BackgroundLow-grade alimentary lymphoma (LGAL) is characterised by the infiltration of neoplastic T-lymphocytes, typically in the small intestine. The incidence of LGAL has increased over the last ten years and it is now the most frequent digestive neoplasia in cats and comprises 60 to 75% of gastrointestinal lymphoma cases. Given that LGAL shares common clinical, paraclinical and ultrasonographic features with inflammatory bowel diseases, establishing a diagnosis is challenging. A review was designed to summarise current knowledge of the pathogenesis, diagnosis, prognosis and treatment of feline LGAL. Electronic searches of PubMed and Science Direct were carried out without date or language restrictions.ResultsA total of 176 peer-reviewed documents were identified and most of which were published in the last twenty years. 130 studies were found from the veterinary literature and 46 from the human medicine literature. Heterogeneity of study designs and outcome measures made meta-analysis inappropriate. The pathophysiology of feline LGAL still needs to be elucidated, not least the putative roles of infectious agents, environmental factors as well as genetic events. The most common therapeutic strategy is combination treatment with prednisolone and chlorambucil, and prolonged remission can often be achieved. Developments in immunohistochemical analysis and clonality testing have improved the confidence of clinicians in obtaining a correct diagnosis between LGAL and IBD. The condition shares similarities with some diseases in humans, especially human indolent T-cell lymphoproliferative disorder of the gastrointestinal tract.ConclusionsThe pathophysiology of feline LGAL still needs to be elucidated and prospective studies as well as standardisation of therapeutic strategies are needed. A combination of conventional histopathology and immunohistochemistry remains the current gold-standard test, but clinicians should be cautious about reclassifying cats previously diagnosed with IBD to lymphoma on the basis of clonality testing. Importantly, feline LGAL could be considered to be a potential animal model for indolent digestive T-cell lymphoproliferative disorder, a rare condition in human medicine.

Background Differentiation of low‐grade intestinal T‐cell lymphoma (LGITL) from lymphoplasmacytic enteritis (LPE) in cats is a diagnostic challenge for pathologists. Objective Characterize histologic, immunohistochemical, and molecular features of LGITL and LPE. Animals Forty‐four client‐owned cats, 22 diagnosed with LGITL and 22 with LPE. Methods Prospective, cohort study. Clinical suspicion of LGITL or LPE was based on persistent gastrointestinal signs, unresponsive to empirical treatments. All cats underwent a standardized diagnostic evaluation, including biopsy (preferentially full‐thickness), and were diagnosed with LGITL or LPE after review of clinical, laboratory, sonographic, histologic, immunohistochemical, and clonality results. Results A monomorphic lymphocytic population (22/22, 100%) and in‐depth mucosal infiltration (15/22, 68%) were hallmarks of LGITL. Epithelial patterns (nests and plaques) were significantly more frequent in LGITL (11/22, 50%) than in LPE (1/22, 5%) cases (P = .001). A CD3+ lymphocytic apical‐to‐basal gradient was observed in 9/22 (41%) of LGITL vs 1/22 (5%) of LPE cases (P = .004). Most LPE cases (17/18, 94%) featured marked fibrosis in the superficial part of the lamina propria. The Ki‐67 20%‐ and 30%‐thresholds discriminated between LGITL and LPE within both the epithelium (specificity >95%) and lamina propria (specificity >95%), respectively. All LGITL cases were CD3+ pSTAT3− and pSTAT5+. T‐cell receptor gamma chain gene rearrangements indicated monoclonality in 86% of LGITL cases. Surprisingly, 70% of LPE cases featured monoclonality (40%) or monoclonality on a polyclonal background (30%). Conclusions and Clinical Importance We identified new histologic, immunohistochemical, and clonality criteria to distinguish LGITL from LPE.

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Background Low‐grade intestinal T‐cell lymphoma (LGITL) is the most common intestinal neoplasm in cats. Differentiating LGITL from lymphoplasmacytic enteritis (LPE) is challenging because clinical signs, laboratory results, diagnostic imaging findings, histology, immunohistochemistry, and clonality features may overlap. Objectives To evaluate possible discriminatory clinical, laboratory and ultrasonographic features to differentiate LGITL from LPE. Animals Twenty‐two cats diagnosed with LGITL and 22 cats with LPE based upon histology, immunohistochemistry, and lymphoid clonality. Methods Prospective, cohort study. Cats presented with clinical signs consistent with LGITL or LPE were enrolled prospectively. All data contributing to the diagnostic evaluation was recorded. Results A 3‐variable model (P < .001) consisting of male sex (P = .01), duration of clinical signs (P = .01), and polyphagia (P = .03) and a 2‐variable model (P < .001) including a rounded jejunal lymph node (P < .001) and ultrasonographic abdominal effusion (P = .04) were both helpful to differentiate LGITL from LPE. Conclusions and Clinical Importance Most clinical signs and laboratory results are similar between cats diagnosed with LGITL and LPE. However, male sex, a longer duration of clinical signs and polyphagia might help clinicians distinguish LGITL from LPE. On ultrasonography, a rounded jejunal lymph node, and the presence of (albeit small volume) abdominal effusion tended to be more prevalent in cats with LGITL. However, a definitive diagnosis requires comprehensive histopathologic and phenotypic assessment.

Objectives The first aim of this survey was to report client experiences associated with the administration of common medications, particularly glucocorticoids and bronchodilators, in managing cats with feline lower airway disease (FLAD). The second aim was to ascertain client perception of response to treatment and level of satisfaction. Methods This was a prospective cross-sectional study. An online survey was distributed worldwide to cat owners caring for cats with a chronic cough. Only cats reported to have FLAD were included. Results A total of 153 complete responses describing cats with FLAD were analyzed. Glucocorticoids and bronchodilators were the predominantly prescribed therapeutics for 140/153 (92%) and 80/153 (52%) of FLAD cats, respectively. Oral and inhalant administration routes were reported most commonly: glucocorticoids (64% oral and 75% inhalant) and bronchodilators (21% oral and 88% inhalant). A review of how air quality could be improved was conducted for 54% of cats. Almost half (43%) of owners reported adverse effects secondary to glucocorticoid administration, the most frequent being polyphagia (26%) and polydipsia (21%). Only 10% of owners reported bronchodilator-associated side effects, with restlessness (9%) being the most common. Difficulties giving glucocorticoid or bronchodilator tablets orally were reported for 33% and 71% of owners, respectively. Glucocorticoid or bronchodilator inhalant therapies were difficult to administer for 28% and 31% of owners, respectively. Frequency and severity of coughing were significantly lower after at least 2 months of treatment, with median numerical input on a slider scale (0–100) of 48 and 42 before, and 10 and 7 after treatment, respectively ( P <0.0001). Median numerical input of owner satisfaction was 83%. Conclusions and relevance Despite significant improvements in client-reported responses to treatment, challenges associated with the administration of medications and their adverse effects still exist. Promoting awareness of client experiences can facilitate appropriate follow-up, guidance and empathy to further optimize outcomes.

Case summary A 7-month-old intact female Maine Coon cat was presented with a 2-month history of regurgitations. Contrast radiographic and endoscopic examinations revealed a diffuse megaoesophagus secondary to a severe lower oesophageal stricture. An epiphrenic diverticulum was noted. Endoscopic balloon dilation was unsuccessful. Gastrotomy was thus performed in order to incise the oesophageal wall radially along the stricture site, and then to dilate the stricture. A diameter of 20 mm was reached. With the aim of preventing stricture recurrence, submucosal injections of triamcinolone acetonide were performed. An 18 Fr oesophagogastric feeding tube was placed and a left gastropexy was performed in order to exert some traction on the gastroesophageal junction, with the aim of reducing the oesophageal diverticulum. Twelve months postoperatively, clinical signs had completely resolved and follow-up radiographs revealed marked improvement of the oesophageal dilatation. Relevance and novel information Lower oesophageal strictures should be considered when evaluating regurgitations or megaoesophagus in a kitten. Surgical mucosal radial incision is a therapeutic option in cases of lower oesophageal stricture refractory to balloon dilation, and can lead to a marked improvement of clinical signs and of the oesophagus diameter leading to clinical success.

A 7‐year‐old, neutered, male miniature pinscher was presented with a 36‐hour history of acute life‐threatening haematochezia and severe anaemia (haematocrit 4.9%). A diagnosis of acquired colonic vascular ectasia was ultimately made from the characteristic gross morphologic vascular abnormalities visualised during colonoscopy. A combination ethinyl estradiol and norethindrone acetate tablet was prescribed. On recheck 6 weeks after starting hormone therapy, the patient had not had haematochezia for the previous 4 weeks (haematocrit 34%). On the recheck visit 12 months after starting hormone therapy, haematocrit was within reference range (50%) and the patient had not had diarrhoea or haematochezia for the preceding 9 months. This is the first case report describing a successful medical management of an acute haemorrhagic crisis related to acquired colonic vascular ectasia without endoscopic‐assisted argon therapy or colectomy.

A 6-year-old castrated male Labradoodle was referred in uncompensated hypovolemic shock, with a 72-h history of lethargy, vomiting and diarrhea that had acutely worsened with subsequent development of profuse hemorrhagic diarrhea in the last 24 h after a visit to the groomer. In most respects this case was classic for a patient with a primary hypoadrenocortical crisis. After initial attempts to address hypovolemia and refractory hypotension, no clinical improvement was seen, and the respiratory rate had increased acutely to 80 bpm with crackles detected on thoracic auscultation and serosanguineous fluid began draining from the nose and mouth. An arterial blood gas sample while breathing room air revealed moderate hypoxemia (PaO2 59.9: RI 95–100 mmHg), an elevated alveolar-arterial (A-a) gradient at 54.7 (RI &lt; 15 mmHg) and a PaO2:FiO2 ratio of 285 mmHg. Thoracic radiographs revealed severe bilateral alveolar lung pattern largely limited to the perihilar and caudodorsal lung fields. The radiographic findings, along with signs of ongoing hypovolemia, the lack of evidence of typical long-standing acquired cardiac disease, and the rapid resolution of the pulmonary edema without the need for diuretics or long-term cardiac medications supported non-cardiogenic pulmonary edema. The proposed cause of the non-cardiogenic pulmonary edema was speculated to be neurogenically mediated. Oxygen supplementation along with mineralocorticoid and glucocorticoid replacement therapy was sufficient for the management of the non-cardiogenic pulmonary edema in this case.