Lymphocytic Inflammation of the Liver
Does anyone have any information regarding lymphocytic inflammation located in the liver (causes, treatment, etc.)?
Rodney (DOB: 5/5/2013) is an albino MF gib. In December 2015, he presented with lethargy and was vetted. At December 1, 2015 visit, his bloodwork was as follows:
Vetscan Comprehensive Mammal (1+ lipemia, other quality control parameters WNL): ALB 3.8, ALP
48, ALT 483 (65-346), AMY 27, TBILI 0.3, BUN 25, Ca++ 8.8, PHOS 5.2, CRE 0.9 (0.2-0.7), GLU 105,
Na+ 148, K+ 5.0, TP 6.3, GLOB 2.5
Rodney went home that day with a trial of Baytril. Follow up bloodwork 3 weeks later showed one enzyme had slightly decreased and the other had no change. We proceeded and he seemed to stabilize. In June of 2016, he received a Lupron injection for sexual aggression, with no new coat changes. In August, he received his first Des implant. 5 days following the implant, he was lethargic, nauseated with tooth grinding, and anorexia. He was admitted into the hospital after radiographs showed abnormal gas pattern suggesting non-obstructed foreign object (ulcer). We continued that day with a barium radiograph, where barium lingered within the stomach until radiographs were repeated the following morning. Radiographs also suggested left ventricular enlargement within the heart. Rodney was sent home with Famotidine and an appointment the next week for cardiac and abdominal US.
During US, Rodney went into respiratory arrest and was resuscitated using flumazenil IM and exhibited arrhythmia and brief bradycardia. US results are as follows:
Formal report: There is mild IV septal thickness upper normal limits, this and other mild changes
suggest early onset cardiomyopathy; repeat ultrasound is recommended in 6 months. No pericardial or
There are no abnormalities of the liver noted.
Review of radiographs: slight enlargement of cardiac silhouette and rounding of the apex.
Following the US, Rodney continued to expressed lethargy, nausea, and anorexia. Less than a week after the US, Rodney went back to his vet clinic. We drew more blood. Bloodwork concluded that his liver enzyme levels had spiked more than 200 points since the last. Those results from 8.26.2016 are as follows:
Vetscan Comprehensive Mammal panel: ALB 4.2, ALP 81(8-72), ALT 671 (65-346), AMY 17, TBIL 0.3,
BUN 12, CA 9.8, PHOS 3.3 (3.6-7.3), CRE 0.4, GLU 87, NA 149, K 4.5, TP 7.2, GLOB 2.9
QC Hem 2+
Our PVC is 58%, TP of 6.6%
Following this appointment, Rodney was placed on a 2-week trial of Amoxicillin and Metro for possible bacterial hepatitis. Recheck bloodwork was completed at the end of the trial. Those results from 9.7.2016 are as follows:
Vetscan Comprehensive Mammal panel: ALB 3.7, ALP 76(8-72), ALT 874 (65-346), AMY 28, TBIL 0.3, BUN 23, CA 9.4, PHOS 4.7 (3.6-7.3), CRE 0.9, GLU 82, NA 152, K 4.6, TP 6.9, GLOB 3.2
After this bloodwork, I suggested we sent off CBC to Antech and send urine sample for UA due to creatinine level increase. Antech CBC taken on 9.14.2016 is as follows:
Complete Blood Count Verified on:09/15/16
Test Results Meter Normals Test Results Meter Normals
WBC 10-3/uL 4.9 |-*---| 3.0 - 9.0 Hets/Neuts % 58 |---*-| 11 – 82
RBC 10-6/uL 6.28 |-*---| 4.5 - 9.5 Abs.# / uL 2842
PCV % 55 |---*-| 40 - 59 Lymphocytes % 40 |-*---| 25 – 65
Buffy Coat % 0 |*----| 0 - 0.5 Abs.# / uL 1960
MCV fl 88 Basophils % 2 |---*-| 0 – 3
HGB g/dL 17.0 |---*-| 13.5 - 18.0 Abs.# / uL 98
MCHC g/dL 30.9 Eosinophils % 0 |*----| 0 – 5
Total Protein 8.4 |-----|* 5.0 - 7.0 Abs.# / uL 0
NRBC /100 WBC 0 |---*-| 0 - 0 Monocytes % 0 |*----| 0 – 4
Polychromasia Normal Normal - Abs.# / uL 0
Anisocytosis Normal Normal - Azurophils % N/A |*----| 0 – 0
Parasites P.O.F. Not Seen |---*-| 0 - 0 Abs.# / uL N/A
Parasite Type N/A N/A - Thrombos/Plats Present
HCT Plasma /
Serum Condition Sl-Hmls
Urinalysis: Specific gravity is 1.032; trace protein, pH is 6.5, negative for blood, ketones. Scant positive bilirubin.
After all of the continued testing, I decided to get Rodney healthy before considering biopsy. I began with 4x daily soup and he began to feel better and gain weight. We also added a liver supplement per vet instruction (lactulose, dandelion root, and milk thistle). However, in December 2016, he began experiencing more lethargy and occasional tooth grinding -- I administered Pepto Bismol until his appointment a couple of days later. We did another blood panel. The blood panel concluded that while ALT levels had decreased, only very slightly.
He underwent Liver biopsy January 19, 2017. A week later, his histopathology results were back and are as follows:
LIVER: MODERATE TO SEVERE LYMPHOCYTIC CHOLANGITIS, SEE COMMENT COMMENT The cell population within the portal triads and extending along portal tracts is a fairly uniform population of small well-differentiated lymphocytes. Few other cell populations are recognized. No significant effacement of the hepatic architecture is recognized. Even without the effacement, I would still consider that this might be an early lesion of lymphoma based on the monomorphic population of cells. Systemic evaluation is suggested. It is also possible to consider immunohistochemistry to classify the lymphocytes (mixed population is probably inflammation, one cell line is neoplastic).
The pathologist suggested an immunochemistry stain to determine whether it was in fact lymphoma or lymphocytic inflammation. Fast forward 5 weeks for wait time on pricing and on test results -- results do not support lymphoma but rather lymphocytic inflammation. My exotic vet is currently researching treatment and other information. I would appreciate any ideas from the veterinarians and experienced ferret researchers here.
Also note: After implanting with Des, it took approx. 3 months for sexual behaviors to decrease. However, I am already noticing sexual drive increase. No hair loss still. He has also had 3 random occasions of vomiting between roughly December 2016 to March 2017.
- I only just saw this. The anorexia and teeth grinding do suggest ulcer to me. You might try treating for 4 weeks instead of two. I would give carafate suspension 3x day on an empty stomach at least 20 min before ulcer meds.
I would also avoid pepto bismol as the salicylates it contains could exacerbate an ulcer situation. If giving flagyl is difficult, switch to clarithromycin (Biaxin). It's actually not expensive if you get it thru a human pharmacy and have them apply a discount code.
I would also consider treating for IBD. Start with switching to a novel protein since you wouldn't want to start immunosuppressants til you've ruled out infectious agents.
Not a vet, just a tech and ferret caregiver for ~20 yrs. And apparently a magnet for ferrets with GI disease....
Sent from my iPhone
> On Mar 6, 2017, at 12:33 AM, jazzy_cat_2002@... [ferrethealth] <firstname.lastname@example.org> wrote:
- Thanks for responding. The post was really about the lymphocytic inflammation as I have never heard of it before. However, my vet has since put him on a trial of high dose prednisolone, and also a 2 week run of Helicobacter treatment to avoid a flare up. He just had his post 2-week recheck bloodwork to determine if pred was working. It is!
His ALP is normal now, ALT down to 480 from the 759 it was in December, and Creatnine is .2 instead of .9. She has lowered his pred dose by half but suspects he will be on pred for the remainder of his life.
Interesting about the Pepto. They have never offered Carafate, even when I have asked for it when he did seemingly have an ulcer. He has began doing the chewing/grinding motion again, even throughout the recent Helicobacter prevention treatment that which did also include a 2x daily dose of Pepto with the other meds. Hmmmm.... He is only doing it when he wakes up, I've noticed.
He is off the Helicobacter and Pepto regimen. So, I will continue to monitor this chewing behavior and talk with his doc if it continues. We have another recheck in a month to see if his ALT drops back into normal range and probably lower pred again if the numbers suggest we can. --------------------------------------------
- Quoting Dr. Bruce Williams, a ferret pathology expert (with his
Probably the most common misinterpretation that I see on a routine
basis is in the area of hepatic enzymes. Remember, that the ferret,
being by nature an obligate carnivore, has an extremely short digestive
tract, and requires meals as often as every four to six hours. Should
food not be available, it possesses the ability to quickly mobilize
peripheral fat stores in order to meet energy requirements. When this
physiologic mechanism is activated, the liver is literally flooded with
fat, which results in hepatocellular swelling which may be marked. The
result of this swelling is the leakage of membrane enzymes such as
alanine aminotransferase, and as the hepatocellular swelling increases,
occlusion of bile canaliculi occurs, resulting, over time, in elevation
of alkaline phosphatase.
In conjunction with this physiologic change, elevations of ALT up to
800 mg/dl can be seen, and alkaline phosphatase up to approximately
100 mg/dl. This often causes confusion to practitioners, who render an
erroneous diagnosis of unspecified hepatic disease. However, hepatic
disease is quite uncommon in this species; the most common cause of
true hepatic disease in the ferret is neoplasia, with lymphosarcoma
causing 95% of cases. Rarely bacterial infections of the liver or
biliary tree may be seen.
The diagnosis of hepatic disease in the ferret must be based not only
on ALT and alkaline phosphatase, but other clinical indicators in the
CBC and chem panel. Clinical elevation of icterus or an elevated
bilirubin is an excellent indicatior of primary hepatic disease, or
concomitant leukocytosis or pyrexia may lend additional credence to
a diagnosis of primary hepatic disease.
END QUOTED SECTION
Dr. Bruce Williams is a ferret veterinary pathology expert, one of the
Sent from my iPad
- Interesting information. Rodney has access to food at all times. Even when we first saw the spike in ALT, he was in relatively good health besides a sudden onset of minor lethargy. His eating habits then were great. It was only after his Des implant this past August that I noticed any sign of nausea and anorexia.
He was put on meds and a 4x daily soup schedule with kibble mix left out for him at all times (as usual). He had not experienced any other poor eating habits since then and, yet, ALT continued to rise. We sent biopsy sample to not one, but two labs. One for preliminary results and the second for the stain. And with treatment working, I am inclined to believe we are on track.
I will share this with his vet. While I do understand that vets don't always get it right, I am at least taking my ferrets to the only biard certified exotic specialist in Indiana. She has not lead me wrong thus far. But, outside information is always good for vets to read. --------------------------------------------