Explore the vast range of titles available.

In a randomized trial, patients with acute pericarditis were assigned to either colchicine or placebo in addition to conventional antiinflammatory therapy. Colchicine significantly reduced the incidence of incessant or recurrent pericarditis. Colchicine has been used for centuries to treat and prevent gouty attacks 1 and more recently has been recommended to treat and prevent serositis in patients with familial Mediterranean fever and recurrent pericarditis. 2 , 3 Preliminary data from nonrandomized trials have also supported the use of colchicine for the treatment and prevention of acute pericarditis. 4 In a single-center, open-label, randomized trial, called the Colchicine for Acute Pericarditis (COPE) study, the addition of colchicine to conventional therapy with either aspirin or glucocorticoids halved the recurrence rate after an initial attack of acute pericarditis. 5 Our study, called the Investigation on Colchicine for Acute Pericarditis . . .

Colchicine is effective for the treatment of acute pericarditis and first recurrences. However, conclusive data are lacking for the efficacy and safety of colchicine for treatment of multiple recurrences of pericarditis. We did this multicentre, double-blind trial at four general hospitals in northern Italy. Adult patients with multiple recurrences of pericarditis (≥two) were randomly assigned (1:1) to placebo or colchicine (0·5 mg twice daily for 6 months for patients weighing more than 70 kg or 0·5 mg once daily for patients weighing 70 kg or less) in addition to conventional anti-inflammatory treatment with aspirin, ibuprofen, or indometacin. Permuted block randomisation (size four) was done with a central computer-based automated sequence. Patients and all investigators were masked to treatment allocation. The primary outcome was recurrent pericarditis in the intention-to-treat population. This trial is registered with ClinicalTrials.gov, number NCT00235079. 240 patients were enrolled and 120 were assigned to each group. The proportion of patients who had recurrent pericarditis was 26 (21·6%) of 120 in the colchicine group and 51 (42·5%) of 120 in the placebo group (relative risk 0·49; 95% CI 0·24–0·65; p=0·0009; number needed to treat 5). Adverse effects and discontinuation of study drug occurred in much the same proportions in each group. The most common adverse events were gastrointestinal intolerance (nine patients in the colchicine group vs nine in the placebo group) and hepatotoxicity (three vs one). No serious adverse events were reported. Colchicine added to conventional anti-inflammatory treatment significantly reduced the rate of subsequent recurrences of pericarditis in patients with multiple recurrences. Taken together with results from other randomised controlled trials, these findings suggest that colchicine should be probably regarded as a first-line treatment for either acute or recurrent pericarditis in the absence of contraindications or specific indications. Azienda Sanitaria 3 of Torino (now ASLTO2).

Amyloidosis is a group of protein-misfolding disorders characterized by the accumulation of amyloid in organs, both in humans and animals. AA-amyloidosis is considered a reactive type of amyloidosis and in humans is characterized by the deposition of AA-amyloid fibrils in one or more organs. In domestic shorthair cats, AA-amyloidosis was recently reported to be frequent in shelters. To better characterize this pathology, we report the distribution of amyloid deposits and associated histological lesions in the organs of shelter cats with systemic AA-amyloidosis. AA-amyloid deposits were identified with Congo Red staining and immunofluorescence. AA-amyloid deposits were then described and scored, and associated histological lesions were reported. Based on Congo Red staining and immunofluorescence nine shelter cats presented systemic AA-amyloidosis. The kidney (9/9), the spleen (8/8), the adrenal glands (8/8), the small intestine (7/7) and the liver (8/9) were the organs most involved by amyloid deposits, with multifocal to diffuse and from moderate to severe deposits, both in the organ parenchyma and/or in the vascular compartment. The lung (2/9) and the skin (1/8) were the least frequently involved organs and deposits were mainly focal to multifocal, mild, vascular and perivascular. Interestingly, among the organs with fibril deposition, the stomach (7/9), the gallbladder (6/6), the urinary bladder (3/9), and the heart (6/7) were reported for the first time in cats. All eye, brain and skeletal muscle samples had no amyloid deposits. An inflammatory condition was identified in 8/9 cats, with chronic enteritis and chronic nephritis being the most common. Except for secondary cell compression, other lesions were not associated to amyloid deposits. To conclude, this study gives new insights into the distribution of AA-amyloid deposits in cats. A concurrent chronic inflammation was present in almost all cases, possibly suggesting a relationship with AA-amyloidosis.

The spleen is one of the organs most commonly injured by blunt abdominal trauma. It plays an important role in immune response to infections, especially those sustained by encapsulated bacteria. Nonoperative management (NOM), comprising clinical and radiological observation with or without angioembolization, is the treatment of choice for traumatic splenic injury in patients who are hemodynamically stable. However, this strategy carries a risk of failure, especially for high-grade injuries. No clear predictors of failure have been identified, but minimally invasive surgery for splenic injury is gaining popularity. Laparoscopic surgery has been proposed as an alternative to open surgery for hemodynamically stable patients who require surgery, such as after failed NOM. We reviewed research articles on laparoscopic surgery for hemodynamically stable patients with splenic trauma to explore the current knowledge about this topic. After presenting an overview of the treatments for splenic trauma and the immunological function of the spleen, we try to identify the future indications for laparoscopic surgery in the era of NOM.

AA amyloidosis is a systemic disease characterized by deposition of misfolded serum amyloid A protein (SAA) into cross-β amyloid in multiple organs in humans and animals. AA amyloidosis occurs at high SAA serum levels during chronic inflammation. Prion-like transmission was reported as possible cause of extreme AA amyloidosis prevalence in captive animals, e.g. 70% in cheetah and 57–73% in domestic short hair (DSH) cats kept in zoos and shelters, respectively. Herein, we present the 3.3 Å cryo-EM structure of AA amyloid extracted post-mortem from the kidney of a DSH cat with renal failure, deceased in a shelter with extreme disease prevalence. The structure reveals a cross-β architecture assembled from two 76-residue long proto-filaments. Despite >70% sequence homology to mouse and human SAA, the cat SAA variant adopts a distinct amyloid fold. Inclusion of an eight-residue insert unique to feline SAA contributes to increased amyloid stability. The presented feline AA amyloid structure is fully compatible with the 99% identical amino acid sequence of amyloid fragments of captive cheetah. Here, the authors report the cryoEM structure of AA amyloid from a cat shelter with extreme disease prevalence and reveal the feline-specific sequence insert in the fibril core. The sequence is 99% identical to AA amyloid from cheetah with reported prion-like transmission in zoos.

Lack of dental eruption may be accompanied by development of dentigerous cysts and has also been rarely associated with neoplasia. However, little information is available on prevalence of unerupted teeth and associated lesions in dogs and cats. The main objective of this study was to describe the epidemiologic data of canine and feline dental patients with unerupted teeth, and assess the prevalence of associated dentigerous cysts and tumors. Secondary aims included the evaluation of possible factors implicated in cystic development, and description of the histological features of dentigerous cysts. Medical and dental records, intraoral photographs, intraoral radiographs of client-owned dogs and cats with clinically missing teeth examined between 2001 and March 2018 were reviewed. Collected data included signalment, reason for presentation, number, type, depth of inclusion and angulation of unerupted teeth, presence of cystic lesions or tumors, abnormalities affecting involved teeth, histopathological findings, performed treatment and outcome. Seventy-three animals (69 dogs and 4 cats) with 113 unerupted teeth were included. The most frequent unerupted tooth in dogs was the first premolar teeth (78%), followed by the canine and third molar teeth. Dentigerous cysts were diagnosed associated with 48 (44.4%) teeth in dogs and one out of five unerupted teeth in cats. The affected teeth in dogs were predominantly in horizontal inclination (40%) and in soft tissue inclusion (77%). Brachycephalic canine breeds were overrepresented. The only unerupted tooth in boxer dogs was the first premolar tooth (32 teeth). Ninety percentage of boxers with unerupted teeth developed associated lesions (25 dentigerous cysts and one tumor). Two ameloblastomas (one in a dog and one in a cat) and one osteosarcoma (in a dog) were diagnosed in association with three unerupted teeth. Histology was essential in diagnosing two odontogenic cysts not evident on radiographs. In all cases that were followed-up, treatment (i.e., extraction, extraction and surgical curettage, or operculectomy) appeared successful. Untreated dentigerous cysts showed progression at re-examination. None of the unerupted teeth without evidence of cyst at the time of diagnosis showed incipient cystic development. None of the evaluated factors were associated with lack of eruption and/or development of associated lesions.

Epithelial-to-mesenchymal transition (EMT) is a process by which epithelial cells acquire mesenchymal properties. EMT has been closely associated with cancer cell aggressiveness. The aim of this study was to evaluate the mRNA and protein expression of EMT-associated markers in mammary tumors of humans (HBC), dogs (CMT), and cats (FMT). Real-time qPCR for SNAIL, TWIST, and ZEB, and immunohistochemistry for E-cadherin, vimentin, CD44, estrogen receptor (ER), progesterone receptor (PR), ERBB2, Ki-67, cytokeratin (CK) 8/18, CK5/6, and CK14 were performed. Overall, SNAIL, TWIST, and ZEB mRNA was lower in tumors than in healthy tissues. Vimentin was higher in triple-negative HBC (TNBC) and FMTs than in ER+ HBC and CMTs (p < 0.001). Membranous E-cadherin was higher in ER+ than in TNBCs (p < 0.001), whereas cytoplasmic E-cadherin was higher in TNBCs when compared with ER+ HBC (p < 0.001). A negative correlation between membranous and cytoplasmic E-cadherin was found in all three species. Ki-67 was higher in FMTs than in CMTs (p < 0.001), whereas CD44 was higher in CMTs than in FMTs (p < 0.001). These results confirmed a potential role of some markers as indicators of EMT, and suggested similarities between ER+ HBC and CMTs, and between TNBC and FMTs.

Systemic AA-amyloidosis is a protein-misfolding disease characterized by fibril deposition of serum amyloid-A protein (SAA) in several organs in humans and many animal species. Fibril deposits originate from abnormally high serum levels of SAA during chronic inflammation. A high prevalence of AA-amyloidosis has been reported in captive cheetahs and a horizontal transmission has been proposed. In domestic cats, AA-amyloidosis has been mainly described in predisposed breeds but only rarely reported in domestic short-hair cats. Aims of the study were to determine AA-amyloidosis prevalence in dead shelter cats. Liver, kidney, spleen and bile were collected at death in cats from 3 shelters. AA-amyloidosis was scored. Shedding of amyloid fibrils was investigated with western blot in bile and scored. Descriptive statistics were calculated. In the three shelters investigated, prevalence of AA-amyloidosis was 57.1% (16/28 cats), 73.0% (19/26) and 52.0% (13/25), respectively. In 72.9% of cats (35 in total) three organs were affected concurrently. Histopathology and immunofluorescence of post-mortem extracted deposits identified SAA as the major protein source. The duration of stay in the shelters was positively associated with a histological score of AA-amyloidosis (B = 0.026, CI95% = 0.007–0.046; p = 0.010). AA-amyloidosis was very frequent in shelter cats. Presence of SAA fragments in bile secretions raises the possibility of fecal-oral transmission of the disease. In conclusion, AA-amyloidosis was very frequent in shelter cats and those staying longer had more deposits. The cat may represent a natural model of AA-amyloidosis.

Abstract Background Amyloid A (AA) amyloidosis is a protein misfolding disease arising from serum amyloid A (SAA). Systemic AA amyloidosis recently was shown to have a high prevalence in shelter cats in Italy and was associated with azotemia and proteinuria. Objectives Investigate urine protein profiles and diagnostic biomarkers in cats with renal AA amyloidosis. Animals Twenty-nine shelter cats. Methods Case-control study. Cats with renal proteinuria that died or were euthanized between 2018 and 2021 with available necropsy kidney, liver and spleen samples, and with surplus urine collected within 30 days before death, were included. Histology was used to characterize renal damage and amyloid amount and distribution; immunohistochemistry was used to confirm AA amyloidosis. Urine protein-to-creatinine (UPC) and urine amyloid A-to-creatinine (UAAC) ratios were calculated, and sodium dodecyl sulfate-agarose gel electrophoresis (SDS-AGE) and liquid chromatography-mass spectrometry (LC-MS) of proteins were performed. Results Twenty-nine cats were included. Nineteen had AA amyloidosis with renal involvement. Cats with AA amyloidosis had a higher UPC (median, 3.9; range, 0.6-12.7 vs 1.5; 0.6-3.1; P = .03) and UAAC ratios (median, 7.18 × 10−3; range, 23 × 10−3-21.29 × 10−3 vs 1.26 × 10−3; 0.21 × 10−3-6.33 × 10−3; P = .04) than unaffected cats. The SDS-AGE identified mixed-type proteinuria in 89.4% of cats with AA amyloidosis and in 55.6% without AA amyloidosis (P = .57). The LC-MS identified 63 potential biomarkers associated with AA amyloidosis (P < .05). Among these, urine apolipoprotein C-III was higher in cats with AA amyloidosis (median, 1.38 × 107; range, 1.85 × 105-5.29 × 107 vs 1.76 × 106; 0.0 × 100-1.38 × 107; P = .01). In the kidney, AA-amyloidosis was associated with glomerulosclerosis (P = .02) and interstitial fibrosis (P = .05). Conclusions and Clinical Importance Renal AA amyloidosis is associated with kidney lesions, increased proteinuria and increased urine excretion of SAA in shelter cats. Additional studies are needed to characterize the role of lipid transport proteins in the urine of affected cats.