https://doi.org/10.52973/rcfcv-e34495

Received: 24/07/2024 Accepted: 14/09/2024 Published: 23/12/2024

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Revista Científica, FCV-LUZ / Vol. XXXIV, rcfcv-e34495

ABSTRACT

A 10–year–old Pomeranian with chronic ulcerative and bullous

lesions, that did not respond to previous treatment with amoxicillin,

cephalexin, levothyroxine and trilostane, was presented. A primary

immune–mediated process was suspected on examination, and

multifocal supercial pyoderma was identied. A skin biopsy revealed

panniculitis of pancreatic or sterile nodular origin. Further tests

conrmed that the dog had ongoing pancreatitis and glomerulopathy.

Ultrasonography revealed enlargement of the pancreatic tissue

and hyperechogenicity. Treatment with cyclosporine, tetracycline,

niacinamide and omega–3 for 8 weeks resulted in a favorable

response. However, 4 weeks after clinical improvement of the skin,

the dog suddenly became paraplegic and lost deep nociception. Spinal

cord compression type Acute Non–compressive Nucleus Pulposus

Extrusion (ANNPE) was suspected, but could not be conrmed. This

case documents the presentation of pancreatic panniculitis in a

Pomeranian and the concomitant occurrence of possibly associated

glomerulopathy and spinal cord trauma.

Key words: Steatitis; pancreas; canine; glomerulopathy; ANNPE

RESUMEN

Se presenta el caso de un pomerania de 10 años de edad con lesiones

ulcerosas y ampollosas crónicas, que no respondieron al tratamiento

previo con amoxicilina, cefalexina, levotiroxina y trilostano. En la

exploración clínica se sospechó un proceso inmunomediado primario

y se identicó pioderma supercial multifocal. Una biopsia cutánea

reveló paniculitis de origen pancreático o nodular estéril. Las pruebas

paraclínicas confirmaron que el canino padecía pancreatitis y

glomerulopatía. La ecografía reveló agrandamiento del tejido

pancreático e hiperecogenicidad heterogénea del parénquima. El

tratamiento con ciclosporina, tetraciclina, niacinamida y omega–3

durante 8 semanas dio lugar a una respuesta favorable. Sin embargo,

4 semanas después de la mejoría clínica de la piel, el paciente

quedó súbitamente parapléjico y perdió la nocicepción profunda.

Se sospechó una compresión medular del tipo “extrusión aguda

no compresiva del núcleo pulposo”, más no pudo confirmarse.

Este caso documenta la presentación de paniculitis pancreática

en un Pomerania y la aparición concomitante de glomerulopatía

posiblemente asociada y traumatismo medular.

Palabras clave: Esteatitis, páncreas, canino, glomerulopatía, hernia

de disco intervertebral

Pancreatic panniculitis and glomerulopathy in a Pomeranian dog

Clinical case

Paniculitis pancreática y glomerulopatía en un perro Pomerania

Caso clínico

Paula Bermúdez* , Iovana Castellanos

Universidad de La Salle, Facultad de Ciencias Agropecuarias, Programa de Medicina Veterinaria. Bogotá, Colombia.

*Corresponding author: pabermudez@unisalle.edu.co

FIGURE 1. Appearance of the skin of a canine with pancreatic panniculitis before

treatment

Pancreatic panniculitis and glomerulopathy in a dog / Bermúdez and Castellanos _________________________________________________

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INTRODUCTION

Panniculitis is the inammation of subcutaneous fat, a condition

of low prevalence in canines with multiple clinical associations.

Clinically, it is characterized by subcutaneous nodules, focal or

multiple, distributed classically over the trunk, with draining tracts

(“melted cysts”), that cause mild pain, fever, lymphadenopathy or

ndings of systemic disease at physical examination. Nodules may

ulcerate and drain an exudate (oily, yellow, brown or bloody) or scar

with crusts and brous tissue. Fat inammation can be triggered

by infections (bacteria, fungi, or atypical mycobacteria), immune–

mediated conditions (lupus, erythema nodosum, or vasculitis,

arthropod bites), trauma (ischemia or chronic pressure), neoplastic

conditions (multicentric mastocytoma, cutaneous lymphoma, or

pancreatic tumor), nutritional deciencies (vitamin E deciency,

excess of polyunsaturated fatty acids), drug reactions (vaccines,

corticosteroids), or unknown reasons [1, 2, 3, 4, 5, 6, 7, 8].

Pancreatic panniculitis can lead to abnormal test results such as

leukocytosis (neutrophilia and left shift or eosinophilia), anemia,

and elevated levels of alkaline phosphatase, lipase, amylase,

trypsin or hyperlipemia. Blood tests and ultrasound scans can

help diagnose pancreatitis. Classic cases of pancreatitis may also

include hypoglycemia, hypocalcemia, and hypoalbuminemia [2, 7].

Conrmation of diagnosis involves a biopsy and culture to determine

sterile or contaminated panniculitis with a secondary infection [2].

Treatment options for skin lesions include surgical removal

or antimicrobial therapy combined with immunosuppressants,

tetracyclines, niacinamide, and vitamin E [2]. Recovery usually takes

3–6 weeks although it could take longer. However, the prognosis for

pancreatic causes is poor due to high recurrence and progression

rates [1, 5, 9].

MATERIALS AND METHODS

Case description

A 10–year–old Pomeranian dog (Canis lupus familiaris) with chronic

skin disease and hormonal imbalances was presented at the Veterinary

Clinic of La Salle University in Bogotá. Six months ago, the patient

had a lesion on the ventral tail region, which later spread to the dorsal

region. The ulcerous–crusted lesion then extended to the skin of

the thorax and neck. The patient also experienced severe itching,

blisters, and bullae, which became ulcer and scab lesions. The patient

had been treated with oral ampicillin and cephalexin (unknown dose)

with chlorhexidine shampoos during the illness period, however, the

response was only partial and inconsistent. Also, the dog had been

diagnosed previously with hypothyroidism and hyperadrenocorticism

(based on reduced total T

and free T

hormones and cortisol more

than 1.4 μg·dL

-1

at 8 hours in a low–dose dexamethasone suppression

test performed at another veterinary center) but did not respond

accordingly to levothyroxine and trilostane.

On physical inspection, physiological constants were within

normal ranges; blood pressure was 152/108 (137) mmHg (SunTech

Vet20 Veterinary Blood pressure Monitor, Miami, USA). Dermatologic

inspection revealed bilateral hypotrichosis, symmetrical extended to all

four limbs, with perineal and tail alopecia, multifocal hyperpigmentation

(accentuated in the perineal region) accompanied by erythema,

desquamation and epidermal collarettes with pustules and bullae

generating severe pruritus (FIG. 1). There were secondary lesions to

the pruritus, with multifocal petechiae and ecchymosis as well as

scabs and scars. Skin biopsy was performed under local anaesthesia

and amoxicillin/clavulanic acid at 12.5 mg·kg

-1

every 12 hours (h) for 28

continuous days (d), amitriptyline 3 mg·kg

-1

every 12 h for 28 continuous

d and enalapril at 0.25 mg·kg

-1

every 12 h, plus topical cleaning of lesions

with chlorhexidine and cream with neomycin/bacitracin and zinc oxide.

Nutraceuticals like omega 3, and vitamins A, and E were also given.

RESULTS AND DISCUSSION

The results of the paraclinical examinations performed on the

patient during the diagnostic approach are presented in TABLE I.

The ultrasound ndings showed that there were structural changes

in the kidneys, liver, and pancreas (Vinno D650, Veterinary model,

Suzhou, China). The pancreas had increased echogenicity and a larger

size on the right branch. The liver had mild hepatomegaly and reduced

differentiation of portal wall visualization. The kidneys showed less

TABLE I

Paraclinical examinations of a 10–year–old, entire male Pomeranian

canine with chronic presentation of ulcerative, crusty, blistering,

pustular lesions, and symmetrical truncal alopecia

Parameter

Pre–treatment

value

Post–treatment

value

Unit of

Measurements

Reference

range

Erythrocytes 7.4 7.07 10

cells·µL

-1

5.4 – 7.8

Haemoglobin 16 14.3 g·L

-1

13 – 19

Haematocrit 52 46 % 37 – 54

Leukocytes 13.6 14.6 10

cells·µL

-1

6 – 17

Neutrophils 11.2 13.1 10

cells·µL

-1

3 – 11.5

Lymphocytes 1.4 0.7 10

cells·µL

-1

1 – 4.8

Monocytes 0.8 0.4 10

cells·µL

-1

0.1 – 1.4

Eosinophils 0.3 0.3 10

cells·µL

-1

0 – 0.9

Platelets 237 934 10

cells·µL

-1

160 – 430

Plasma proteins 5.5 6.4 – 6 – 7.8

Blood biochemistry

Albumin – 2.7 g·dL

-1

2.3 – 4.0

Globulins – 5.3 g·dL

-1

2.1 – 4.5

ALT – 158 U·L

-1

5 – 125

FA – 209 U·L

-1

17 – 212

Creatinine – 0.59 mg·dL

-1

0.27 – 1.07

BUN – 16.9 mg·dL

-1

7 – 27

Glucose – 126 mg·dL

-1

74 – 143

Cholesterol 385 – mg·dL

-1

110 – 350

HDL 256.6 – mg·dL

-1

> 100

LDL 274 – mg·dL

-1

< 50

Triglycerides 85 – mg·dL

-1

21 – 87

Amylase 593 U·L

-1

388 – 1007

Pre–treatment

pancreas–

specic lipase

547.2 937.7 ng·mL

-1

< 200 ng·mL

-1

Uroanalysis

Specic gravity 1022 1019 – >1030

pH 8 7 – 6.5 – 7.5

Crystals – – mg·dL

-1

Negative

Cylinders Hialines + Hialines + cylinder/eld < 1

Erythrocytes 0 – 2 1 – 4 cells/eld < 5

Leukocytes 0 – 2 0 – 2 cells/eld < 5

Bacteria – + – 0

Squamous cells 0 – 1 0 – 2 cells/eld < 5

Transitional cells 0 – 1 0 – 2 – < 5

UPC (inactive

sediment)

1.9 11.7 – < 0.2

FIGURE 2. Ultrasound images of kidneys, liver, pancreas and adrenal glands of

canine with pancreatic panniculitis

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The cutaneous tissue was taken with punch biopsy (biopsy

punch 8 mm, India). The report indicated severe bleeding in the

hypodermis, with multiple eosinophilic areas of amorphous material

(lipid saponication) surrounded by PMN, along with adipose tissue

necrosis. Intralobular PMN inltration in the adipose tissue and

interstitial inltration in the supercial and deep dermis were present.

The epidermis was normal, with atrophy of appendages, and the

presence of hair follicles in the telogen phase. There were areas

of bleeding in the supercial and deep dermis. The nal diagnosis

proposed was an inammatory pattern suggestive of panniculitis

and a possible association with pancreatic panniculitis or idiopathic

nodular panniculitis.

After receiving the biopsy results, it was decided to start a

treatment plan for the patient. The plan included cyclosporine at a

dosage of 5 mg per kg every 8 h, tetracycline at 250 mg every 8 h, and

niacinamide at 250 mg every 8 h. This treatment was continued for 8

weeks and some dietary modications (low–fat maintenance diet). It

was also decided to gradually discontinue trilostane.

After eight weeks of treatment, there was a signicant improvement

in the quality of the coat, with regrowth in the dorsal, thoracic, and

cortico–medullary differentiation, hyperechogenicity of the renal

cortex compared to the spleen, and irregular contour. Additionally,

the adrenal glands were identied with bilateral hyperplasia but had

a normal sonographic appearance (FIG. 2).

FIGURE 3. Clinical evolution of the appearance of the skin of a canine with pancreatic panniculitis 8 weeks after treatment

FIGURE 4. Latero–lateral radiographs of the thoracolumbar and lumbar regions in a

canine with pancreatic panniculitis and sudden spinal trauma of undetermined origin

Pancreatic panniculitis and glomerulopathy in a dog / Bermúdez and Castellanos _________________________________________________

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abdominal regions. There were no more ulcerative, crusty, bullous,

or complicated lesions with collars and papules, as shown in FIG. 3.

However, there were still some areas with uneven coat growth, such

as the cervical, perineal region, and the entire tail. Additionally, there

was still generalized desquamation in certain regions like the groin

and belly. The canine–specic pancreatic lipase continued to be

elevated compared to the initial value, as shown in TABLE I.

During the paraclinical examinations, it was found that the patient

had persistent proteinuria, suggesting an ongoing glomerulopathy.

As a result, the patient has been classified in IRIS stage I, non–

hypertensive proteinuric. Amlodipine 0.1 mg·kg

-1

every 24 h was added

to the iECA therapy to treat his condition. However, due to economic

reasons, the owner refused the diagnostic approach to identify the

probable cause of glomerulopathy.

About four weeks later, the patient started showing symptoms

of acute spontaneous trauma in the spinal cord, which led to non–

ambulatory paraparesis to paraplegia. The patient also experienced

progressive loss of deep sensation within 24 h of the onset of these

signs, initial spinal hyperesthesia, urinary retention, and fecal

incontinence. Neurological examination suggested a high motor

neuron lesion for the hind limbs in the thoracolumbar segment.

Radiographs [VIVIX. 2024. Flat Panel for Digital Radiography

VIVIX–F. VIVIX Corp. Seongnam, Corea del Sur] did not evidence an

abnormality consistent with spinal cord compression from Hansen

type I disc herniations, fractures or dislocations of the vertebral

bodies (FIG. 4). It was not possible to perform an MRI to rule out or

conrm other possible differential diagnoses (brocartilaginous

embolism). Following the clinical scenario, the owner decided to

request humane euthanasia of the animal given the compromise of

the patient’s future quality of life. Due to the owner’s dissent, it was

also not possible to perform the necropsy of the patient.

Paniculitis associated with pancreatic disease in dogs is a rare and

poorly documented condition. The rst post–mortem report in a dog

with nodular hyperplasia was made in 1982 [10] and the rst ante–

mortem report was made in 2003 [1]. It is believed to occur due to

the saturation of lipase, amylase, trypsin and/or phospholipase–A in

the portal or thoracic circulation, which, upon reaching the systemic

circulation, results in vascular hyper–permeability, causing the release

of lipids into the extracellular space from inamed adipocytes. The

released lipids undergo hydrolysis to become glycerol and fatty acids

that trigger inammatory events, local piogranulomatous reactions in

the subcutaneous space and fat necrosis, given their pro–inammatory

effect [4, 5, 11]. The associated pancreatic conditions have been

nodular hyperplasia, chronic inammation, necrosis, adenoma, and

adenocarcinoma/carcinoma [1, 3, 4, 9, 12]. In this case, the panniculitis

associated with ongoing chronic pancreatitis was documented through

the elevation of canine–specic lipase and ultrasound ndings.

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In Human Medicine, it has been proposed that the association

between pancreatitis and panniculitis may be due to a deciency of

an enzyme inhibitor (alpha–1 antitrypsin) or a reduction in alpha–2–

macroglobulin [1, 8, 9]. It has also been documented that the presence

of high concentrations of lipase and cytotoxic concentrations of fatty

acids in the skin of patients with panniculitis and polyarthritis is one

of the triggering factors [9]. However, in canines, the association

between alpha–1 antitrypsin has not been conrmed [13], although it

is not ruled out as a probable contributing factor [6]. In this patient,

the simultaneous occurrence of both diagnoses is suggestive of the

disease presentation, and furthermore, the cutaneous therapeutic

response to immunosuppression.

Skin biopsy ndings were key to the identication of panniculitis.

It is recommended to perform a skin culture to diagnose a clinically

evident secondary bacterial infection. In addition, a suspicion of

mycobacteria causing cutaneous/subcutaneous pyogranulomas

and panniculitis (such as Actinomyces, Nocardia, Blastomyces,

Histoplasma, Coccidioides, Cryptococcus, Sporothrix, Aspergillus,

Leishmania, Bartonella and/or mycobacteria) can only be conrmed

or ruled out through cultures, differential stains, and respective

serologies of each entity. These procedures were not documented

in this case [4, 6, 7, 14].

In a study of 14 cases of sterile nodular panniculitis in dogs, it

was found that 5 cases (35.7%) had a urinary protein to creatinine

(UPC) ratio greater than 0.5 (range 0.9 – 3.61) [7]. This suggests

that glomerulopathy may be related to the primary cause of

panniculitis. In the same study, 8 of the 14 dogs (57%) had chronic

kidney disease caused by protein–losing nephropathy. In human

medicine, it is believed that this association is due to the leakage of

oxidized lipids, leading to inammation and brosis, or to immune

complex–mediated glomerulonephritis.

In the previously mentioned study, 21.4% of dogs were found to

have adrenomegaly without any suspected functional adrenal disease

[7]. In this patient, despite clinical and paraclinical suspicion, as

well as ultrasound ndings consistent with hyperadrenocorticism,

the comorbidity with panniculitis pancreatic biased the correct

diagnosis and increased the probability of a false positive HAC case.

The lack of response to trilostane supports this hypothesis. It is

worth noting that in this case, the low–dose suppression test with

dexamethasone led to a false–positive result, highlighting the need

to apply the ACVIM consensus about HAC to minimize the possibility

of ambiguous results. The sensitivity and specicity of the test have

been estimated to be between 85–100% and 44–73%, respectively [15].

Spinal cord compression caused by idiopathic sterile

pyogranulomatous inammation of the epidural fat has been found

in Dachshunds. This condition can lead to paraparesis or paraplegia

in these dogs even though there may not be any obvious radiographic

abnormalities. Evidence of extradural compression has been found

in myelography [16]. The origin of the spinal cord trauma could not

be identied in this case. It could be associated with Acute Non–

degenerated Nucleus Pulposus Extrusion (ANNPE) or Hydrated

Nucleus Pulposus compressive Extrusion (HNPE). Alternatively, it

could be due to a brocartilaginous embolism [17]. However, a more

precise diagnosis cannot be made without MRI data.

Regarding the treatment of panniculitis, previous studies have

shown that a single administration of antibiotics does not result in

a permanent improvement of cutaneous signs [7, 12, 18]. Therefore,

immunosuppression (using glucocorticoids, azathioprine, or

cyclosporine) is often used as an additional part of the treatment

for pancreatic panniculitis [1, 2, 3, 4, 5, 7, 18]. In this particular case,

cyclosporine was chosen as the immunosuppressive treatment after

gradually reducing trilostane, having ruled out hyperadrenocorticism.

Additionally, the use of corticosteroids is controversial as it may

potentially cause chronic pancreatitis, which is why it was not

prescribed [19]. According to a report by O’Kell et al. (2010), one case

achieved the therapeutic success of pancreatic panniculitis once

pancreatitis was treated, while seven of eight patients treated with

corticosteroids showed improvement [7].

It has been reported that pancreatic panniculitis has responded

well to a combination of oral tetracycline and niacinamide. This

treatment appears to have an immune–mediated effect, although

the exact mechanism is not yet fully understood [2, 4]. Some studies

suggest that the combination of tetracycline and niacinamide may

suppress leukocyte chemotaxis and leukocyte protease release,

which are caused by complement activation from antigen–antibody

complexes [20]. Tetracyclines have also been used to treat alpha–1

antitrypsin deciency related to panniculitis in human medicine [21].

It is believed that this is due to the potential collagenase–inhibitory

effect of tetracyclines. In this particular case, doxycycline was chosen

due to its ecacy against common Gram–positive skin bacteria

(such as Staphylococcus spp., including methicillin–resistant S., and

Streptococcus spp.), and its potential immunomodulatory effects

when combined with niacinamide [20].

The selection of ciclosporin as an immunosuppressant for

this case was due to its effect on reducing the proliferation of T

lymphocytes. This is achieved through blocking the transcription

of cytokines, particularly IL–2. Additionally, ciclosporin has anti–

inammatory and cytostatic effects on leukocytes, Langerhans cells,

and keratinocytes [20].

CONCLUSIONS

In conclusion, pancreatic panniculitis is a condition that is not

well–known in dogs. The case study presented here is of a canine

with chronic pancreatic panniculitis who partially responded to

immunosuppressive therapy but developed severe glomerulopathy

and spinal cord trauma. It is suspected that there may be a link

between panniculitis and glomerulopathy and/or spinal cord trauma.

Conict of interest

The case report was conducted without any potential conict

of interest.

Role of the authors

PB: case analysis, methodology, research, writing, reviewing and

editing. IC: case analysis, methodology and reviewing. The authors

declare that no ethical or legal standards were omitted in this research.

BIBLIOGRAPHIC REFERENCES

[1] Mellanby RJ, Stell A, Baines E, Chantrey JC, Herrtage ME.

Panniculitis associated with pancreatitis in a cocker spaniel.

J. Small Anim. Pract. [Internet] 2003; 44(1):24–28. doi: https://

doi.org/dk4vm4

Pancreatic panniculitis and glomerulopathy in a dog / Bermúdez and Castellanos _________________________________________________

6 of 6

[2] Helton Rhodes K. Chapter 19 – Panniculitis. In: Helton Rhodes

K, Werner A, editors. Blackwell’s Five–minute veterinary consult

clinical companion: small animal dermatology. 2

ed. West

Sussex (UK): John Wiley & Son; 2018. p. 197–202.

[3] Torres SM. Sterile nodular dermatitis in dogs. Vet. Clin. North

Am. Small Anim. Pract [Internet]. 1999; 29(6):1311–1323. doi:

https://doi.org/g8vnkh

[4] German AJ, Foster AP, Holden D, Hotston–Moore A, Day MJ,

Hall EJ. Sterile nodular panniculitis and pansteatitis in three

weimaraners. J. Small Anim. Pract. [Internet]. 2003; 44(10):449–

455. doi: https://doi.org/bwz9fc

[5] Harvey RG, McKeever PJ. Sección 2 – Dermatosis nodulares:

Paniculitis. In: Harvey RG, McKeever PJ, editors. Manual ilustrado

de enfermedades de la piel en perro y gato. Madrid (España):

Grass editions; 2006. p. 66–67.

[6] Mellor PJ, Fetz K, Maggi RG, Haugland S, Dunning M, Villiers

EJ, Mellanby RJ, Williams D, Breitschwerdt E, Herrtage ME.

Alpha1–proteinase inhibitor deciency and Bartonella infection

in association with panniculitis, polyarthritis, and meningitis in

a dog. J. Vet. Intern. Med. 2006; 20(4):1023–1028. doi: https://

doi.org/d2cq33

[7] O’Kell AL, Inteeworn N, Diaz SF, Saunders GK, Panciera DL. Canine

sterile nodular panniculitis: A retrospective study of 14 cases.

J. Vet. Intern. Med. [Internet]. 2010; 24(2):278–284. doi: https://

doi.org/d3xvc9

[8] Yamagishi C, Momoi Y, Kobayashi T, Ide K, Ohno K, Tsujimoto

H, Iwasaki T. A retrospective study and gene analysis of canine

sterile panniculitis. J. Vet. Med. Sci. [Internet]. 2007; 69(9):915–

924. doi: https://doi.org/bqjnnz

[9] Gear RNA, Bacon NJ, Langley–Hobbs S, Watson PJ, Woodger

N, Herrtage ME. Panniculitis, polyarthritis and osteomyelitis

associated with pancreatic neoplasia in two dogs. J. Small Anim.

Pract. [Internet]. 2006; 47(7):400–404. doi: https://doi.org/

bzmt67

[10] Moreau PM, Fiske RA, Lees GE, Corrier DE. Disseminated

necrotizing panniculitis and pancreatic nodular hyperplasia

in a dog. J. Am. Vet. Med. Assoc. [Internet]. 1982 [cited 6 Aug.

2024]; 180(4):422–425. PMID: 7061328. Available in: https://

goo.su/Vd0AH

[11] Kunovsky L, Dite P, Brezinova E, Sedlakova L, Trna J, Jabandziev

P. Skin manifestations of pancreatic diseases. Biomed Pap

.[Internet]. 2022; 166(4):353–358. doi: https://doi.org/g8vnkj

[12] Brown PJ, Mason KV, Merrett DJ, Mirchandani S, Miller RI.

Multifocal necrotizing steatites associated with pancreatic

carcinoma in three dogs. J. Small Anim. Pract. [Internet]. 1994;

35(3):129–132. doi: https://doi.org/f4xr

[13] Hughes D, Goldschmidt MH, Washabau RJ, Kueppers F. Serum

alpha 1–antitrypsin concentration in dogs with panniculitis. J.

Am. Vet. Med. Assoc. [Internet]. 1996; 209(9):1582–1584. doi:

https://doi.org/nw2c

[14] Malik R, Love DN, Wigney DI, Martin P. Mycobacterial nodular

granulomas affecting the subcutis and skin of dogs (canine

leproid granuloma syndrome). Aust. Vet. J. [Internet]. 1998;

76(6):403–407. doi: https://doi.org/b95dzv

[15] Behrend EN, Kooistra HS, Nelson R, Reusch CE, Scott–Moncrieff

JC. Diagnosis of spontaneous canine hyperadrenocorticism:

2012 ACVIM Consensus Statement (Small Animal). J. Vet. Intern.

Med. [Internet]. 2013; 27(6):1292–1304. doi: https://doi.org/

f5htt3

[16] Aikawa T, Yoshigae Y, Kanazono S. Epidural idiopathic

sterile pyogranulomatous inammation causing spinal cord

compressive injury in ve miniature Dachshunds. Vet. Surg.

[Internet]. 2008; 37(6):594–601. doi: https://doi.org/dpbshq

[17] De Decker S, Fenn J. Acute herniation of nondegenerate nucleus

pulposus. Vet. Clin. North Am. Small Anim. Pract. [Internet].

2018; 48(1):95–109. doi: https://doi.org/g8vnkk

[18] Post K. Nodular panniculitis in a female toy poodle. Can. Vet. J.

[Internet]. 1983 [cited 6 Aug. 2024]; 24(5):152–153. Available in:

https://goo.su/1ca6ALI

[19] Mansfield C. Acute pancreatitis in dogs: Advances in

understanding, diagnostics, and treatment. Top. Companion

Anim. Med. [Internet]. 2012; 27(3):123–132. doi: https://doi.org/

f4f39s

[20] Koch SN, Torres SMF, Plumb DC. Canine and feline dermatology

drug handbook. Iowa (USA): John Wiley & Sons. 2013. Section

1, Systemic drugs; p 76–201.

[21] Humbert P, Faivre B, Gibey R, Agache P. Use of anti–collagenase

properties of doxycycline in the treatment of alpha 1–antitrypsin

deciency panniculitis. Acta Derm. Venereol. 1991; 71(3):189–194.

PMID: 1678218