SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Parturient paresis (hypocalcemia) is most likely to affect dairy cattle around the time of parturition. It causes progressive neuromuscular dysfunction and flaccid paralysis. Older dairy cows, cows with a history of parturient paresis during a previous lactation, high-producing cows, and cows from the Jersey and Guernsey breeds are at highest risk for developing parturient paresis. Nonparturient hypocalcemia may also occur and is related to events other than parturition, such as severe stress, that temporarily overwhelm the mechanisms of calcium homeostasis. Beef cattle, sheep, and goats are affected less frequently by hypocalcemia than are dairy cows. Because these species are not as stressed for milk production as dairy cattle, nonparturient hypocalcemia makes up a higher proportion of cases in nondairy ruminants. Clinical signs of hypocalcemia in beef cattle, sheep, and goats tend toward hyperesthesia and tetany rather than the classic flaccid paralysis that occurs in dairy cattle with parturient hypocalcemia. Prompt and effective treatment of hypocalcemia helps to reduce the incidence of secondary complications, such as muscle damage or mastitis. The standard treatment regimen of 500 ml of 23 per cent calcium gluconate, administered intravenously, will elicit a favorable response in approximately 75 per cent of recumbent cows within 2 hours of treatment. Relapses following successful initial therapy are common and may be prevented in part by supplementation of intravenous treatment with an additional 500 ml of 23 per cent calcium gluconate administered subcutaneously. Proper nursing care following treatment speeds recovery and reduces the incidence of secondary complications owing to hypocalcemia.
Parturient paresis (milk fever) is a hypocalcemic disorder caused by the onset of lactation in the dairy cow. In most cows a complete recovery follows a single iv calcium treatment to correct the acute hypocalcemia. However, about 20% of cows treated for parturient paresis experience recurring episodes of hypocalcemia (relapses) requiring further treatment. Analysis of plasma from 8 nonrelapsing parturient paretic and 11 relapsing parturient paretic cows revealed differences in plasma 1,25-dihydroxyvitamin D [1,25-(OH)2D] concentrations before and during the development of hypocalcemia. In nonrelapsing cows, plasma 1,25-(OH)2D increased to 4- to 5-fold as plasma calcium concentrations declined during the first stage of parturient paresis. In relapsing cows, decreases in plasma calcium concentrations during the first stage of parturient paresis were accompanied by just a 2- to 2.5-fold increase in plasma 1,25-(OH)2D. Plasma 1,25-(OH)2D eventually increased 4- to 5-fold in the relapsing cows, but this response was delayed 24-48 h compared with the response in the nonrelapsing cows. Plasma PTH concentration profiles were similar in relapsing and nonrelapsing cows, suggesting that renal 25-hydroxyvitamin D 1 alpha-hydroxylase was temporarily refractory to stimulation by PTH in the relapsing cows. In both groups of cows recovery from parturient paresis began about 12-24 h after plasma 1,25-(OH)2D concentrations had increased 4- to 5-fold. These data imply that lack of production of 1,25-(OH)2D is an important factor in predisposing the cow to relapses of parturient paresis and is critical for recovery from the hypocalcemia associated with the onset of lactation.
The prophylactic effect in parturient paresis of an intramuscular injection of 10 million i.u. vitamin D3 one week prior to the expected calving date, was investigated in 84 cows which had previously suffered from parturient paresis. Clinical observations in connection with the development of parturient paresis after injection of vitamin D3 were compared with corresponding observations made on cows within the same population at the previous calving when no vitamin D3 was administered. The incidence of clinical parturient paresis in cows given vitamin D3 was 44.3 per cent. There were no significant differences in the incidence of parturient paresis in cows injected with vitamin D3 during the periods less than 2, 2--4, 5--8 and greater than 8 days before parturition. Average plasma calcium levels (mg/100 ml) before first calcium treatment, results of treatment, and the incidence of retained placenta in vitamin D3 injected cows did not differ significantly from corresponding data for cows with clinical parturient paresis which had not been given vitamin D3 before calving. It is concluded that vitamin D3 does not have any prophylactic effect in parturient paresis in cows in Eastern Norway.
Forty-one aged Jersey cows were fed a high Ca diet prior to parturition to predispose them to parturient paresis. Twenty-one of the cows were treated with 24-F-1,25-dihydroxyvitamin D3, a synthetic analogue of 1,25-dihydroxyvitamin D3, 7 d before the expected parturition. Treated cows received either 100 micrograms (n = 7) or 150 micrograms (n = 14) of 24-F-1,25-dihydroxyvitamin D3, intramuscularly at 7-d intervals until the cow calved. Incidence of parturient paresis among untreated animals was 85% (17/20). Injections of 100 micrograms of 24-F-1,25-dihydroxyvitamin D3 reduced the incidence of parturient paresis to 43% (3/7), whereas 150 micrograms injections of 24-F-1,25-dihydroxyvitamin D3 reduced the incidence of parturient paresis to 29% (4/14). Plasma concentrations of hydroxyproline were not elevated prior to parturition in 24-F-1,25-dihydroxyvitamin D3-treated cows, indicating that treatment did not stimulate bone resorption and that the ability of 24-F-1,25-dihydroxyvitamin D3 to prevent parturient paresis likely resides in its ability to stimulate intestinal Ca absorption prior to parturition. Further, cows treated with 24-F-1,25-dihydroxyvitamin D3 that developed parturient paresis had lower than normal plasma concentrations of 1,25-dihydroxyvitamin D, indicating that 24-F-1,25-dihydroxyvitamin D3 treatment impairs the metabolism of 25-hydroxyvitamin D in response to hypocalcemia. These data suggest that injection of 24-F-1,25-dihydroxyvitamin D3, delivered at 7-d intervals prior to parturition, can effectively reduce incidence of parturient paresis in dairy cows.
Dry cow feeding and management were examined for predisposing factors for parturient paresis in 1,983 Holstein cows from New York Dairy Herd Improvement Cooperative records, monthly technician visits to 31 farms, and questionnaires. Variables were estimated transmitting ability, season of calving, lactation number, parturient paresis, estimated potential hours per day of exercise, and estimated nutrient intakes (protein, calcium, phosphorus, and energy) during the preceding dry period. Nutrient intakes were estimated by farmers for the average dry cow (season dependent) in their herd for the early (greater than or equal to 3 wk prepartum) and late portions of the dry period. Intakes were percentages of National Research Council requirements for a 550 kg dry cow in the last 2 mo of gestation. Nutrient intakes were coded by ranking the herds by percentage of each requirement. Codes represented the approximate lower third, middle third, and top third of the herds. Individual cows were assigned their herd nutrition codes by their season of calving. For stepwise discriminant analysis, the group variable was parturient paresis (94 cases, 1,889 controls). As lactation number (most important) and estimated transmitting ability (second most important) increased, incidence of parturient paresis increased. Parturient paresis was reduced with high dietary protein fed during the early stage of the dry period, with low phosphorus and high energy (lead feeding) closer to calving, and with decreased opportunity for exercise. Most cows were overfed calcium, especially in the late stage of the dry period, but calcium intake was not important when phosphorus was low.
Twenty-one aged Jersey cows were fed a high calcium diet prior to parturition to predispose them to parturient paresis. Eleven cows were implanted subcutaneously with pellets containing 24F-1,25-dihydroxyvitamin D3 7 d before the expected date of parturition and thereafter at 7-d intervals until parturition. Ten cows were left untreated to serve as controls. Incidence of parturient paresis among control animals was 80% (8/10). Treatment reduced the incidence of parturient paresis to 9% (1/11). The mean observed plasma calcium concentration nadir of implanted cows was 6.61 +/- .40 mg/dl, which was significantly greater than the plasma calcium nadir of 4.45 +/- .39 mg/dl observed in the control cows. Two steers were implanted with and three nonpregnant, nonlactating cows received intramuscular injections of 24F-1,25 dihydroxyvitamin D3 to contrast circulating plasma concentrations achieved by the two routes. Intramuscular injection and implantation resulted in plasma 24F-1,25 dihydroxyvitamin D3 concentrations above 300 pg/ml for the first 48 h after administration. From d 4 until d 11 after administration, plasma concentration was maintained between 164 and 89 pg/ml in the implanted steers. Plasma concentration was undetectable 7 d after an intramuscular injection. These data indicate that, with refinement, sustained release of 24F-1,25 dihydroxyvitamin D3 can be successfully used to reduce the incidence of parturient paresis.
A synthetic biologically active derivative of vitamin D (350 microgram of 1alpha-hydroxycholecalciferol [1alpha(OH)CC]) was injected into 2 nonlactating 7-year-old Israeli-Friesian cows. Plasma calcium values increased after 24 hours, peaked at 48 hours, and returned to base-line values 120 hours after injection. An injection of 350 microgram of 1alpha(OH)CC was given to 23 parturient-paresis-prone Israeli-Friesian cows from 7 days to 6 hours prepartum; 13 cows were injected once, 6 were injected twice, and 4 were injected 3 times, all at 48-hour intervals. Parturient-paresis-prone cows (n = 23) of the same breed were used as controls. Within 0 to 36 hours postpartum, plasma calcium concentrations were found to be higher in cows injected with 1alpha(OH)CC than in the control cows. The increase was highly significant (P less than 0.01) in cows injected at least twice. None of the cows injected with 1alpha(OH)CC, within 72 to 24 hours prior to calving developed parturient paresis; but 9 of 23 control cows developed parturient paresis. Prior to calving, none of the injected cows developed hypercalcemia and there was no local or systemic clinically detectable signs of toxiosis. When given at the right time prepartum, 1alpha(OH)CC is considered to be an improvement over previous methods of preventing bovine parturient paresis.
Four trials involved intravenous or intramuscular injections of 1alpha-hydroxyvitavin D3 to test efficacy in preventing parturient paresis. Use of .1 mg intravenously afforded total protection compared with an incidence of 33% (2/6) in controls. Intramuscular injections of .1 mg in 2 ml propylene glycol and .3, .5, and 1.0 mg in 5 ml corn oil resulted in 0, 15.7, 20, and 0% incidence of parturient paresis compared with 33, 16.7, 37.5, and 37.5% incidence of parturient paresis in the controls. There was a rapid increase in serum calcium (12 to 24 h) in response to intravenous treatment, whereas the response to intramuscular injections was gradual but was maintained longer. To evaluate the safety of 1alpha-hydroxyvitamin D3, eight cows, two per treatment, were given intramuscular doses of .5, 1.0, 1.5, or 3.0 mg (three 1.0 mg injections) in 5 ml corn oil. No clinical or pathological evidence of hypervitaminosis C or soft tissue calcification was found. Tissue taken from the injection site 15 days after last injection contained 3 to 38 IU vitamin D activity per 100 g wet tissue compared with control of 8 to 15 IU per 100 g. Total vitamin D activity of milk taken the 11th milking postpartum from cows receiving .5 or 1.0 mg had a mean of 13.4 and 22.6 IU vitamin D activity per liter compared to 19 IU per liter for control milk. Milk from the 5th milking postpartum in the cows receiving .5 mg had a mean activity of 14.5 IU per liter. Milk from animals slaughtered for retention studies had a mean activity of 22 IU per liter.
Forty-eight Holstein cows with two or more previous lactations and no history of parturient paresis were randomly assigned to one of four prepartum diets in a 2 x 2 factorial design to determine the effect of dietary supplementation with ammonium salts and Ca intake on serum Ca concentrations at calving. Four diets provided either 53 g total dietary Ca/d or 105 g Ca/d and were either supplemented with ammonium salts [100 g/d each of NH4Cl and (NH4)2SO4] or unsupplemented. Anion-cation balance of the diets, calculated as milliequivalents (Na + K)--(Cl + S), was -75 meq/kg DM with ammonium salts and +189 meq/kg DM without ammonium salts. Experimental diets were fed from 21 d prior to expected parturition until calving. Calcium intake during the feeding period did not affect the incidence of parturient paresis or serum concentrations of ionized Ca at calving. The incidence of parturient paresis was 4% with and 17% without the ammonium salts. Cows fed diets containing ammonium salts had higher serum ionized and total Ca concentrations at parturition. Serum concentrations of Mg, P, Na, K, and Cl on the day of parturition were unaffected by dietary treatment.
The effectiveness of a combination of 1 alpha-hydroxyvitamin D3 and 25-hydroxyvitamin D3 for reducing incidence of parturient paresis in aged Holstein cows was tested. Intramuscular injection of .5 mg of 1 alpha-hydroxyvitamin D3 plus 4 mg of 25-hydroxyvitamin D3 increased plasma 1,25-dihydroxyvitamin D concentrations through parturition. Treatment with 1 alpha-hydroxyvitamin D3 plus 25-hydroxyvitamin D3 raised prepartum serum Ca approximately 2 mg/dl and prepartum serum P approximately 4 to 5 mg/dl higher than untreated controls. Both treated and control cows had approximately a 2-mg/dl decrease in serum Ca following parturition. The prepartum diet of alfalfa silage and hay was supplemented with a grain mixture supplying 100 g of Ca/d from ground limestone. Under these dietary conditions, incidence of parturient paresis was reduced from 33 to 8%. In a separate experiment, treatment with 1 alpha-hydroxyvitamin D3 plus 25-hydroxyvitamin D3 did not reduce incidence of parturient paresis when cows consumed mixed diets of different feed-stuff composition. Further experiments are required to determine specifically the factor or factors responsible for the difference in response to active vitamin D compound administration between the two experiments. Prepartum dietary Ca intake may be one such factor.
Intravenous infusion of synthetic bovine parathyroid hormone for 96 h increased 1,25-dihydroxyvitamin D, Mg, Ca, and hydroxyproline in plasma of pregnant cows within 16, 24, 48, and 72 h, respectively. Plasma Ca concentration was maximal at the end of the 96-h infusion (15.1 mg/100 ml). Plasma concentration of 1,25-dihydroxyvitamin D at 96 h was twice that before parathyroid hormone infusion, indicating that parathyroid hormone stimulated 1,25-dihydroxyvitamin D production in the presence of hypercalcemia. The urinary excretion of hydroxyproline indicated that at least 48 h of parathyroid hormone stimulation was required to stimulate bone resorption in the pregnant cow. Eight periparturient cows were on a high Ca diet prepartum. Four cows were treated with intravenous parathyroid hormone prior to parturition. Four cows were untreated. All four untreated cows developed parturient paresis. None of the cows treated with parathyroid hormone developed parturient paresis. However, two cows that received parathyroid hormone for less than 24 h prior to parturition became hypocalcemic, but not recumbent. Plasma Ca concentrations remained within normal limits in the two other cows that received greater than 60 h parathyroid hormone infusion prior to parturition. We conclude that exogenous parathyroid hormone (1-34) can prevent parturient paresis if administered at least 60 h prior to parturition.
Fifty percent (7/14) of aged cows treated with 4 mg 24,25-dihydroxyvitamin D3 intramuscularly precalving developed parturient paresis shortly after calving compared with 7% (1/14) of controls. Injection of 24,25-dihydroxyvitamin D3 increased concentrations in blood plasma 15 times that in control cows. Blood plasma 1,25-dihydroxyvitamin D concentrations were elevated in all groups on day of calving but were not different. Injection of 24,25-dihydroxyvitamin D3 did not alter the typical plasma profile for calcium, phosphorus, or 1,25-dihydroxyvitamin D of paretic or nonparetic cows around parturition. Although injection of 24,25-dihydroxyvitamin D3 was associated with an increased incidence of parturient paresis, the mechanism remains unknown.
The degree of hypocalcaemia was determined from serum total, and serum ionized calcium concentrations in 27 cows with parturient paresis. Electrocardiographic recordings were made just before the start of the intravenous calcium treatment. The T-oTc interval was determined, but could only be adequately measured in 16 cases because of inherent difficulties in recording from paretic animals. No significant correlation was found between the degree of hypocalcaemia and Q-oTc interval, whether the hypocalcemia was determined from serum total or serum ionized calcium concentrations. This study indicated that measurement of the Q-oTc interval was of very little value as a clinical test for detection of hypocalcaemia and indication of the degree of hypocalcaemia in parturient paresis.
During 1967, 1968 and 1969, blood samples were taken from 83 cows affected by parturient paresis. Whole blood glucose estimations were made on these samples. The range was 1.33 to 10.22 mmol/1 with an average of 3.94 mmol/1. Eighteen cows known to have been affected less than 4 hours had average levels of 3.06 +/- 1.11 mmol/1. All (except one) "previously untreated" cows with levels less than 3.33 mmol/1 were on their feet within 10 minutes whereas cows with higher levels than this had a 28.6% delayed recovery rate. The evidence suggests that low levels have no clinical significance but that higher levels are significant in that they occur as a result of prolongation of attacks of parturient paresis.
Sixty-four cows with parturient paresis were given a standard treatment of 500 ml calcium gluconate (10.7 g Ca++) infusion solution. Twelve of these cows (experimental group = EG 1) additionally received 420 micrograms 1-alpha-hydroxycholecalciferol (1-alpha-OHD3) with 4 mg 25-hydroxycholecalciferol (25-OHD3) by the intramuscular route. A further 9 and 10 cows were given 210 micrograms 1-alpha-OHD3 and 2 mg 25-OHD3 (EG 3) with the calcium infusion, while 10 cows received either 420 micrograms 1-alpha-OHD3 (EG 4) or 210 micrograms 1-alpha-OHD3 (EG 5). Twenty-three cows (EG 2 and 4) which were given a calcium infusion alone acted as controls. The incidence of recurrence could not be reduced by the administration of Vitamin D3 metabolites concurrently with a calcium infusion, although calcium and phosphorus levels were higher between 24 and 48 hours after calcium infusion alone. The combination of 1-alpha-OHD3/25-OHD3 at the higher dosage resulted in the highest calcium levels.