Osteoartropatía hipertrofiante néumica canina : un caso clínico

Se describe un caso de osteoartropatía hipertrofiante néumica (OAHN) en un perro mastín español de 8 años de edad.A case of hypertrophic pulmonary osteoarthropathy in a spanish mastin, eight years old, is presented

Equine Pleuropneumonia

consiste en colonización bacteriana del parénquima pulmonar, desarrollo de una neumonía o abscesos pulmonares y la consiguiente extensión del proceso hacia la pleura visceral y el espacio pleural provocando pleuritis. Generalmente, su desarrollo se asocia con cualquier condición que favorezca la aspiración de secreciones faríngeas o impida su eliminación (transporte, enfermedades víricas, ejercicio extenuante, anestesia general, etc). Los signos clínicos pueden variar según se trate de un problema agudo o crónico, predominando en el primer caso: fiebre, letargia, descarga nasal, tos, intolerancia al ejercicio, disnea y pleurodinia. En los casos crónicos suele aparecer fiebre intermitente, pérdida de peso y edema subesternal El diagnóstico se basa fundamentalmente en la ecografía de la región torácica y el análisis microbiológico y citológico de las secreciones traqueales y pleurales. Su tratamiento se centra en antibioterapia sistémica para inhibir el crecimiento bacteriano, drenaje del exceso de líquido pleural (en los casos que dificulte la capacidad respiratoria del animal o sea claramente séptico), administración de terapia antiinflamatoria y analgésica y tratamiento de soporte a base de fluidoterapia, oxigenoterapia y broncodilatadores. El pronóstico de la pleuroneumonía es favorable en los casos que se identifican precozmente y reciben tratamiento agresivo, empeorando mucho en casos crónicos o con complicaciones como la laminitis, colitis asociada a antibióticos y trombosis yugular. Las principales secuelas de este proceso incluyen la formación de abscesos pulmonares, fístulas broncopleurales, neumotórax, y pericarditis restrictiva.Pleuropneumonia is a frequent and severe disease in the horse. It is produced by the bacterial colonization of pulmonary parenchyma, development of pneumonia or pulmonary abscesses and subsequent extension of the infection to the visceral pleura and pleural cavity, which causes pleuritis. Risk factors include transport, viral infections, exhausting exercise, general anesthesia, and any condition that enhances aspiration of oropharyngeal microrganisms or that impairs their clearance. Clinical signs may vary in acute or chronic diseases. In acute pleuropneumonia, horses have fever, lethargy, nasal discharge, cough, exercise intolerance, dispnea and pleurodinia. In chronic cases, intermittent fever, weight loss and subesternal edema are more frequent. Diagnosis is based mainly in thoracic ultrasonography and in the cytologic and biochemical analysis and culture of the pleural and tracheal fluids. Treatment consists on administration of systemic antibiotics to inhibit bacterial growth, removal of excessive pleural fluid, antiinflammatory and analgesic drugs, and supportive care (fluid therapy, oxygen and bronchodilators). Prognosis can be favorable when the disease is identified early and aggressive treatment is provided. In chronic cases or when complications like laminitis, colitis or thrombosis develop, prognosis is guarded to poor. The most common sequelae of pleuropneumonia are pulmonary abscesses, bronchopleural fistulae, pneumothorax and restrictive pericarditis

Chronic obstructive pulmonary disease - Recurrent Airway obstruction

Los procesos inflamatorios de vías respiratorias bajas constituyen una de las patologías más importantes en clínica equina. Aunque la etiopatogenia de la obstrucción aérea recurrente no se conoce con exactitud, parecen estar implicados tanto procesos alérgicos, como infecciosos y la presencia de elementos irritantes o tóxicos. La presentación clínica más habitual de esta enfermedad son caballos de edad media o avanzada que tosen frecuentemente y presentan disnea espiratoria incluso en reposo, agravándose el problema de forma estacional y con la exposición a los factores desencadenantes. En los casos más avanzados se puede presentar pérdida de peso, enfisema pulmonar e hipertrofia de la musculatura espiratoria. El diagnóstico se realiza fundamentalmente basándose en signos clínicos (hiperreactividad respiratoria, auscultación pulmonar anormal e incremento del campo de percusión pulmonar), la endoscopia traqueobronquial y el estudio citológico de las secreciones respiratorias, aunque existen otros métodos más complejos de evaluación como la medición de presión intratorácica y la gasometría arterial. El pronóstico siempre es reservado puesto que se trata de una enfermedad crónica que, si no se controla adecuadamente, tenderá a progresar. El tratamiento se centra en dos grupos de medidas terapéuticas: a) el tratamiento higiénico-dietético y b) el tratamiento farmacológico. El primer grupo tiene como objetivos la eliminación del polvo tanto de la alimentación como de la cama y la presencia de una buena ventilación, siendo la medida ideal en muchos casos mantener los caballos al aire libre El tratamiento farmacológico consiste en la aplicación de antiinflamatorios esteroideos y broncodilatadores, pudiendo complementarse con otros productos como por ejemplo los mucolíticos.Lower airway inflammatory disease is a frequent disese in horses. Although the ethiology of recurrent airway obstruction (RAO) is not completely known, allergic and infectious processes and the presence of irritant or toxic particles seem to be involved. The most common presentation of the disease is middle-advanced age horses that cough frequently and have expiratory dyspnoea even at rest. This problem worsens seasonally and with the exposition to trigger factors. In severe cases, weight loss, pulmonary emphysema, and expiratory muscle hypertrophy (heavy line) can be observed. The diagnosis is based on clinical signs (respiratory hypereactivity, abnormal pulmonary auscultation and expanded lung field), tracheobronchial endoscopy, and cytology of respiratory secretions. More complex techniques, like arterial blood gases or intrapleural pressure measurement, can also be used for the diagnosis of RAO. Prognosis is always guarded since it is a chronic disease that is going to worsen if is not controlled. The treatment consists on management measures and medical therapy. The objective of the management measures is to minimize the presence of dust, not only in the food but also in the bedding, and to provide good ventilation. Unless pasture exacerbates the condition, horses should ideally be kept outside. Medical management is based on corticosteroids and bronchodilators but other adjunctive drugs like mucolytics can also be use

Caloric Intake in Renal Patients: Repercussions on Mineral Metabolism

The aim of this paper is to review current knowledge about how calorie intake influences mineral metabolism focussing on four aspects of major interest for the renal patient: (a) phosphate (P) handling, (b) fibroblast growth factor 23 (FGF23) and calcitriol synthesis and secretion, (c) metabolic bone disease, and (d) vascular calcification (VC). Caloric intake has been shown to modulate P balance in experimental models: high caloric intake promotes P retention, while caloric restriction decreases plasma P concentrations. Synthesis and secretion of the phosphaturic hormone FGF23 is directly influenced by energy intake; a direct correlation between caloric intake and FGF23 plasma concentrations has been shown in animals and humans. Moreover, in vitro, energy availability has been demonstrated to regulate FGF23 synthesis through mechanisms in which the molecular target of rapamycin (mTOR) signalling pathway is involved. Plasma calcitriol concentrations are inversely proportional to caloric intake due to modulation by FGF23 of the enzymes implicated in vitamin D metabolism. The effect of caloric intake on bone is controversial. High caloric intake has been reported to increase bone mass, but the associated changes in adipokines and cytokines may as well be deleterious for bone. Low caloric intake tends to reduce bone mass but also may provide indirect (through modulation of inflammation and insulin regulation) beneficial effects on bone. Finally, while VC has been shown to be exacerbated by diets with high caloric content, the opposite has not been demonstrated with low calorie intake. In conclusion, although prospective studies in humans are needed, when planning caloric intake for a renal patient, it is important to take into consideration the associated changes in mineral metabolism

Vitamin E protects against extraskeletal calcification in uremic rats fed high fat diets

Background: High fat diets are implicated in the pathogenesis of metabolic syndrome, obesity and renal disease. Previous studies have revealed that high fat diets promote vascular calcification in uremic rats. Moreover, vitamin E has been shown to prevent uremic calcifications in genetically obese Zucker rats fed standard diet. The objective of this study was to investigate the influence of vitamin E supplementation on the development of extraskeletal calcifications in non-obese (wild type) uremic rats fed high fat diets. Methods: Wistar rats ( n = 32) were preconditioned by feeding either a normal (NF) or high fat (HF) diet for 45 days and subsequently were subjected to 5/6 nephrectomy (Nx). Just before performing the first Nx step, a blood sample (Pre-Nx) was obtained. After Nx rat s were switched to a diet with 0.9% phosphorus and supplemented with calcitriol. Also, after Nx, half of the rats from each group (NF and HF) were treated with vitamin E (VitE) in the diet (30,000 mg/kg) and the ot her half were maintained on basic VitE requirements (27 mg/kg). Thus, rats were allotted to four experimental groups: Nx-NF ( n = 8), Nx-NF-VitE ( n =8),Nx-HF( n =8)and Nx-HF-VitE ( n = 8). At the time of sacrifice (day 66), blood and tissue samples were obtained. Results: Feeding a HF diet for 45 days did not increase body weight but elicited hyperglycemia, hypertriglyceridemia, an increase in plasma fibroblast growth factor 23 and a reduction in plasma calcitriol concentrations. After Nx, rats fed HF diet showed substantial extraskeletal calcification with aortic calcium content that was higher than in rats fed NF diet. Supplementation with VitE significantly ( p < 0.05) reduced aortic (from 38.4 ± 8.8 to 16.5 ± 1.4 mg/g), gastric (from 5.6 ± 2.7 to 1.2 ± 0.4 mg/g) and pulmonary (from 1.8 ± 0.3 to 0.3 ± 0.2 mg/g) calcium content in rats on HF diets. Conclusions: Uremic rats fed HF diets developed more severe extraosseous calcifications than their normocaloric-fed counterparts and dietary VitE supplementation protected against uremic calcifications in rats fed HF diets. Thus, eating energy-rich foods should be discouraged in patients with renal disease and their deleterious effect may be ameliorated with adequate antioxidant suppl

Chronic Vitamin D Intoxication in Captive Iberian Lynx (Lynx pardinus)

To document the biochemical and pathologic features of vitamin D intoxication in lynx and to characterize mineral metabolism in healthy lynx, blood samples were obtained from 40 captive lynx that had been receiving excessive (approximately 30 times the recommended dose) vitamin D3 in the diet, and from 29 healthy free ranging lynx. Tissue samples (kidney, stomach, lung, heart and aorta) were collected from 13 captive lynx that died as a result of renal disease and from 3 controls. Vitamin D intoxication resulted in renal failure in most lynx (n = 28), and widespread extraskeletal calcification was most severe in the kidneys and less prominent in cardiovascular tissues. Blood minerals and calciotropic hormones in healthy lynx were similar to values reported in domestic cats except for calcitriol which was higher in healthy lynx. Changes in mineral metabolism after vitamin D intoxication included hypercalcemia (12.0 ± 0.3 mg/dL), hyperphosphatemia (6.3 ± 0.4 mg/dL), increased plasma calcidiol (381.5 ± 28.2 ng/mL) and decreased plasma parathyroid hormone (1.2 ± 0.7 pg/ mL). Hypercalcemia and, particularly, hyperphosphatemia were of lower magnitude that what has been previously reported in the course of vitamin D intoxication in other species. However, extraskeletal calcifications were severe. The data suggest that lynx are sensitive to excessive vitamin D and extreme care should be taken when supplementing this vitamin in captive lynx diets

Increased 1,25(OH)2-Vitamin D Concentrations after Energy Restriction Are Associated with Changes in Skeletal Muscle Phenotype

The influence of energy restriction (ER) on muscle is controversial, and the mechanisms are not well understood. To study the effect of ER on skeletal muscle phenotype and the influence of vitamin D, rats (n = 34) were fed a control diet or an ER diet. Muscle mass, muscle somatic index (MSI), fiber-type composition, fiber size, and metabolic activity were studied in tibialis cranialis (TC) and soleus (SOL) muscles. Plasma vitamin D metabolites and renal expression of enzymes involved in vitamin D metabolism were measured. In the ER group, muscle weight was unchanged in TC and decreased by 12% in SOL, but MSI increased in both muscles (p < 0.0001) by 55% and 36%, respectively. Histomorphometric studies showed 14% increase in the percentage of type IIA fibers and 13% reduction in type IIX fibers in TC of ER rats. Decreased size of type I fibers and reduced oxidative activity was identified in SOL of ER rats. An increase in plasma 1,25(OH)2-vitamin D (169.7 ± 6.8 vs. 85.4 ± 11.5 pg/mL, p < 0.0001) with kidney up-regulation of CYP27b1 and down-regulation of CYP24a1 was observed in ER rats. Plasma vitamin D correlated with MSI in both muscles (p < 0.001), with the percentages of type IIA and type IIX fibers in TC and with the oxidative profile in SOL. In conclusion, ER preserves skeletal muscle mass, improves contractile phenotype in phasic muscles (TC), and reduces energy expenditure in antigravity muscles (SOL). These beneficial effects are closely related to the increases in vitamin D secondary to ER

Phosphorus restriction does not prevent the increase in fibroblast growth factor 23 elicited by high fat diet

This study was designed to evaluate the influence of phosphorus (P) restriction on the dele- terious effects of high fat diets on mineral metabolism. Twenty-four rats were allotted to 3 groups (n = 8 each) that were fed different diets for 7 months. Rats in group 1 were fed nor- mal fat-normal P (0.6%) diet (NF-NP), rats in group 2 were fed high fat- normal P diet (HF- NP) and rats in group 3 were fed high fat-low P (0.2%) diet (HF-LP). Blood, urine and tissues were collected at the end of the experiments. When compared with the control group (NF- NP), rats fed HF diets showed increases in body weight, and in plasma concentrations of tri- glycerides and leptin, and decreased plasma calcitriol concentrations. In rats fed HF-NP plasma fibroblast growth factor 23 (FGF23) was higher (279.6 ± 39.4 pg/ml vs 160.6 ± 25.0 pg/ml, p = 0.018) and renal klotho (ratio klotho/GAPDH) was lower (0.75 ± 0.06 vs 1.06 ± 0.08, p < 0.01) than in rats fed NF-NP. Phosphorus restriction did not normalize plasma FGF23 or renal klotho; in fact, rats fed HF-LP, that only ingested an average of 22.9 mg/day of P, had higher FGF23 (214.7 ± 32.4 pg/ml) concentratio ns than rats fed NF-NP (160.6 ± 25. 0 pg/ml), that ingested and average of 74.4 mg/day of P over a 7 month period. In conclusion, our results demonstrate that severe P restriction over a prolonged period of time (7 months) does not normalize the increase in circulating FGF23 induced by HF diets. These data indi- cate that the deleterious effects of high fat diet on the FGF23/klotho axis are not eliminated by reduced P intake

Oral Acid Load Down-Regulates Fibroblast Growth Factor 23

Increased dietary acid load has a negative impact on health, particularly when renal function is compromised. Fibroblast growth factor 23 (FGF23) is a bone-derived hormone that is elevated during renal failure. The relationship between metabolic acidosis and FGF23 remains unclear. To investigate the effect of dietary acid load on circulating levels of FGF23, rats with normal renal function and with a graded reduction in renal mass (1/2 Nx and 5/6 Nx) received oral NH4Cl for 1 month. Acid intake resulted in a consistent decrease of plasma FGF23 concentrations in all study groups when compared with their non-acidotic control: 239.3 ± 13.5 vs. 295.0 ± 15.8 pg/mL (intact), 346.4 ± 19.7 vs. 522.6 ± 29.3 pg/mL (1/2 Nx) and 988.0 ± 125.5 vs. 2549.4 ± 469.7 pg/mL (5/6 Nx). Acidosis also decreased plasma PTH in all groups, 96.5 ± 22.3 vs. 107.3 ± 19.1 pg/mL, 113.1 ± 17.3 vs. 185.8 ± 22.2 pg/mL and 504.9 ± 75.7 vs. 1255.4 ± 181.1 pg/mL. FGF23 showed a strong positive correlation with PTH (r = 0.877, p < 0.0001) and further studies demonstrated that acidosis did not influence plasma FGF23 concentrations in parathyroidectomized rats, 190.0 ± 31.6 vs. 215 ± 25.6 pg/mL. In conclusion, plasma concentrations of FGF23 are consistently decreased in rats with metabolic acidosis secondary to increased acid intake, both in animals with intact renal function and with decreased renal function. The in vivo effect of metabolic acidosis on FGF23 appears to be related to the simultaneous decrease in PTH