Vitamin E protection of obesity-enhanced vascular calcification in uremic rats.

This study aimed to determine the extent of extraskeletal calcification in uremic Zucker rats, by comparing obese and lean phenotypes, and to evaluate the influence of vitamin E (VitE) on the development of calcifications in both uremic rats and human vascular smooth muscle cells (HVSMCs) cultured in vitro. Zucker rats of lean and obese phenotypes with normal renal function [control (C); C-lean and C-obese groups] and with uremia [5/6 nephrectomy (Nx); Nx-lean and Nx-obese groups] and uremic rats treated with VitE (Nx-lean + VitE and Nx-obese + VitE groups) were studied. Uremic groups were subjected to Nx, fed a 0.9% phosphorus diet, and treated with calcitriol (80 ng/kg ip). The aortic calcium concentration was significantly higher (P < 0.05) in Nx-obese rats (10.0 ± 2.1 mg/g tissue) than in Nx-lean rats (3.6 ± 1.3 mg/g tissue). A decrease in plasma glutathione peroxidase activity was observed in Nx-obese rats compared with Nx-lean rats (217.2 ± 18.2 vs. 382.3 ± 15.5 nmol·min(-1)·ml(-1), P < 0.05). Treatment with VitE restored glutathione peroxidase activity and reduced the aortic calcium concentration to 4.6 ± 1.3 mg/g tissue. The differences in mineral deposition between Nx-lean, Nx-obese, Nx-lean + VitE, and Nx-obese + VitE rats were also evidenced in other soft tissues. In HVSMCs incubated with high phosphate, VitE also prevented oxidative stress and reduced calcium content, bone alkaline phosphatase, and gene expression of core-binding factor-α1. In conclusion, uremic obese rats develop more severe calcifications than uremic lean rats and VitE reduces oxidative stress and vascular calcifications in both rats and cultures of HVSMCs.

Comparison of different treatments for oestrous induction in seasonally anovulatory mares.

The aim of this study was to evaluate the effects of different treatments for induction and synchronization of oestrus and ovulation in seasonally anovulatory mares. Fifteen mares formed the control group (C), while 26 mares were randomly assigned to three treatment groups. Group T1 (n = 11) were treated with oral altrenogest (0.044 mg/kg; Regumate(®) ) during 11 days. Group T2 (n = 7) was intravaginally treated with 1.38 g of progesterone (CIDR(®) ) for 11 days. In group T3 (n = 8), mares were also treated with CIDR(®) , but only for 8 days. All mares received PGF2α 1 day after finishing the treatment. Sonographic evaluation of follicles, pre-ovulatory follicle size and ovulation time was recorded. Progesterone and leptin levels were analysed. Results show that pre-ovulatory follicles were developed after the treatment in 88.5% of mares. However, the pre-ovulatory follicle growth was dispersal, and sometimes it was detected when treatment was not finished. While in mares treated with intravaginal device, the follicle was soon detected (1.5 ± 1.2 days and 2.3 ± 2.0 days in T2 and T3 groups, respectively), in T1 group, the pre-ovulatory follicle was detected slightly later (3.9 ± 1.6 days). The interval from the end of treatment to ovulation did not show significant differences between groups (T1 = 13.1 ± 2.5 days; T2 = 11.0 ± 3.6 days; T3 = 13.8 ± 4.3 days). The pregnancy rate was 47.4%, similar to the rate observed in group C (46.7%; p > 0.05). Initial leptin concentrations were significantly higher in mares, which restart their ovarian activity after treatments, suggesting a role in the reproduction mechanisms in mares. It could be concluded that the used treatments may be effective for oestrous induction in mares during the late phase of the seasonally anovulatory period. Furthermore, they cannot synchronize oestrus, and then, it is necessary to know the reproductive status of mares when these treatments are used for oestrous synchronization.

High-speed plasma measurements with a plasma impedance probe.

Plasma impedance probes (PIPs) are a type of RF probe that primarily measures electron density. This work introduces two advancements: a streamlined analytical model for interpreting PIP-monopole measurements and techniques for achieving ≥1 MHz time-resolved PIP measurements. The model's improvements include introducing sheath thickness as a measurement and providing a more accurate method for measuring electron density and damping. The model is validated by a quasi-static numerical simulation, which compares the simulation with measurements, identifies sources of error, and provides probe design criteria for minimizing uncertainty. The improved time resolution is achieved by introducing higher-frequency hardware, updated analysis algorithms, and a more rigorous approach to RF calibration. Finally, the new model and high-speed techniques are applied to two datasets: a 4 kHz plasma density oscillation resolved at 100 kHz with densities ranging between 2 × 1014 and 3 × 1015 m-3, and a 150 kHz oscillation resolved at 4 MHz with densities ranging between 4 × 1014 and 6 × 1014 m-3.

Spontaneous electromagnetic emission from a strongly localized plasma flow.

Laboratory observations of electromagnetic ion-cyclotron waves generated by a localized transverse dc electric field are reported. Experiments indicate that these waves result from a strong E×B flow inhomogeneity in a mildly collisional plasma with subcritical magnetic field-aligned current. The wave amplitude scales with the magnitude of the applied radial dc electric field. The electromagnetic signatures become stronger with increasing plasma ß, and the radial extent of the power is larger than that of the electrostatic counterpart. Near-Earth space weather implications of the results are discussed.

Metabolic acidosis inhibits soft tissue calcification in uremic rats.

Metabolic acidosis is common in patients with chronic kidney disease, which is known to affect bone metabolism. We examined the effect of metabolic acidosis on the development of vascular and other soft-tissue calcifications in uremic rats treated with calcitriol. Extraskeletal calcification was measured in vivo, in control rats and rats with a remnant kidney model of uremia with or without ammonium chloride-induced acidosis. Soft-tissue calcification was assessed histologically, by measurement of the expression of the sodium-dependent phosphate cotransporter Pit-1 and by quantification of tissue calcium and phosphorus. Calcitriol administration to uremic rats resulted in significant deposition of material positive for von Kossa stain in the aorta, stomach, and kidney, elevated aortic calcium and phosphorus, increased aortic Pit-1 expression, and high mortality. Calcitriol-treated uremic rats with acidosis did not develop aortic or soft-tissue calcification, did not increase aortic Pit-1 expression, and had significantly lower mortality. Additionally, an acidotic environment prevented calcification of vascular smooth muscle cells in vitro. Our study shows that metabolic acidosis inhibits extraskeletal calcification.

The influence of anticoagulants on the measurement of total protein concentration in equine peritoneal fluid.

The aim of this study was to evaluate the influence of two commonly used anticoagulants (K3EDTA and lithium heparin) on refractometric and spectrophotometric measurement of total protein (TP) concentration in equine peritoneal fluid samples. The influence of a commercial solution of K3EDTA, a solution of K3EDTA in distilled water and lithium heparin on the refractometric and spectrophotometric (biuret) quantification of TP content in peritoneal fluid samples was assessed. Total protein concentration measured by refractometry was consistently overestimated in samples with commercial K3EDTA. The solution of K3EDTA in distilled water only caused TP overestimation at high K3EDTA concentrations (>5 micromol/ml). By contrast, lithium heparin did not influence the refractometric values of TP. Neither anticoagulant modified TP values when measured by the biuret method. In conclusion, the use of K3EDTA as anticoagulant may result in a significant overestimation of TP values of peritoneal fluid samples measured by refractometry.

Endocrine, morphometric, and ultrasonographic characterization of neck adiposity in Andalusian horses.

Equine metabolic syndrome (EMS) can be diagnosed by hormonal measurements; however, it would be important to find simpler measurements that allow easy identification of affected or at risk individuals. In horses, the dorsal neck region is one of the most frequent anatomical sites for fat deposition and neck obesity has been linked to EMS. The aim of this study was to evaluate the association of hormonal markers of obesity (leptin) and insulin resistance (insulin) with morphometric and ultrasonographic neck measurements in Andalusian horses. Plasma leptin and insulin concentrations were measured by RIA in 127 Andalusian horses. Neck circumferences (NC) were measured at 3 equidistant locations at 25%, 50%, and 75% of neck length (NC-25%, NC-50%, and NC-75%). At the same 3 locations, subcutaneous fat thickness (SFT-25%, SFT-50%, and SFT-75%) was measured ultrasonographically. In the population under study, a tendency to adiposity was confirmed by the elevated plasma leptin levels (7.47 ± 5.03 ng/mL). However, plasma insulin concentrations (4.05 ± 3.74 µIU/mL) were within normal range in most horses. Our results indicate that NC showed significant sexual dimorphism and did not correlate well with hormonal measurements. Ultrasonographic assessment of fat thickness at the base of the neck (SFT-75%) was significantly correlated with both plasma leptin and insulin and did not show differences between males and females. Thus, in the search for a single objective parameter which can be used in large populations, SFT-75% is a potential candidate and may be a meaningful parameter to predict EMS.

Eosinophilic Enteritis in Horses with Motor Neuron Disease.

BACKGROUND: Equine motor neuron disease (EMND) is a neuromuscular disorder that affects adult horses. Although EMND has been linked to vitamin E deficiency, its etiopathogenesis is poorly understood. OBJECTIVES: To describe clinical features, laboratory results, and postmortem findings in a series of young horses with motor neuron disease (MND). ANIMALS: A herd of 15 young Andalusian horses with weakness, weight loss, muscle atrophy, and muscle fasciculations related to restricted intake of green forage. METHODS: A case series is presented in which horses were subjected to a clinical examination and plasma vitamin E measurement. Five severely affected horses were euthanized for detailed postmortem examination. Muscle specimens were taken from the M. sacrocaudalis dorsalis medialis and the M. gluteus medius for histopathologic and morphometric evaluation. RESULTS: MND was diagnosed in 5 horses based on clinical signs, low serum levels of vitamin E (0.11 ± 0.05 mg/dL; normal range,: 0.3-1.5 mg/dL), changes in muscle histopathology (neurogenic atrophy), and spinal cord lesions (neuronal chromatolysis in ventral horns). An unexpected postmortem finding was the presence of intestinal inflammation (catarrhal enteritis, edema, and eosinophilic infiltrate) associated with the presence of giant ciliated protozoa in all of the horses. CONCLUSIONS: Although a mechanistic link could not be established, it is hypothesized that intestinal inflammation may have been involved in the decreased absorption of vitamin E, thus favoring the development of MND.

The influence of the progression of secondary hyperparathyroidism on the set point of the parathyroid hormone-calcium curve.

The influence of secondary hyperparathyroidism (2 HPT) on the set point of the parathyroid hormone (PTH)-Ca(2+) curve is controversial. In vitro experiments have shown an increase in the set point. However, clinical studies with hemodialysis patients have provided a variety of results (increases, decreases and no changes in the set point have been reported). The present study was designed to investigate the influence of the progression of 2 HPT on the set point of the PTH-Ca(2+) curve. The PTH-Ca(2+) curve and the expression of parathyroid calcium receptor (CaR mRNA) and vitamin D receptor (VDR mRNA) have been studied in normal rabbits (group I, n=9) and in nephrectomized rabbits (group II, n=18) at two stages after inducing 2 HPT: 2-3 weeks (group IIA) and 5-6 weeks (group IIB). In group I, the set point of the PTH-Ca(2+) curve was 1.63+/-0.03 mM. A progressive hypocalcemia was detected during the evolution of 2 HPT (groups IIA and IIB). Rabbits from group IIA had a significant (P<0.001) decrease in the set point to values of 1.45+/-0.02 mM. However, the set point increased significantly in group IIB (P<0.001) to 1.56+/-0.03 mM. CaR mRNA was similarly decreased in groups IIA (39+/-12%) and IIB (48+/-7%). No changes were detected in VDR mRNA. In conclusion, a reduction in the set point of the PTH-Ca(2+) curve in response to decreased extracellular Ca(2+) was detected in the early phases of 2 HPT. However, with the progression of 2 HPT the set point tended to increase even though extracellular Ca(2+) was markedly decreased. The increase in the set point in the course of 2 HPT seems to be a complex process that cannot be fully explained by changes in parathyroid CaR mRNA or VDR mRNA.

Diurnal variations in the plasma concentration of parathyroid hormone in dogs.

The plasma concentrations of parathyroid hormone (PTH), ionised calcium (Ca(2+)), total calcium, albumin and inorganic phosphorus, and the pH were measured in blood samples obtained from nine dogs during a period of 26 hours. The plasma pth levels fluctuated slightly during the day, by about 20 pg/ml, but there was a distinct peak (42.8 [8.8] pg/ml) at 07.00. Plasma Ca(2+) showed a diurnal pattern in which two peaks (increases of 0.03 mmol/l) were observed at 05.00 and 17.00, and the plasma concentration of inorganic phosphorus showed a similar pattern. There were no diurnal changes in total calcium or albumin.

Nonlinear Generation of Electromagnetic Waves through Induced Scattering by Thermal Plasma.

We demonstrate the conversion of electrostatic pump waves into electromagnetic waves through nonlinear induced scattering by thermal particles in a laboratory plasma. Electrostatic waves in the whistler branch are launched that propagate near the resonance cone. When the amplitude exceeds a threshold ~5 × 10(-6) times the background magnetic field, wave power is scattered below the pump frequency with wave normal angles (~59°), where the scattered wavelength reaches the limits of the plasma column. The scattered wave has a perpendicular wavelength that is an order of magnitude larger than the pump wave and longer than the electron skin depth. The amplitude threshold, scattered frequency spectrum, and scattered wave normal angles are in good agreement with theory. The results may affect the analysis and interpretation of space observations and lead to a comprehensive understanding of the nature of the Earth's plasma environment.

Effects of two calculolytic diets on parameters of feline mineral metabolism.

OBJECTIVES: To evaluate the influence of two feline calculolytic diets on selected parameters of mineral metabolism. MATERIALS AND METHODS: Two dry commercial diets designed for struvite urolith dissolution were evaluated in 14 cats. The study was designed as a two-sequence, four-period crossover protocol with a baseline period, two 60-day "run-in" periods in which calculolytic diets (Diet 1 and Diet 2) were fed and one 30-day "wash-out" period. Data are expressed as median (range). RESULTS: Feeding the calculolytic diets for two months did not alter plasma concentrations of calcium, phosphorus, magnesium and parathyroid hormone. A significant (P < 0.05 in each case) decline in calcitriol was observed after administering both diets from 236.4 (122.4-429.6) to 170.4 (108.0-394.3) pmol/L (Diet 1) and from 278.4 (153.6-492.0) to 177.1 (87.6-392.4) pmol/L (Diet 2). Cats fed Diet 1 showed a significant increase in urine calcium concentration (from 0.3 (0.2-0.5) to 0.4 (0.3-0.7) mmol/L). Magnesium concentration in urine was significantly increased with both diets, from 1.4 (0.1-1.7) to 1.5 (1.3-2.4) mmol/L (Diet 1) and from 1.1 (0.4-1.9) to 2.0 (0.1-3.1) mmol/L (Diet 2). CLINICAL SIGNIFICANCE: Both diets resulted in an increased urinary concentration of magnesium, through different mechanisms: urine acidification (Diet 1) and increased sodium load (Diet 2).

Hysteresis of the PTH-calcium curve during hypocalcemia in the dog: effect of the rate and linearity of calcium decrease and sequential episodes of hypocalcemia.

Several studies have shown the presence of hysteresis of the parathyroid hormone (PTH)-calcium relationship in both normal humans and hemodialysis patients; for hypocalcemia, hysteresis is defined as a lower PTH level for the same serum calcium during the recovery from than the induction of hypocalcemia. However, some have questioned whether hysteresis is only a function of the rate and/or direction of change in calcium, and others have proposed that hysteresis is due to depletion of PTH stores. To address these issues, two groups of dogs were studied. To induce hypocalcemia, sodium EDTA (50 mg/kg) was infused either over 60 (termed slow) or 30 (termed fast) minutes; immediately after the cessation of the ethylenediamine tetracetate (EDTA) infusion, calcium chloride (0.75 mEq/kg) was infused over 60 or 30 minutes, respectively, to correct the hypocalcemia. The EDTA infusion produced a linear decrease in serum calcium by progressively increasing the infusion rate at regular intervals. A second cycle of hypocalcemia and recovery using the same protocol was started immediately after the completion of the first cycle. To determine whether a nonlinear decrease in the serum calcium affected the PTH response to hypocalcemia, a third group of dogs, termed superfast, was studied; in this group, EDTA was infused for 30 minutes at a constant rate of 50 mg/kg. The hysteretic loops of PTH produced by the two sequential slow and fast cycles and the superfast cycle during the induction of and recovery from hypocalcemia were similar. Moreover, the maximal PTH level for the two sequential slow and fast cycles and the superfast cycle was not different even though the rates of calcium decrease varied and the calcium decrease was nonlinear in the superfast cycle. In conclusion, (1) since hysteresis was reproducible and the maximal PTH was not different during two sequential cycles of hypocalcemia, hysteresis is not due to PTH depletion; (2) the PTH-calcium curve is not affected by the rate at which hypocalcemia is induced; and (3) the maximal PTH level is not influenced by either the rate or linearity of the reduction in serum calcium.

Effect of phosphate on parathyroid hormone secretion in vivo.

Alterations in phosphate homeostasis play an important role in the development of secondary hyperparathyroidism in renal failure. Until recently, it was accepted that phosphate retention only increased parathyroid hormone (PTH) secretion through indirect mechanisms affecting calcium regulation and calcitriol synthesis. However, recent in vitro studies have suggested that phosphate may directly affect PTH secretion. Our goal was to determine whether in vivo an intravenous phosphate infusion stimulated PTH secretion in the absence of changes in serum calcium. Three different doses of phosphate were infused intravenously during 120 minutes to increase the serum phosphate concentration in dogs. Sulfate was also infused intravenously as a separate experimental control. A simultaneous calcium clamp was performed to maintain a normal ionized calcium concentration throughout all studies. At the lowest dose of infused phosphate (1.2 mmol/kg), serum phosphate values increased to approximately 3 mM, but PTH values did not increase. At higher doses of infused phosphate (1.6 mmol/kg and 2.4 mmol/kg), the increase in serum phosphate to values of approximately 4 mM and 5 mM, respectively, was associated with increases in PTH, even though the ionized calcium concentration did not change. Increases in PTH were not observed until 30-60 minutes into the study. These increases were not sustained, since by 120 minutes PTH values were not different from baseline or controls despite the maintenance of marked hyperphosphatemia. During the sulfate infusion, serum sulfate values increased by approximately 3-fold, but no change in PTH values were observed. In conclusion, an acute elevation in serum phosphate stimulated PTH secretion in the intact animal, but the magnitude of hyperphosphatemia exceeded the physiologic range. Future studies are needed to determine whether PTH stimulation is more sensitive to phosphate loading in states of chronic phosphate retention. Moreover, the mechanisms responsible for the delay in PTH stimulation and the failure to sustain the increased PTH secretion need further evaluation.

Both duration and degree of hypercalcemia influence the reduced parathyroid hormone response to hypocalcemia after hypercalcemia.

The stimulation of parathyroid hormone (PTH) secretion by hypocalcemia is reduced when hypocalcemia is preceded by hypercalcemia. The present study investigates whether the duration and degree of hypercalcemia influence the reduced PTH response to hypocalcemia after hypercalcemia. In addition, the implication of the arachidonic acid (AA) signaling pathway in this effect is evaluated. The PTH response to hypocalcemia has been studied in a control group and in four groups of rabbits subjected to hypercalcemia for different periods of time (between 30 and 120 min) and at two levels of hypercalcemia (1 x 9 and 2 x 1 mM). AA levels have been measured in parathyroid glands from rabbits subjected to hyper- and hypocalcemia. When compared with controls, rabbits that had been hypercalcemic (2 x 1 mM) for 2 h showed a markedly attenuated PTH response to hypocalcemia (50% of normal PTHmax), rabbits that had been in hypercalcemia (2 x 1 mM) for 75 min had an intermediate PTH response to hypocalcemia (70% of normal PTHmax) and rabbits that had been subjected to either 30 min hypercalcemia of 2 x 1 mM or 120 min hypercalcemia of 1 x 9 mM had a normal PTH response to hypocalcemia. AA levels increased in hypercalcemia and decreased in hypocalcemia; however, no differences were observed at either calcium level in short-time (30 min) versus long-time (120 min) hypercalcemia. In conclusion, the attenuated PTH response to hypocalcemia after hypercalcemia is dependent on both the period of time that the parathyroid glands have been exposed to hypercalcemia and the degree of hypercalcemia. In addition, this reduced PTH response does not seem to be related to changes in the AA signaling pathway.

The influence of acute and chronic hypercalcemia on the parathyroid hormone response to hypocalcemia in rabbits.

OBJECTIVE: To investigate the influence of acute and chronic hypercalcemia on the parathyroid hormone (PTH) response to hypocalcemia. DESIGN: The PTH response to hypocalcemia has been evaluated in three groups of rabbits: Group I, normal rabbits, Group II, normal rabbits subjected to an acute hypercalcemic clamp (induced by CaCl(2) infusion) and Group III, rabbits with chronic hypercalcemia (due to surgical reduction of renal mass). RESULTS: In Group I (baseline Ca(2+)=1.69+/-0.02 mM), hypocalcemia resulted in stimulation of PTH secretion which reached a maximum (PTHmax) of 91.7+/-6.4 pg/ml. In rabbits from Group II, which also had normal baseline Ca(2+) (1.70+/-0.02 mM), plasma Ca(2+) was maintained at an elevated level for 2 h, at around 2.05 mM. The PTH response to hypocalcemia in Group II was attenuated and the PTHmax in these rabbits was 45.6+/-7.4 pg/ml. In rabbits from Group III, baseline Ca(2+) was elevated (2.06+/-0.06 mM) for 1 month. The PTH response to hypocalcemia in Group III was esentially the same as in Group I and PTHmax reached levels of 94.8+/-9.9 pg/ml. CONCLUSIONS: A difference in PTH response to hypocalcemia has been found in rabbits after exposure to either acute or chronic hypercalcemia. After acute hypercalcemia, an attenuated PTH response to hypocalcemia has been identified. Chronic hypercalcemia, however, did not influence the PTH response to hypocalcemia.

A reduced PTH response to hypocalcemia after a short period of hypercalcemia: a study in dogs.

The relationship between PTH and calcium is best represented as a sigmoidal curve. In the normal animal and human, basal PTH is positioned at approximately 25% of maximal PTH and responds rapidly to small changes in calcium in either direction. Since PTH secretion is designed to respond to either hypo- or hypercalcemia, the study was performed to evaluate whether the parathyroid gland would respond differently to hypocalcemia when the reduction in serum calcium was initiated from sustained hypercalcemia with maximal PTH suppression. Nine dogs were studied and the experimental protocol consisted of two separate parts in which the same dogs were used and the order of study was randomly assigned. For the hypercalcemic part, calcium chloride was infused intravenously to increase serum calcium to between 1.60 and 1.70 mM at 30 minutes and then continued for another 90 minutes to clamp the serum calcium at this level. Sodium EDTA was then infused to lower the serum calcium at a constant rate to less than 0.85 mM. For the normocalcemic part, 5% dextrose in water was infused for two hours to control for fluid volume and time, and then EDTA was infused to lower the serum calcium at a constant rate to less than 0.85 mM. The results show that for the same serum calcium concentration at every 0.05 mM decrement in serum calcium below normal, PTH was less in the hypercalcemic than the normocalcemic dogs (P < 0.02). During the induction of hypocalcemia in the normocalcemic dogs, a characteristic sigmoidal curve was observed in which a small decrease in the serum calcium induced a brisk increase in PTH and a maximal PTH level was rapidly attained; however, during the induction of hypocalcemia in the hypercalcemic dogs, the increase in PTH was progressive, but linear and it was not certain that a maximal PTH level was attained. In conclusion, a sustained period of hypercalcemia resulted in a decreased PTH response to hypocalcemia and reduced the efficiency of the sigmoidal PTH-calcium relationship. Whether the mechanism for this difference in PTH secretion is due to secretory products, modification of the calcium receptor, or changes in intercellular communication among parathyroid cells deserves further study.

Significance of CA 72-4 in colorectal carcinoma. Comparison with CEA and CA 19-9.

In order to evaluate the usefulness of CA 72-4 tumour-associated antigen assay in colorectal carcinoma, we have studied 70 patients with benign colorectal diseases and 127 patients with colorectal cancer at different stages. The results were compared with those obtained by CEA and CA 19-9. No significant differences were found in any of the stages according to Dukes' classification when comparing stages A, B and C. However, there were differences with CEA (P < 0.001), CA 19-9 (P < 0.001) and CA 72-4 (P < 0.001) when comparing stages A, B and C with stage D. In the ROC curve, at a specificity of 95%, the sensitivities of CEA, CA 19-9 and CA 72-4 were 46.4%, 20.5% and 40.1%, respectively. In conclusion, CA 72-4 showed better sensitivity and specificity scores than CA 19-9. CEA increased individual sensitivity from 46.4% to 59.8% when combined with CA 72-4, showing a decrease of merely 0.9% in specificity.

Vitamin C status, cervico-vaginal infection and premature rupture of amniotic membranes.

A prospective study to evaluate the role of vitamin C and cervico-vaginal infection in the premature rupture of amniotic membranes (PROM) was designed. The leukocyte vitamin C levels of 44 pregnant women that did not consume vitamin supplements was evaluated at weeks 20, 28 and 32 of pregnancy. On each evaluation the presence of cervico-vaginal infection was diagnosed and treated. The leukocyte vitamin C level throughout gestation showed a decrease towards week 28 and then it recovered at the end of pregnancy. Six of every ten women had normal flora in their vaginal secretion cultures. Eleven cases had PROM (0.24), no association was found between cervico-vaginal infection and PROM. The leukocyte vitamin C levels on week 20 of gestation showed an association with PROM. (chi 2 = 6.34, p < 0.05, odds ratio 6.75 [CI 1.26-26.03]).