Chronic diarrhea secondary to canine leishmaniosis: Case series.

Chronic diarrhea is a clinical sign associated with canine leishmaniosis, varying from 3 % to 30 % of prevalence. However, its occurrence in dogs has been mostly associated with chronic kidney or liver disease. Leishmania organisms can cause inflammation of the digestive tract with chronic diarrhea as the only clinical manifestation, although it has been poorly documented in dogs. The aim of this retrospective observational study was to describe dogs with chronic diarrhea as the main clinical sign associated with leishmaniosis. All cases had a complete blood count, biochemistry, urinalyses, and diagnostic tests for leishmaniosis. Exclusion criteria included renal or hepatic disease and/or previous diagnosis of gastrointestinal disease. Twenty-three dogs were included. Small bowel diarrhea was present in 7/23 (30.4 %), large bowel diarrhea in 9/23 (39.2 %) and mixed diarrhea in 7/23 (30.4 %). Gastrointestinal biopsies were performed in 8/23 dogs and Leishmania amastigotes were found in all of them. In the others, leishmaniosis was diagnosed by serology in 10/15 dogs (66.7 %), serology plus blood PCR in 3/15 (20.0 %), lymph node cytology in 1/15 (6.7 %), and blood PCR in 1/15 (6.7 %). All dogs treated had a complete resolution of diarrhea with specific treatment for leishmaniosis alone, based on meglumine antimoniate (75-100 mg/kg SID SC for 1 month) plus allopurinol (10 mg/kg BID PO ≥ 6 months). This study suggests that leishmaniosis should be also included in the differential diagnosis of dogs from endemic areas presenting with the primary problem of large-bowel, small-bowel, or mixed-bowel chronic diarrhea.

Clinical findings, neurological manifestations and survival of dogs with insulinoma: 116 cases (2009-2020).

OBJECTIVES: To review the clinical findings and outcome in dogs diagnosed with insulinoma, and to assess which factors are predictors of overall survival. Additionally, to describe the neurological manifestations of this population and their correlation with survival. MATERIALS AND METHODS: Retrospective multicentric study of canine insulinoma cases (2009 to 2020). Signalment, clinical history, neurological examination, diagnostic findings, treatment and outcome were obtained from clinical records. Univariate and multivariate analyses were used to compare the overall survival. RESULTS: One hundred and sixteen cases were included. Median duration of clinical signs before presentation was 1.5 months. The most common presenting clinical signs were weakness (59.5%), epileptic seizures (33.6%) and changes in consciousness or behaviour (27.6%). Three dogs were suspected to have paroxysmal dyskinesia. Thirty-two dogs had an abnormal neurological examination, most commonly showing obtundation (28.1%), decreased withdrawal reflexes (21.9%) and absent menace response (18.8%). Overall survival for dogs undergoing surgery (20 months) was significantly longer than in medically treated (8 months; adjusted hazard ratio: 0.33; 95% confidence interval: 0.18, 0.59). Presence of metastases was the only other variable associated with prognosis (adjusted hazard ratio 1.72; 95% confidence interval: 1.02, 2.91). CLINICAL SIGNIFICANCE: Clinical signs of canine insulinoma are vague and non-specific. Weakness, epileptic seizures and changes in mentation or behaviour were the most commonly reported. Obtunded mentation and forebrain neurolocalisation were the main neurological manifestations. Dogs undergoing surgery had a longer overall survival compared to medically treated cases, and dogs with metastasis had a shorter overall survival regardless of treatment modality. Abnormalities in the neurological examination did not correlate with prognosis.

Role of adipocytokines in hepatic fibrosis.

Hepatic fibrosis is a dynamic process whereby the liver responds to conditions of persistent damage. This leads to deposition of fibrillar extracellular matrix, altered hepatocyte regeneration, deranged microvascular architecture and cirrhosis. Accumulating data demonstrate that obesity and insulin resistance are associated with a more severe and faster progression of the fibrogenic process indifferent chronic liver diseases, and attention has focused on possible links between the adipose tissue and liver repair.ADIPOCYTOKINEs are cytokines secreted primarily by adipose tissue, they are relevant for adipose tissue physiology and metabolism.Alterations in the adipocytokine pattern are involved in different obesity-related diseases, such as hypertension, atherosclerosis and type II diabetes mellitus (T2DM).Numerous recent studies have analyzed the role played by adipocytokines in the process of hepatic 'wound healing' and fibrogenesis. In particular, data have accumulated on the role of adiponectin and leptin. This review summarizes the more significant and recent findings concerning the role played by different adipocytokines in hepatic fibrogenesis, discussing the actions of adipocytokines on the biology of liver cells, and their effects in different animal models. The variations in the circulating levels and intrahepatic expression of different adipocytokines in patients with fibrogenic liver diseases are also discussed.

Review article: the pathogenesis of fibrosis in non-alcoholic steatohepatitis.

Non-alcoholic steatohepatitis has been recognized as a significant cause of end-stage liver disease and hepatic decompensation. Despite the growing interest in this condition, the molecular mechanisms underlying the development of fibrosis in this setting are only partially understood. In this article, the cellular and molecular basis of fibrosis in chronic liver disease are briefly outlined. In addition, mechanisms specifically operating in the context of fatty liver and steatohepatitis are examined, including: insulin resistance, oxidative stress, and inflammation. Finally, recent developments indicating the possible contribution of cytokines derived from adipose tissue (adipokines) to liver fibrosis is discussed.

Adipokines and liver fibrosis.

Liver fibrosis involves different cell types, and should be regarded as a "wound healing" response that occurres in conditions of chronic liver injury and is characterized by inflammation, activation of matrix-producing cells, matrix deposition and remodeling, and epithelial cell regeneration or an attempt thereof. Liver damage may be caused by several agents or conditions, resulting in different degrees and types of tissue inflammation and in activation of matrix-producing cells, such as the hepatic stellate cells (HSC). HSC undergo a phenotypic transition (known as "activation") to myofibroblast-like cells that synthesize different extracellular matrix components. Obesity is associated with the development of NASH, and has been indicated as an independent factor for the progression to fibrosis. In liver diseases, the biologic actions of the adipokines, such as leptin, adiponectin and resistin, released by adipocytes or locally produced by liver and/or inflammatory cells, may contribute to clarify the mechanisms of progression in NASH. The clinical and experimental findings accumulating on this class of molecules could represent the basis to devise a better management strategy for the patients with chronic liver disease.