Page 1215 - Cote clinical veterinary advisor dogs and cats 4th

Lymphoma, Gastrointestinal 605

RISK FACTORS Etiology and Pathophysiology ○ Hypocobalaminemia is associated with
feline GI LSA
Cause of most cases of GI LSA is unknown. Most lymphomas are thought to arise from • Three-view thoracic radiographs to look for
VetBooks.ir • Epidemiologic studies implicate exposure to events, which may be random or induced by • Abdominal ultrasonography with guided Diseases and Disorders
abnormal somatic cell DNA recombination
• Chronic inflammatory bowel disease (IBD
[p. 543]) is a predisposing factor.
metastasis
retroviral infection, environmental carcinogen
phenoxy herbicides (2,4-D) and environmen-
tal cigarette smoke in lymphomagenesis. exposure, or chronic infection/inflammation fine-needle aspiration cytology of thickened
that increases lymphoid cell population
bowel and/or enlarged lymph nodes (p. 1112)
• Helicobacter pylori infection is implicated in expansion. ○ Normal bowel wall thickness (dog, cat)
human GI LSA, but that association has <5 mm
not been firmly established in veterinary DIAGNOSIS ○ Any layer may be thickened; thickening
medicine. may be focal or diffuse (diffuse more
• Underlying immune disorders may predis- Diagnostic Overview common), and mesenteric lymphadeno-
pose. • The diagnosis is suspected in a patient with megaly is common but not specific to
persistent vomiting, diarrhea, systemic signs lymphoma. Intestinal mural layering is
CONTAGION AND ZOONOSIS such as weight loss, or some combination of commonly preserved with diffuse disease.
No infectious or zoonotic cause is known in these. Suspicion increases when abdominal ○ Thickened small intestinal wall and mus-
dogs. In cats, retroviral infection with FeLV ultrasound reveals gastric or intestinal cularis propria layer is commonly observed
and/or feline immunodeficiency virus (FIV) is wall thickening, GI masses or mesenteric in cats with small cell GI T-cell lymphoma;
rarely associated with GI lymphoma. lymphadenomegaly. these changes are also common in cats
• Confirmation requires cytology or biopsy; with IBD.
ASSOCIATED DISORDERS endoscopic biopsies are less invasive but
• Anemia and panhypoproteinemia may occur may be insufficient; full-thickness biopsies Advanced or Confirmatory Testing
secondary to chronic GI blood loss. are the gold standard but require laparoscopy • Biopsy of gastric, duodenal, or colorectal
• Hypercalcemia may be associated with canine or laparotomy. lesions to make the diagnosis by histopatho-
GI LSA, but it is rare in cats. • Interpretation of histologic features in some logic tissue exam
• LSA metastatic to the liver may be associated cases is difficult and may require advanced ○ Endoscopy is less invasive and therefore
with biliary obstruction. staining or other techniques such as poly- generally preferred to surgical biopsy
merase chain reaction for antigen receptor (p. 1098).
Clinical Presentation rearrangement (PARR), with some samples ○ Surgical full-thickness biopsy may be
DISEASE FORMS/SUBTYPES remaining permanently ambiguous. necessary for LSA in the deeper layers of
• GI LSA may be of the B-cell, T-cell, or large the GI tract or in portions of the intestine
granular lymphocyte (LGL) type. LGL LSA Differential Diagnosis not reached by endoscopy (jejunum).
typically has a T-cell origin, although it can Depends on the form and location of the LSA ○ Avoid full-thickness biopsy of the colon.
be a null cell phenotype of natural killer lesion(s): • Tumor staging for extent of systemic
(NK) cells. • IBD involvement:
• Lesions may be focal masses or diffusely • Chronic endoparasitism ○ Bone marrow cytology for staging and/
infiltrative throughout the gut. • GI foreign body or intussusception or as indicated by cytopenias (p. 1068)
• Lesions may be submucosal, epitheliotropic, • Chronic pancreatitis (especially cats) ○ Peripheral node aspiration or biopsy for
or transmural. • Other causes of liver disease such as hepatitis, staging and/or as indicated for lymphad-
• GI LSA may be a low-grade disease of cholangiohepatitis, toxic hepatopathy, or enomegaly
cellular accumulation due to impaired feline hepatic lipidosis • Immunohistochemical phenotyping for
apoptosis, as in human MALT lymphoma, • Benign GI disease such as gastric ulcer, polyp, B-cell, T-cell, or LGL subtypes
or may be high-grade disease with rapid cell or adenoma ○ CD3 for T-cell subset
replication. • Other GI tumors, including mast cell ○ CD79a or CD20 for B-cell disease
disease, adenocarcinoma, and mesenchymal ○ CD3 and CD57 for LGL subtype
HISTORY, CHIEF COMPLAINT tumors ○ PARR for monoclonality by B-cell (immu-
• GI LSA is associated with GI signs: • Granulomatous enteritis secondary to bacte- noglobulin gene rearrangement) or T-cell
○ Evidence of malassimilation such as weight rial, fungal, algal, or oomycotic infection (T-cell receptor gene rearrangement) clonal
loss (p. 395) expansion rather than polyclonal lesions
○ Anorexia seen in lymphoplasmacytic enteritis
○ Vomiting and/or diarrhea, often chronic Initial Database
○ Melena, hematemesis, hematochezia • Minimum database: CBC, serum chemistry TREATMENT
• Polyuria/polydipsia if hypercalcemia present panel, urinalysis, fecal exam for parasites,
Giardia antigen test, T 4 assay (cats), FeLV/ Treatment Overview
PHYSICAL EXAM FINDINGS FIV tests (cats) • It is extremely unlikely that dogs and cats
• Poor body condition and ill-kempt appear- ○ Normal, or can find evidence of GI with diffuse, nodal, or visceral organ involve-
ance, especially cats bleeding (e.g., anemia, hypoproteinemia, ment can be cured.
• Palpable abdominal mass(es) and intra- increased blood urea nitrogen [BUN]) or • For most cases, the goal is to prolong life
abdominal lymphadenomegaly hepatopathy (e.g., increased liver enzymes, with good quality while avoiding adverse
• With diffuse intestinal infiltration, turgid, hyperbilirubinemia) effects of therapy.
thickened intestinal walls often palpable ○ These tests are important to rule out • Focal GI LSA lesions can be surgically
• Signs of anemia (e.g., pallor, lethargy, alternative diagnoses, including parasitism, cured by excision with complete margins if
tachycardia) or hypercalcemia (e.g., muscle before undertaking more invasive tests neoplastic cells have not disseminated.
weakness) may be evident. (i.e., biopsy).
• Hepatosplenomegaly may be present. • Evaluation for chronic pancreatic or GI Acute General Treatment
• Rectal exam may reveal melena, hematoche- disease (trypsin-like immunoreactivity General supportive care:
zia, or abnormal rectal mucosa. [TLI], cobalamin/folate, or pancreatic lipase • Rehydration and restoring electrolyte
• Physical exam may be normal. immunoreactivity [PLI]) homeostasis

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