Effects of different cereal grains in diets for laying hens on production parameters and liver fat content

Two experiments were conducted with White Leghorn laying hens to study the effects of different cereal grains on production criteria and liver fat content. The results of Experiment 1, in which pullets 21 weeks of age were used for a period of 22 weeks indicated that Gaines wheat or triticale (Trailblazer) were equal to corn in supporting egg production, egg weight and body weight, with comparable feed consumption. Henry wheat(a hard red winter class) was slightly, yet significantly (P less than 0.05) inferior to corn for the above criteria. No significant differences were observed among four treatments in wet liver weight and liver fat content. Hens fed the corn diet had significantly (P less than 0.05) lower carcass fat followed by the hens fed triticale in comparison with those fed Gaines or Henyry wheat. Mortality was very low and not related to dietary treatments. Neither dietary fat nor energy content was related to fat content of liver and carcass of the hens. Body weight and liver fat content were not closely related to each other. Wet liver weight was the only significantly (P less than 0.05) related factor to liver fat content. In the second experiment, in which hens 33 weeks of age were used for an experimental period of 20 weeks, opaque-2 corn was slightly superior to normal corn and triticale was comparable to normal corn in supporting egg production and egg weight. Supplementation of the diets containing the two corns and triticale with lysine failed to improve egg production and egg weight. Hens fed the diets containing either normal corn or opaque-2 corn as the only grain in the diet had significantly (P less than 0.05) higher liver fat content in comparison with hens fed the diet containing triticale as the only grain. Mortality, however, was much higher among hens fed triticale-containing diets in comparison with groups fed corn-containing diets in spite of the fact that they had significantly lower liver fat content. Regardless of dietary treatments or grains used, the hens that died were diagnosed to have fatty liver hemorrhagic syndrome. Dietary fat content was postively and significantly (P less than 0.05) related to liver fat content. Dietary energy or body weight was not closely related to liver content. Liver fat content and mortality were negatively related to each other. The higher for content did not adversely affect laying performance.     

Metabolic insights and nutrition of poultry

Excessive specialization and high production requirements place high demands on the metabolism of poultry. A number of metabolic problems, such as disturbances of energy metabolism (affecting mainly hens) and mineral balance (affecting mainly laying hens), affect performance. Nearly all these problems are multifactorial in nature, but diet, and in particular the interaction between diet and phenotype, plays an important role. The problem of ascites in broiler hens is discussed in relation to external and genetic causative factors. Genetic factors can be further subdivided into structural and functional causative factors. This distinction has important consequences. For example, sudden death syndrome can be distinguished as a separate entity. Fatty liver syndrome in laying hens, and gout and urolithiasis in chicks and hens are briefly discussed. Finally, some of the most important or most common skeletal problems affecting poultry, namely, tibial dyschondroplasia, battery fatigue, rickets, and chondrodystrophy, are briefly discussed in the context of the dietary factors that underlie these disorders or which can be used as treatment.     

Liver lipid accumulation and performance of hens as affected by cage density and initial body weight

Hens housed in individual cages (25 46 cm.) laid significantly more eggs, consumed significantly more feed and had significantly larger livers with a higher lipid content than hens housed three to a cage in two experiments. Body weight gain was significantly higher for individually housed birds in experiment 1, but not in experiment 2. No difference was observed in mean egg weight or kg. feed per dozen eggs. In experiment 2 hens housed two to a cage laid slightly fewer eggs and accumulated slightly less liver fat but the differences were not significantly different fromthose housed individually. Hens socially dominant in three bird pens had higher liver fat accumulation than hens lower on the peck order but liver fat accumulation for the dominant hens still averaged less than hens housed either two or one per cage. Comparison of two strains in experiment 1 revealed a significant difference in rate of egg production and feed efficiency but no difference in liver fat accumulation. Pullets placed in four body weight classes prior to the start of the experiment did not differ significantly in liver fat accumulation per unit of body weight or percentof dry matter of the liver at the end of the experiment. Rate of egg production and feed efficiency were also not significantly different among the body weight classes.     

The relationship of various tibia bone measurements in hens

Tibias from 50 Single Comb White Leghorn hens were used to study the relationships among various bone measurements. The bone ash (BA), length, wet bone volume (V), fat-free dry matter (FFDM), fat-free bone density (BD; mass per unit bone volume), and bone breaking force (BF) were measured, and the BA concentration (BA/V) and BA as a percentage of FFDM (BA/FFDM) were calculated. Bone ash was highly correlated with FFDM (r = 0.975). The BD was poorly correlated with any of the parameters measured in the present study. The BF was highly correlated with BA (r = 0.922) and FFDM (r = 0.918), but less well correlated with BA/FFDM (r = 0.496) and BA/V (r = 0.694). However, the inclusion of volume2 significantly improved the BF predicting models when BA/V was used as predictor (R2 = 0.855), indicating that BF is not only a function of BA density but also of bone size. The BF adjusted for V may better reflect treatment effect upon bone status than BF alone. The coefficient of variation of BA/FFDM and BD was smaller (0.007) than the CV with BA/V (0.026), which may indicate the BA/V is potentially a better indicator of bone status than BA/FFDM and BD. Bone length was poorly correlated with BA, FFDM, and BF, but highly correlated with V (r = 0.844). The volume of the same bone measured by the water weight change method gave the most consistent measurement. The data showed that BA/V may be a better measurement to reflect the bone status changes of hens than other measurements tested. When BA, FFDM, or BF are used in laying hen's bone status studies, the data analysis needs to be adjusted for V, an V is closely correlated with these variables.     

Osteoporosis in men. New insights into aetiology, pathogenesis, prevention and management

Osteoporosis is increasingly recognised in men. Low bone mass, risk factors for falling and factors causing fractures in women are likely to cause fractures in men. Bone mass is largely genetically determined, but environmental factors also contribute. Greater muscle strength and physical activity are associated with higher bone mass, while radial bone loss is greater in cigarette smokers or those with a moderate alcohol intake. Sex hormones have important effects on bone physiology. In men, there is no abrupt cessation of testicular function or 'andropause' comparable with the menopause in women; however, both total and free testosterone levels decline with age. A common secondary cause of osteoporosis in men is hypogonadism. There is increasing evidence that estrogens are important in skeletal maintenance in men as well as women. Peripheral aromatisation of androgens to estrogens occurs and osteoblast-like cells can aromatise androgens into estrogens. Human models exist for the effects of estrogens on the male skeleton. In men aged > 65 years, there is a positive association between bone mineral density (BMD) and greater serum estradiol levels at all skeletal sites and a negative association between BMD and testosterone at some sites. It is crucial to exclude pathological causes of osteoporosis, because 30 to 60% of men with vertebral fractures have another illness contributing to bone disease. Glucocorticoid excess (predominantly exogenous) is common. Gastrointestinal disease predisposes patients to bone disease as a result of intestinal malabsorption of calcium and colecalciferol (vitamin D). Hypercalciuria and nephrolithiasis, anticonvulsant drug use, thyrotoxicosis, immobilisation, liver and renal disease, multiple myeloma and systemic mastocytosis have all been associated with osteoporosis in men. It is possible that low-dose estrogen therapy or specific estrogen receptor-modulating drugs might increase BMD in men as well as in women. In the future, parathyroid hormone peptides may be an effective treatment for osteoporosis, particularly in patients in whom other treatments, such as bisphosphonates, have failed. Men with idiopathic osteoporosis have low circulating insulin-like growth factor-1 (IGF-1; somatomedin-1) concentrations, and IGF-1 administration to these men increases bone formation markers more than resorption markers. Studies of changes in BMD with IGF-1 treatment in osteoporotic men and women are underway. Osteoporosis in men will become an increasing worldwide public health problem over the next 20 years, so it is vital that safe and effective therapies for this disabling condition become available. Effective public health measures also need to be established and targeted to men at risk of developing the disease.     

Inactivation of Kupffer cells prevents early alcohol-induced liver injury

It is well recognized that consumption of alcohol leads to liver disease in a dose-dependent manner; however, the exact mechanisms remain unclear. Hypoxia subsequent to a hypermetabolic state may be involved; therefore, when it was observed recently that inactivation of Kupffer cells prevented stimulation of hepatic oxygen uptake by alcohol, the idea that Kupffer cells participate in early events that ultimately lead to alcohol-induced liver disease became a real possibility. The purpose of this study was to test that hypothesis. Male Wistar rats were exposed to ethanol continuously by means of intragastric feeding for up to 4 weeks using the model developed by Tsukamoto and French. In this model, ethanol causes fatty liver, necrosis and inflammation--changes characteristic of alcohol-induced liver disease in human beings. Kupffer cells were inactivated by twice weekly treatment with gadolinium chloride (GdCl3), a selective Kupffer cell toxicant. AST levels were elevated to 192 +/- 13 and 244 +/- 56 IU/L in rats exposed to ethanol for 2 and 4 wk, respectively (control value, 88 +/- 7). This injury was prevented almost completely by GdCl3 treatment. Fatty changes, inflammation and necrosis were also all reduced dramatically by GdCl3 treatment. The average hepatic pathological score of rats treated with ethanol for 4 wk was 4.3 +/- 0.6, which was reduced significantly in ethanol- and GdCl3-treated rats to 1.8 +/- 0.5 (p < 0.05). Rates of ethanol elimination were elevated 2- to 3-fold in rats exposed to ethanol for 2 to 4 wk. This elevation was blocked by GdCl3 treatment.(ABSTRACT TRUNCATED AT 250 WORDS)     

Diagnosis of fatty liver in dairy cows

From 27 dairy cows with a mean milk yield of 6900 kg FCM (4% milk fat) per 305 day lactation period liver bioptates 2 weeks post partum (p.p.), milk samples 2, 4 weeks p.p., blood samples 0 (partus), 2, 4 week p.p., measurement of backfat thickness 2 weeks prior to calving, 0, 6, 17 weeks p.p. were taken and body weight and milk yield were determined. Fertility results and disorders appearance were recorded too. Total lipid and triglyceride content were analysed in liver tissue. Acetone concentration was determined in milk and 15 clinical-chemical parameters were elucidated in blood samples. Liver fat concentration shows a great variability from 3.9% to 24%. There is no strong reference value for the distinction between physiological and pathological liver fat concentration. Assessment as to whether increased liver fat levels in dairy cow are indicative of liver damage due to a pathological process should include detection of liver cell damage on the basis of plasma enzymes with closest possible specificity of liver. Glutamate-dehydrogenase (GLDH) is recommended. Liver fat content clearly could be defined exclusively from investigation of liver tissue rather than from analysis of blood or milk parameters. Measurement of backfat thickness provided useful information on the post partum lipolysis rate with a good correlation to liver fat (r to -0.72).     

Electromyography of the sphincter vesicae externus muscle. Technique, indications and outcome

In the past several years significant attention has been directed to the study of adynamic bone disease in uremic patients. Several reports have provided additional information about the prevalence of adynamic bone disease in different countries. It has now become clear that the pathogenesis of adynamic bone disease cannot be ascribed to one single aetiological factor, but rather to a host of complex factors. From recently published papers we have learned about the mechanism of downregulation of the parathyroid hormone/parathyroid hormone-related peptide receptor on osteoblast-like cells, which may be a very important step in the pathogenesis of adynamic bone disease. A provocative hypothesis attempts to link the widespread use of erythropoietin to the emergence of adynamic bone disease-lacking excessive aluminium accumulation. It appears from some studies that bone-specific alkaline phosphatase might become a valuable tool in differentiating high turnover from low/normal turnover bone disease; however, further studies are needed to establish the role of this marker in the diagnosis of adynamic bone disease. Several papers discussed the pros and cons of lowering the calcium concentration of the dialysate in order to prevent adynamic bone disease. The results of these studies help us to understand the pathogenesis and the clinical relevance of this lesion in attempts to provide better care for our patients.     

Prospective study of bacteremia rate after elastic band ligation and sclerotherapy of esophageal varices in patients with hepatosplenic schistosomiasis

Bone scintigraphy was performed in a 69-year-old male patient with adult T-cell leukemia suffering from right lower limb pain. Numerous sites of increased uptake were seen in the skull, left clavicle, bilateral humeri, bilateral radii and right femur and tibia. Bone radiographs showed multiple osteolytic lesions, most of which corresponded to the abnormal deposits on the bone scans with 740 MBq of 99mTc-hydroxymethylene diphosphonate. This pattern is rarely reported, but bone involvement of adult T-cell leukemia is not uncommon. Bone involvement was remarkable on the appendicular skeleton when compared with common metastatic bone tumors. Bone scintigraphy may be useful in detecting bone involvement in adult T-cell leukemia.     

Enhancement of ectopic bone formation in mice with a deficit in Fas-mediated apoptosis

Bone formation is under the control of cytokines as well as growth factors such as bone morphogenetic proteins (BMP). This suggests the possibility that osteogenesis might be modulated by factors which also modulate the immune system. To test whether immune disorders in the host may influence bone formation, we studied BMP-induced bone formation in a C3H/HeJ strain of mice bearing a mutant gene, the lymphoproliferation gene (lpr) or the generalized lymphoproliferative disease gene (gld), both of which are known to be a Fas deletion mutant and a Fas ligand mutant, respectively, and to induce immune disorders via a deficit in Fas-mediated apoptosis. Crude BMP derived from bovine bone were injected into the muscular tissue in the femur of adult C3H/HeJ mice or C3H/HeJ mice bearing an lpr or gld gene. Quantitative analysis of the resulting ectopic bone formation by X-ray photography 2 weeks after injection revealed that the presence of either the lpr or gld gene caused a bone mass significantly larger in dimension than that seen in the wild type mice. Histological examination also revealed the different influence between these mutant genes on the level of bone formation exhibited by hyaline cartilage and bone trabeculae. Based on these results, we discussed the possible mechanisms of the enhanced ectopic bone formation under the deficit in Fas-mediated apoptosis.     

Calcitonin receptor binding properties in bone and kidney of the chicken during the oviposition cycle

The binding property of calcitonin (CT) in the membrane fraction of calvaria and kidney of egg-laying and nonlaying hens was analyzed using a [125I] CT binding assay system. Binding properties of CT receptors in both tissues satisfy the authentic criteria of a receptor-ligand interaction in terms of specificity, reversibility, and saturation. Scatchard plots revealed a single class of binding sites. Values of the equilibrium dissociation constant (Kd) and binding capacity (Bmax) in laying hens showed a decrease during the period between 3 h before and 2 h after oviposition. No change was observed in nonlaying hens. In vivo administration of 17beta-estradiol or progesterone caused the decrease in Kd and Bmax values. The results suggest that the binding affinity and capacity of the CT receptor in the calvaria and the kidney of the hen may be modulated by the ovarian steroid hormone.     

Biochemical markers of bone metabolism: an overview

OBJECTIVES: An overview of biochemical markers of bone metabolism is presented along with indications for their clinical utilization. DESIGN AND METHODS: The structure, cyclical metabolism, and hormone regulation of bone is reflected by markers of resorption, formation and/or turnover. Markers of resorption representing degradation of type 1 collagen, include N-telopeptides, C-telopeptides, hydroxyproline, and the collagen crosslinks pyridinoline and deoxypyridinoline; acid phosphatase, a marker of osteoclast activity, and urinary calcium are also indicators of bone resorption. Bone formation markers indicate osteoblast activity; bone-specific alkaline phosphatase and the N-terminal and C-terminal extension peptides of procollagen reflect formation of organic matrix in bone. Osteocalcin, produced by osteoblasts but also released during osteoclastic degradation, may indicate either formation when resorption and formation are coupled or turnover when they are uncoupled. RESULTS: Bone markers respond to intervention more rapidly than techniques such bone mineral density. Resorption markers respond approximately 1 to 3 months after intervention; markers of formation respond later, after 6 to 9 months. Bone markers may add useful information for assessing fracture risk and for monitoring osteoporosis, Paget's disease of bone, cancer metastasis, and metabolic disease. Various therapeutic interventions may affect release of some bone markers. CONCLUSION: Bone disease has high prevalence in adults so bone markers will become even more important for assessing fracture risk and monitoring therapy as populations age. Characteristics of bone markers are dependent on biology and the assay used. Substantial work remains in characterizing existing assays, identifying better markers and performing the clinical studies to define which bone markers should be measured and when.     

Regulation of phosphoenolpyruvate carboxykinase and fatty acid synthetase in brown fat of suckling rats

Infant rats were injected with prednisolone (0.5-5 mg/100 g wt). This caused phosphoenolpyruvate carboxykinase (PEPCK) activity to rise in liver and to decrease in brown fat. Fatty acid synthetase (FAS) activity remained unchanged in liver but increased in brown fat. A single injection of prednisolone caused hepatic PEPCK activity to remain elevated for at least 7 days. Brown fat FAS also remained high for that period. However, brown fat PEPK activity returned to normal on the third day after the injection. A single injection of prednisolone or cortisone to 5-day-old rats caused a transient elevation of the blood level of insulin and a prolonged decrease in that of growth hormone. No effect on the level of glucagon was noted. Injections of insulin had effects similar to those of prednisolone, i.e. a rise in hepatic and a fall in brown fat PEPCK. Using antibodies prepared to hepatic PEPCK it was shown that the observed changes were due to changes in the rate of synthesis of the enzyme. Using actinomycin D indirect evidence was obtained that changes in FAS activity of brown fat were also due to changes in the synthetic rate.     

]The substitution of protein feed by lysine-supplemented protein-rich wheat during the raisung and laying periods in hens. 6. Report. The effect of graded lysine supplemented on the crude nutritional content of the carcas of laying hen

In the present work 8 hens taken from each of the 16 experimental groups (90 birds per group) were killed at the end of the trial period (52 weeks). The weight of the organs was determined and bones, the utilizable parts and the residual carcass were analyzed for their crude nutrient content. The experimental birds received rations containing a large proportion of high-protein wheat supplemented with varying levels of lysine. Variations in the lysine supply did not affect the mass of blood, feathers, bones, liver, stomach, heart and ovaries, including ovarian follicles. An analysis of the utilizable parts (flesh, stomach, heart, liver, follicles, fat) for crude nutrients showed that the heavier birds receiving adequate amounts of lysine contained less crude protein and more crude fat than the smaller birds. A positive correlation was found to exist between the crude ash content of these samples (expressed as %) and the levels of lysine supplied during the laying period. All the birds receiving the lysine-deficient ration during the time of rearing or during the laying period contained significantly less crude ash in their bones. Alongside with the crude ash content the phosphorus content of the bones decreased when the birds where fed the diet for laying hens.     

Hantavirus pulmonary syndrome in the United States: a pathological description of a disease caused by a new agent

An outbreak of an acute respiratory disease in the southwestern United States has led to the recognition of a new hantaviral illness. This report describes a unique spectrum of antemortem and postmortem pathological findings seen in a case series of nine surviving patients and 13 who died. Clinical, laboratory, and autopsy findings were derived from a consecutive series of individuals confirmed to have hantavirus pulmonary syndrome. Laboratory studies included chemical, hematological, and bone marrow analyses as well as flow cytometric and immunohistochemical phenotyping. Autopsy tissues were examined by routine histological stains, immunohistochemical methods, and transmission electron microscopy. The lung is the primary target organ in this illness. Pulmonary abnormalities include pleural effusions, alveolar edema and fibrin, and an interstitial mononuclear cell infiltrate. Large immunoblast type cells are seen in the lungs, blood, bone marrow, lymph nodes, liver, and spleen. A tetrad of hematological findings includes left-shifted neutrophilic leukocytosis, thrombocytopenia, hemoconcentration in severe cases, and circulating immunoblasts. In contrast to previously described nephropathic hantaviral syndromes, hantavirus pulmonary syndrome is characterized by a unique constellation of pulmonary, hematological, and reticuloendothelial pathological findings. The pulmonary findings are distinguishable from fatal adult respiratory distress syndrome. The data suggest a capillary leak syndrome restricted to the pulmonary circulation. Likewise, the hematological picture is unique and may be valuable in the rapid identification of cases for further diagnostic studies.     

Radiation-induced changes in bone

Radiation therapy has important applications in curative, adjuvant, and palliative therapy for a wide range of malignant conditions. Evidence of radiation therapy may be seen on radiologic images obtained subsequent to therapy. Bone growth disturbances may be observed in the immature axial or appendicular skeleton. Complications in the mature skeleton include osteoradionecrosis, pathologic fracture, and radiation-induced neoplasms. Radiologic features of mandibular osteoradionecrosis include ill-defined cortical destruction without sequestration. In osteoradionecrosis of the ribs, clavicle, scapula, and humerus, radiography may demonstrate osteopenia, disorganization and coarsening of trabecular architecture, and cortical irregularity; computed tomography more clearly depicts subtle fractures, alterations in bone architecture, and dystrophic soft-tissue calcification. In osteoradionecrosis of the spine, hematopoietic cellular elements of the spinal marrow are replaced with fat, which has high signal intensity on T1-weighted magnetic resonance images and intermediate signal intensity on T2-weighted images. Radiation-induced changes in the pelvis include osteopenia, increased bone density, and widening and irregularity of the sacroiliac joints. Radiation-induced osteochondromas are radiographically identical to those that arise spontaneously. Radiographic findings in radiation-induced sarcoma demonstrate an aggressive pattern of bone destruction. Awareness of the varied radiographic manifestations of radiation-induced changes in bone and correlation with clinical features and the radiation field will usually allow distinction of these changes from those associated with other pathologic conditions.     

Odontogenic focus as the etiology of cerebral ischemia]

Several authors have established a relationship between osteoporosis and periodontal disease. The ageing process is associated with a loss of both oral and total bone mass. It has been shown that a reduction of bone mineralization aggravates pathological periodontal changes, resulting in less support for the teeth. The present study investigates the nutritional influences that may condition the appearance of both pathological process. Insufficient dietary calcium and a reduction in the calcium: phosphorous ratio may favour the appearance of both these conditions by promoting bone reabsorption. Bone loss affects the following in descending order: jaw bones (especially alveolar bone), cranial bones, ribs, vertebrae and long bones. Alveolar bone which has the highest rate of renewal, is affected first and consequently is the most severely affected in the long term. The role of calcium in the etiology of osteoporosis is a controversial issue. Nevertheless, its implication has been proven in numerous investigations. The effect of adequate calcium intake on dental health has formed the basis of several recent studies. These investigations have demonstrated that increased calcium intake improves the suffering of inflammatory processes and tooth mobility in patients suffering from gingivitis with haemorrhaging. Based on the results of studies which link dietary calcium and phosphorous to the risk of osteoporosis and periodontal disease, and bearing in mind that in a large proportion of the Spanish population calcium intake is below that recommended, there is a need for a general improvement of the diet. It may be of special interest to increase the calcium intake of patients suffering periodontal disease. It may also help in the prevention of osteoporosis.     

Solution-structure of a peptide designed to mimic the C-terminal hexapeptide of endothelin

Fatty change in donor livers is a risk factor for poor function after orthotopic liver transplantation. Various prevalences of steatosis have been reported in time 0 biopsies. The aim of this research was to determine, in a longitudinal study, the degree (percent of hepatocytes involved) and type (size of vacuoles) of fatty change shown by various histologic techniques. Four staining methods were used on sections from three liver wedge biopsies--at liver procurement, at the back-table, and after reperfusion--from 83 consecutive donor livers. Results in Sudan III-stained (SS) sections showed the greatest sensitivity (87.1%), negative predictive value (91.8%), and agreement rate (k = 0.77) when compared with results in thin (1 micron) plastic-embedded toluidine blue-stained (TBS) sections. High-grade steatosis (> 30% steatotic hepatocytes) was identified in 49.4% of SS sections, 46.9% of TBS sections, 38.5% of frozen hematoxylin-eosin (H&E)-stained sections, and 20.7% of deparaffinated H&E-stained sections. Microscopic observations disclosed two types of steatotic pattern: (1) A predominantly small-droplet lipid vacuolzation (high-grade microsteatosis), similar to the steatosis associated with Reye syndrome, was seen in 29% of SS sections and 25% of TBS sections--approximately one-fourth of grafts; and (2) a combined pattern of large and small fat drops (high-grade macromicrosteatosis) was seen in 20% of SS sections and 22% of TBS sections. We concluded that moderate to severe steatosis is a frequent finding in donor livers. The difficulty in detecting lipidic microvacuoles in H&E-stained sections may be the reason for underestimating the grade of fatty change or even for diagnosing as normal some biopsies with high-grade microsteatosis.     

Influence of fat intake and caloric restriction on bone in aging male rats

Caloric and fat intake may have important skeletal consequences. To evaluate this possibility, skeletal effects of adult-onset caloric restriction (CR) at differing fat intakes were assessed in male Lobund-Wistar rats. At age 17 months, two groups of animals received an anti-obesity diet, restricted approximately 35% from individual ad libitum baseline calorie consumption, and two groups received a diet approximately 50% restricted. Dietary fat concentrations were 5, 15, 15, and 25% by weight, respectively. At ages 20, 24, 28, 30, and 32 months, ex vivo femoral bone densitometry and serum biochemical analyses were performed. Body weight (BW) decreased with time on CR in each group (p < .005), declining faster at the more severe restriction (p = .001). Femoral bone mineral contents (BMC) were also reduced. After adjusting for bone area and BW differences among groups, the only significant difference was a reduction in distal femur BMC in the 25% fat group subjected to more severe CR (p = .02). No differences were observed in serum parathyroid hormone, calcium, phosphorus, or creatinine. Femoral bone loss occurred with CR. This was entirely accounted for by reduction in BW. Higher dietary fat content did not affect BW in CR animals, but did result in lower distal femur BMC.     

Bone disease in patients with primary sclerosing cholangitis: prevalence, severity and prediction of progression

BACKGROUND/AIMS: Osteopenia is a common complication in some chronic cholestatic liver diseases. Our aims were to determine the prevalence and severity of bone disease in patients with primary sclerosing cholangitis; and identify risk factors to predict the presence and progression of osteopenia. METHODS: Eighty-one patients involved in a randomized trial of ursodeoxycholic acid were analyzed. Bone mineral density of the lumbar spine was determined at entry and at annual intervals. RESULTS: Bone mineral density of the lumber spine in primary sclerosing cholangitis patients was significantly lower than expected when compared to normal values adjusted for age, sex and ethnic group at entry (p<0.005), and after 1 year (p<0.05), 2 years (p<0.05), 4 years (p<0.005) and 5 years of follow-up (p<0.005). Seven patients (8.6%) had bone mineral density of the lumber spine below the fracture threshold at entry. These patients were significantly older, had a longer duration of inflammatory bowel disease and more advanced primary sclerosing cholangitis. The rate of bone loss in primary sclerosing cholangitis patients and expected in normal controls was 0.01+/-0.02 g x cm(-2) x year(-1) and 0.003+/-0.003 g x cm(-2) x year(-1), respectively (p = NS), and was similar in patients receiving placebo and ursodeoxycholic acid. Age was the only variable inversely related with baseline bone mineral density of the lumber spine (p<0.0001). None of the variables predicted progression of the bone disease. CONCLUSIONS: Severe osteoporosis occurs in few patients with primary sclerosing cholangitis, but it should be suspected in patients with longer duration of inflammatory bowel disease and more advanced liver disease. Its presence, severity and progression cannot be accurately evaluated by routine clinical, biochemical, or histological variables. Ursodeoxycholic acid does not affect the rate of bone loss in primary sclerosing cholangitis.