Williams Vets Now 24/7 Emergency and Specialty Hospital, ManchesterSearch for more papers by this author First published: 29 June 2019 https://doi.org/10.1136/vr.l4383Citations: 2Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume184, Issue26June 2019Pages 805-806 RelatedInformation

The prevalence of GH-secreting pituitary tumors in domestic cats (Felis catus) is 10-fold greater than in humans. The predominant inhibitory receptors of GH-secreting pituitary tumors are somatostatin receptors (SSTRs) and D2 dopamine receptor (DRD2). The expression of these receptors is associated with the response to somatostatin analog and dopamine agonist treatment in human patients with acromegaly. The aim of this study was to describe pathological features of pituitaries from domestic cats with acromegaly, pituitary receptor expression, and investigate correlates with clinical data, including pituitary volume, time since diagnosis of diabetes, insulin requirement, and serum IGF1 concentration. Loss of reticulin structure was identified in 15 of 21 pituitaries, of which 10 of 15 exhibited acinar hyperplasia. SSTR1, SSTR2, SSTR5, and DRD2 mRNA were identified in the feline pituitary whereas SSTR3 and SSTR4 were not. Expression of SSTR1, SSTR2, and SSTR5 was greater in acromegalic cats compared with controls. A negative correlation was identified between DRD2 mRNA expression and pituitary volume. The loss of DRD2 expression should be investigated as a mechanism allowing the development of larger pituitary tumors.