Idiopathic Hypoparathyroidism in Five Cats

Idiopathic hypoparathyroidism was diagnosed in five young to middle-aged cats of mixed breeding. Three of the cats were male and two were female. Historic signs included lethargy (n = 5), anorexia (n = 5), muscle tremors (n = 4), weakness (n = 4), generalized seizures (n = 3), ataxia (n = 3), mental dullness or disorientation (n = 3), panting (n = 2), pruritus (n = 1), ptyalism (n = 1) and dysphagia (n = 1). Weakness (n = 4), dehydration (n = 2), cataracts (n = 2), hypothermia (n = 1), and bradycardia (n = 1) were found on physical examination. Results of electrocardiography revealed a prolonged Q-T interval in two cats. Results of initial laboratory tests revealed profound hypocalcemia and severe hyperphosphatemia with normal renal function. The diagnosis of hypoparathyroidism was made on the basis of the history, clinical signs, and results serum biochemical testing (i.e., severe hypocalcemia and hyperphosphatemia); in two cats, the diagnosis was also confirmed by histologic examination of parathyroid glands. Initial treatment included intravenous administration of 10% calcium gluconate and oral administration of large loading doses of calcium and vitamin D (dihydrotachysterol). Successful long-term management with dihydrotachysterol and calcium was achieved in all cats. The final dosage of dihydrotachysterol required to maintain normocalcemia in the five cats ranged from 0.004 to 0.04 mg/kg/day (mean = 0.015 mg/kg/day). Long-term calcium supplementation was given to three of the cats in dosages ranging from 29 to 53 mg/kg/day (mean = 42 mg/kg/day) of elemental calcium. One cat died after 28 months of therapy from widely metastatic hemangiosarcoma; the other three cats are still alive and well after 5 to 37 months of treatment.     

Epilepsy in Cats: Theory and Practice

The veterinary literature on epilepsy in cats is less extensive than that for dogs. The present review summarizes the most important human definitions related to epilepsy and discusses the difficulties in applying them in daily veterinary practice. Epileptic seizures can have a wide range of clinical signs and are not necessarily typical in all cases. Whether a seizure event is epileptic can only be suspected based on clinical, laboratory, and neuroimaging findings as electroencephalography diagnostic techniques have not yet been developed to a sufficiently accurate level in veterinary medicine. In addition, the present review aims to describe other diagnoses and nonepileptic conditions that might be mistaken for epileptic seizures. Seizures associated with hippocampal lesions are described and discussed extensively, as they seem to be a special entity only recognized in the past few years. Furthermore, we focus on clinical work‐up and on treatment that can be recommended based on the literature and summarize the limited data available relating to the outcome. Critical commentary is provided as most studies are based on very weak evidence.     

Idiopathic Sterile Granulomatous and Pyogranulomatous Dermatitis in Cats

Abstract— Idiopathic sterile granulomatous or pyogranulomatous dermatitis was diagnosed in four cats. Two distinct clinicopathological syndromes were recognized. Two cats had a pruritic papulonodular dermatitis of the head and pinnae with skin histopathology characterised by perifollicular pyogranulomatous dermatitis. The other two cats had pruritic bilateral preauricular plaques characterised histopathologically by diffuse granulomatous dermatitis with numerous multinucleated histiocytic giant cells and purpura. Haematological, biochemical and urinary abnormalities were not detected and the cats were otherwise healthy. Lesions were not responsive to systemic antibiotics or systemic glucocorticoids at anti-inflammatory doses. Three cats underwent apparently spontaneous, sustained remission after a course of 3 to 9 months. Résumé— Une dermatite granulomateuse idiopathique stérile, ou pyogranulomateuse fut diagnostiquée chez 4 chats. Deux syndromes distincts ont été identifiés. Deux chats avaient une dermatite papulonodulaire prurigineuse de la tête et des oreilles, avec des biopsies cutanées caractérisées par une dermatite pyogranulomateuse périfolliculaire. Les 2 autres chats avaient des plaques prurigineuses préauriculaires bilatérales, caractérisées histologiquement par une dermatite granulomateuse diffuse avec de nombreuses cellules géantes multinucléées et du purpura. Les examens hématologique, biochimique et urinaire étaient par ailleurs normaux et les chats en bon état général. Les antibiotiques et les corticoides à dose antiinflammatoire, tous deux par voie générale, sont restés sans effet. Trois chats ont présenté une rémission spontanée après une évolution de 3 à 9 mois. Zausammenfassung— Bei vier Katzan wurde eine idiopathische sterile granulomatöse oder pyogranulomatöse Dermatitis diagnostiziert. Dabei konnten zwei klinisch-pathologisch abgrenzbare Syndrome erkannt werden. Zwei Katzen wiesen eine pruriginöse, papulo-noduläre Dermatitis am Kopf und an den Ohren auf, wobei histologisch eine perifollikuläre pyogranulomatöse Dermatitis festgestellt wurde. Die beiden anderen Katzen zeigten pruriginöse, bilaterale präaurikuläre Plaques, deron histologisches Bild durch eine diffuse granulomatöse Dermatitis mit zahlreichen vielkernigen histiozytären Riesenzellen und Purpure gekennzeichnet war. Abnormalitäten bezüglich hämatologischer, biochemischer und harnspezifischer Parameter wurden nicht festgestellt, auch waren die Katzen sonst gesund. Die Veränderungen sprachen nicht auf die systemische Behandlung mit Antibiotika oder Glukokortikoiden in einer antiinflammatorischen Dosis an. Bei drei Katzen kam es zu einer spontanen, dauerhaften Remission der Befunde nach einem Krankheitsverlauf von 3 bis 9 Monaten. Resumen En cuatro gatos se diagnosticó una dermatitis piogranulomatosa o granulomatosa esteril idiopática. Se distinguieron dos síndromes clínicopatológicos. Dos gatos presentaban una dermatitis papulonodular prurítica situada en la cabeza y en los pabellones auriculares, con unas biopsias cutáneas caracterizadas por una dermatitis piogranulomatosa perifolicular. Los otros dos animales presentaban placas preauriculares y laterales pruríticas con un cuadro histopatológico caracterizado por una dermatitis granulomatosa difusa con numerosas células gigantes istiocíticas multinucleadas y hemorragias. No se detectaron alteraciones hematológicas, bioquímicas ni en la orina, y los animales se encontraban en buen estado de salud. Las lesiones no respondieron ni al tratamiento con antibióticos sistémicos ni al tratamiento con glucocorticoides a dosis antiinflamatorias. Tres de los animales sufrieron una remisión espontánea después de 3 a 9 meses.     

Clinical Characterization of Epilepsy of Unknown Cause in Cats

Background

The diagnosis of feline epilepsy of unknown cause (EUC) requires a thorough diagnostic evaluation, otherwise the prevalence of EUC could be overestimated.

Hypothesis

Feline EUC is a clinically defined disease entity, which differs from feline hippocampal necrosis by the absence of magnetic resonance imaging (MRI) signal alteration of the hippocampus. The objectives of this study were (1) to evaluate the prevalence of EUC in a hospital population of cats by applying well‐defined inclusion criteria, and (2) to describe the clinical course of EUC.

Animals

Eighty‐one cats with recurrent seizures.

Methods

Retrospective study—medical records were reviewed for cats presented for evaluation of recurrent seizures (2005–2010). Inclusion criteria were a defined diagnosis based on laboratory data, and either MRI or histopathology. Final outcome was confirmed by telephone interview with the owner. Magnetic resonance images were reviewed to evaluate hippocampal morphology and signal alterations.

Results

Epilepsy of unknown cause was diagnosed in 22% of cats with epilepsy. Physical, neurologic, and laboratory examinations, and either 1.5 T MRI and cerebrospinal fluid analysis or postmortem examination failed to identify an underlying cause. Cats with EUC had a higher survival rate (P < .05) and seizure remission occurred frequently (44.4%).

Conclusion and Clinical Importance

A detailed clinical evaluation and diagnostic imaging with MRI is recommended in any cat with recurrent seizures. The prognosis of cats with normal MRI findings and a clinical diagnosis of EUC are good. Standardized imaging guidelines should be established to assess the hippocampus in cats.     

Serum Cytokine Profiling in Cats with Acute Idiopathic Cystitis

Background

Feline idiopathic cystitis (FIC) is a common lower urinary tract disorder of domestic cats that resembles interstitial cystitis/painful bladder syndrome (IC/PBS) in humans. Diagnosis of FIC is based on clinical signs and exclusion of other disorders because of a lack of specific pathologic findings or other objective biomarkers. Cytokines are potential noninvasive biomarkers to define the presence, severity, and progression of disease, and response to treatment.

Objectives

The objective of this pilot study was to determine concentrations of selected cytokines in serum from healthy cats and cats with acute FIC.

Animals

Serum samples from 13 healthy cats and from 12 cats with nonobstructive acute FIC were utilized.

Methods

Multiplex analysis of 19 cytokines (CCL2, CCL5, CXCL1, CXCL12, CXCL8, Flt3L, GM‐CSF, IFN‐γ, IL‐12 (p40), IL‐13, IL‐18, IL‐1β, IL‐2, IL‐4, IL‐6, PDGF‐BB, SCF, sFas, and TNF‐α) was performed with a commercially available feline‐specific multiplex bead‐based assay.

Results

Mean serum concentrations of IL‐12 (p40; P < 0.0001), CXCL12 (P = 0.002), IL‐18 (P = 0.032), and Flt3L (P = 0.0024) were significantly increased in FIC cats compared to healthy cats. GM‐CSF, IL‐1b, IL‐2, and PDGF‐BB were undetectable or detected in an insufficient number of cats to allow meaningful comparisons.

Conclusions and Clinical Importance

We have identified increased serum concentrations of pro‐inflammatory cytokines and chemokines CXCL12, IL‐12, IL‐18, and Flt3L in FIC‐affected cats. These findings suggest potential candidates for noninvasive biomarkers for diagnosis, staging, and therapeutic outcome monitoring of affected cats and provide additional insight into the etiopathogenesis of FIC.     

Bromide Therapy in Refractory Canine Idiopathic Epilepsy

On a retrospective basis, the response to adding chronic oral bromide (BR) to phenobarbital (PB) administration in 23 refractory canine idiopathic epileptics between 1986 and 1991 was studied. The mean age for an observed first seizure was 24 months (range 7 to 72) for all dogs. Thirteen (57%) dogs were males with no breed predisposition observed. All dogs were diagnosed as having idiopathic epilepsy based on normal metabolic and neurologic diagnostic evaluations. Dogs were evaluated before BR therapy for a mean time of 22 months (range 5 to 75 months). Seventeen dogs (74%) received multiple antiepileptic drugs (AEDs) before BR therapy. All animals were maintained on PB at least 4 months before the onset of BR therapy, with a mean trough serum concentration of 37.8 mcg/mL and no improvement in seizure severity or recurrence. Twelve dogs presented with generalized isolated seizures and 11 with generalized cluster seizures (two or more seizures within 24 hours) as their first seizure. The effects of BR therapy were evaluated for a mean time of 15 months (range 4 to 33), with 17 dogs (74%) followed for 12 or more months. The mean BR serum concentration for the 0 to 4 months time period was 117 mg/dL compared with 161 mg/dL for the greater than 4 months period. Overall, response to BR therapy was associated with a reduction in the total number of seizures in 83% of the dogs when compared with their respective pre-BR period. For those followed for 1 year after BR, there was a 53% reduction in the number of seizures compared with the previous 12 months. Furthermore, owners reported a decrease in seizure intensity (65% of dogs) and change to a less severe seizure type (22% of dogs) in those dogs that continued to have seizures. Seizure-free status was obtained in 26% of the dogs with protection continuing up to 31 months in one dog. No correlations could be determined between response to BR and either age of onset of the first seizure or interval from the first AED therapy to BR therapy. Adverse effects of concomitant BR and PB therapy were polydipsia (56% of dogs), polyphagia (30% of dogs), excessive sedation (30% of dogs), and generalized ataxia (17% of dogs). As a result of BR treatment, the PB dosage was reduced in eight dogs (35%). In conclusion, concomitant BR and PB was well tolerated in dogs of this study and was effective in treating refractory canine idiopathic epilepsy, regardless of prior interval of seizure activity or previous treatment. (Journal of Veterinary Internal Medicine 1993; 7:318–327. Copyright © 1993 by the American College of Veterinary Internal Medicine.)     

Cisapride Stimulates Contraction of Idiopathic Megacolonic Smooth Muscle in Cats

We have previously shown that cisapride, a substituted piperidinyl benzamide, stimulates contraction of healthy feline colonic smooth muscle. The purpose of the present investigation was to determine the effect of cisapride on feline idiopathic megacolonic smooth muscle function. Longitudinal smooth muscle strips from ascending and descending colon were obtained from cats with idiopathic megacolon, suspended in a 1.5 mM Ca²⁺-HEPES buffer solution (37°C, 100% O₂, pH 7.4), attached to isometric force transducers, and stretched to optimal muscle length (L₀). Control responses were obtained at each muscle site with acetylcholine (10–⁸ to 10 ⁴ M), substance P (10–¹¹ to 10^-7 M), or potassium chloride (10 to 80 mM). Muscles were then stimulated with cumulative (10–⁹ to 10–⁶ M) doses of cisapride in the absence or presence of tetrodotoxin (10–⁶ M) and atropine (10–⁶ M), or in a 0 calcium HEPES buffer solution. In cats with idiopathic megacolon, cisapride stimulated contractions of longitudinal smooth muscle from both the ascending and the descending colon. Cisapride-induced contractions were similar in magnitude to those induced by substance P and acetylcholine in the ascending colon, but were less than those observed in the descending colon. Cisapride-induced contractions in megacolonic smooth muscle were only partially inhibited by tetrodotoxin and atropine, but were virtually abolished by removal of extracellular calcium. We concluded that cisapride-induced contractions of feline megacolonic smooth muscle are largely smooth muscle mediated and dependent on influx of extracellular calcium. Cisapride-induced contractions in megacolonic smooth muscle are only partially dependent on enteric cholinergic nerves. Thus, cisapride may be useful in the treatment of cats with idiopathic megacolon.     

Lipid Composition of Hepatic and Adipose Tissues From Normal Cats and From Cats With Idiopathic Hepatic Lipidosis

The purpose of this study was to characterize the lipid classes in hepatic and adipose tissues from cats with idiopathic hepatic lipidosis (IHL). Concentrations of triglyceride, phospholipid phosphorus, and free and total cholesterol were determined in lipid extracts of liver homogenates from 5 cats with IHL and 5 healthy control cats. Total fatty acid composition of liver and adipose tissue was also compared. Triglyceride accounted for 34% of liver by weight in cats with IHL (338 ± 38 mg/g wet liver) versus 1% in control cats {9.9 ±1.0 mg/g wet liver, P < .001). The mass of cholesterol ester was significantly higher in triglyceride-free (TG-free) liver from cats with IHL (741 ± 340 μg/g TG-free wet liver) compared to healthy cats (31 ± 11 μg/g TG-free wet liver, P < .05). Total fatty acid composition of hepatic tissue in the 2 groups differed; pa Imitate was higher (19.5 ± 1.1% of total fatty acids in cats with IHL versus 9.2 ± 2.7% in controls, P < .05), stearate was lower (8.5 ± 0.8% versus 16.8 ± 1.1%, P < .05), oleate was higher (41.2 ± 1.6% versus 31.1 ± 1.8%, P < .05), and arachidonate was lower (1.2 ± 0.2% versus 6.0 ± 0.9%, P < .05). The total fatty acid composition of adipose tissue also differed between the 2 groups; palmitate was higher (25.2 ± 1.2% in cats with IHL versus 21.3 ± 0.6% in controls, P < .05), total monounsaturated fatty acids were higher (48.4 ± 1.0% versus 45.0 ± 0.8%, P < .05), linoleate was lower (13.3 ± 1.6% versus 17.5 ± 0.9%, P < .05), total (n-6) fatty acids were lower (13.8 ± 1.38% versus 18.4 ± 0.83%, P < .05), linolenate was lower (0.2 ± 0.04% versus 0.7 ± 0.06%, P < .05), and total (n-3) fatty acids were lower (0.3 ± 0.02% versus 1.3 ± 0.32%, P < .05). The fatty acid composition of both liver and adipose tissue was similar for stearate, oleate, linoleate, and linolenate in cats with IHL. These results support the hypothesis that the origin of hepatic triglyceride in cats with IHL is the mobilization of fatty acids from adipose tissue.     

Association between Estrus and Onset of Seizures in Dogs with Idiopathic Epilepsy

Background

Catamenial epilepsy in humans is defined as changes in seizure frequency over the course of the menstrual cycle. Three hormonally based patterns of seizure exacerbation have been determined.

Objectives

The aim of this study was to evaluate whether there is an association between onset of seizures and the estrous cycle in intact bitches with presumptive idiopathic epilepsy and whether a pattern to the onset of seizures could be recognized.

Animals

Forty‐five intact female dogs from a hospital population with a presumptive diagnosis of idiopathic epilepsy.

Methods

In a retrospective study, the database of a small animal hospital in Sweden was searched for medical records of intact female dogs diagnosed with epilepsy or seizures. The stage of the estrous cycle as reported either by the owner or the veterinarian at the time of the first seizure was noted.

Results

Of the 45 dogs with idiopathic epilepsy, 17 (38%) had their first seizure when in heat and six dogs (13%) had their first seizure 1–3 months after heat. Nine dogs (20%) had seizures reoccurring in relation to their estrous cycle.

Conclusions and Clinical Importance

These findings suggest an association between estrus and onset of seizures in intact bitches with presumptive idiopathic epilepsy. Two hormonally based patterns could be recognized: one during heat and one during a specific time point at the end of diestrus. This could be explained by the proconvulsive effects of estrogen or loss of protective effect against seizures of progesterone, respectively.     

Pancreatitis in Cats

Pancreatitis was considered a rare disease in the cat until a couple of decades ago when several retrospective studies of severe acute pancreatitis were published. It was apparent that few of the diagnostic tests of value in the dog were helpful in cats. With increasing clinical suspicion, availability of abdominal ultrasonography, and introduction of pancreas-specific blood tests of increasing utility, it is now accepted that acute pancreatitis is probably almost as common in cats as it is in dogs, although the etiology(s) remain more obscure. Pancreatitis in cats often co-exists with inflammatory bowel disease, less commonly with cholangitis, and sometimes with both. Additionally, pancreatitis may trigger hepatic lipidosis, while other diseases, such as diabetes mellitus, may be complicated by pancreatitis. Therapy is similar to that used in dogs, with added emphasis on early nutritional support to prevent hepatic lipidosis. Less is known about chronic pancreatitis than the acute form, but chronic pancreatitis is more common in cats than it is in dogs and may respond positively to treatment with corticosteroids.     

Investigation of Known Genetic Mutations of Arabian Horses in Egyptian Arabian Foals with Juvenile Idiopathic Epilepsy

Background

The carrier status of lavender foal syndrome (LFS), cerebellar abiotrophy (CA), severe combined immunodeficiency (SCID), and occipitoatlantoaxial malformation (OAAM1) in foals with juvenile idiopathic epilepsy (JIE) is unknown.

Hypothesis/Objectives

To determine the carrier status of LFS, CA, SCID, and OAAM1 in foals with JIE.

Animals

Ten foals with JIE.

Materials and Methods

Archived DNA samples were tested for known genetic mutations causing LFS, CA, SCID, and OAAM1. The inclusion criteria consisted of having been diagnosed with JIE by ruling out other causes of seizures in foals and supported by electroencephalographic examination.

Results

Ten Egyptian Arabian horses (5 females and 5 males) were phenotyped as foals with JIE by electroencephalography (EEG). All foals were negative for the genetic mutations that cause LFS, CA, SCID, and OAAM1 except for 1 foal that was a carrier of CA.

Conclusions and Clinical Importance

Juvenile idiopathic epilepsy of Egyptian Arabian foals and LFS appear to be phenotypically and genetically distinct disorders. There was no apparent association between JIE and LFS, CA, SCID, and OAAM1.     

Cisplatin Toxicity in Cats

Cisplatin (cis-diamminedichloroplatinum; Platinol, Bristol, Syracuse, NY) was administered to 11 cats, divided into three groups of experimental and clinical patients. In group 1, cisplatin was administered at a dose of 60 mg/m2 to four cats. In an attempt to avoid renal toxicity, saline diuresis was induced by administering 0.9% saline solution intravenously at a rate of 20 ml/kg/hr for 4 hours before and 2 hours after cisplatin administration. All four cats became dyspneic and died 48-96 hours after cisplatin administration. Postmortem findings included severe hydrothorax, pulmonary edema, and mediastinal edema. In group 2, four experimental cats entered a trial comparing the effects of saline diuresis and cisplatin (60 mg/m2) with the effects of saline diuresis and placebo (0.9% saline solution). The cats in the saline control group remained completely normal, while the cats that received cisplatin developed clinical signs and gross postmortem pulmonary changes identical to those in the first group of cats. Histopathologic examination showed that the alveolar septa were thickened and congested, and contained macrophages, occasional neutrophils, thrombi, and small foci of necrosis and fibrin. Microangiopathic changes were seen in the alveolar capillaries. In the third group, three additional cats were treated with a lower dose of cisplatin. Two cats that received 40 mg/m2 of cisplatin developed pulmonary changes similar to, but less severe than, those seen in the cats that received the higher dose of cisplatin. One cat treated with 20 mg/m2 of cisplatin showed no pulmonary changes ante mortem or post mortem. This series of 11 clinical and experimental cases identifies an apparent species-specific, dose-related, primary pulmonary toxicity of cisplatin in cats.     

Acromegaly in 14 Cats

Acromegaly was diagnosed in 14 middle-aged to old cats of mixed breeding. Thirteen (93%) of the cats were male and one was female. The earliest clinical signs in the 14 cats included polyuria, polydipsia, polyphagia, all of which were associated with untreated diabetes mellitus. All developed severe insulin resistance within a few months; peak insulin dosages required to control severe hyperglycemia ranged from 20 to 130 U per day. Other clinical findings weeks to months after diagnosis included enlargement of one or more organs (e.g., liver, heart, kidneys, and tongue) (n = 14), cardiomyopathy (n = 13), increase in body size and weight gain (n = 8), nephropathy associated with azotemia and clinical signs of renal failure (n = 7), degenerative arthropathy (n = 6), and central nervous system signs (i.e., circling and seizures) caused by enlargement of the pituitary tumor (n = 2). The diagnosis of acromegaly was confirmed by demonstration of extremely high basal serum growth hormone concentrations (22 to 131 micrograms/l) in all cats. Computerized tomography disclosed a mass in the region of the pituitary gland and hypothalamus in five of the six cats in which it was performed. Two cats were treated by cobalt radiotherapy followed by administration of a somatostatin analogue (octreotide), whereas two cats were treated with octreotide alone. Treatment had little to no effect in decreasing serum GH concentrations in any of the cats. Eleven of the 14 cats were euthanized or died four to 42 months (median survival time, 20.5 months) after the onset of acromegaly because of renal failure (n = 2), congestive heart failure (n = 1), concomitant renal failure and congestive heart failure (n = 3), progressive neurologic signs (n = 2), persistent anorexia and lethargy of unknown cause (n = 1), the owner's unwillingness to treat the diabetes mellitus (n = 1), or unknown causes (n = 1). Results of necropsy examination in ten cats revealed a large pituitary acidophil adenoma (n = 10), marked left ventricular and septal hypertrophy (n = 7), dilated cardiomyopathy (n = 1), arthropathy affecting the shoulder, elbow, or stifle (n = 5), and glomerulopathy characterized by expansion of the mesangial matrix and variable periglomerular fibrosis (n = 10).