C-reactive protein, leukocyte count and D-dimer monitoring after orthopedic surgery: early diagnosis of infectious or thromboembolic complications. Part two: does d-dimer measurement contribute to the diagnosis of postoperative venous thromboembolism?]

OBJECTIVES: To determine the modification in postoperative D-dimer level as a function of the surgical act and to assess the relevance of this measure for diagnosing thromboembolism. METHOD: A cohort of 179 patients was followed: group 1 comprised 128 patients undergoing lower limb arthroplasty, group 2 comprised 29 patients undergoing lower limb surgery without implant, and group 3 comprised 22 patients undergoing spinal or upper limb surgery. D-dimer level was systematically measured on admission and then once a week for 4 weeks. Doppler ultrasonography was performed on clinical suspicion of deep vein thrombosis. D-dimer levels were compared between patients with and without deep vein thrombosis. RESULTS: D-dimer levels were constantly elevated postsurgery (2- to 6-fold above normal) and returned to normal by week 4 in groups 2 and 3 but remained elevated in group 1 (3-fold above normal). Deep vein thrombosis was suspected in 45 cases and confirmed by Doppler ultrasonography in 10 cases. D-dimer level was not significantly different between patients with deep vein thrombosis and those without. DISCUSSION AND CONCLUSIONS: In the postoperative period, measurement of D-dimer level does not aid in diagnosing thromboembolism since its constant high level obviates any negative predictive value.     

Silastic ring vertical gastric bypass: cohort study with 83% rate of 5-year follow-up

BackgroundSilastic ring vertical gastric bypass (SRVGB) with jejunal interposition is our standard operation for morbidly obese patients. We present the results of 5 years of follow-up in a cohort of patients who underwent SRVGB in 2001.MethodsThe records of all 160 consecutive patients who underwent SRVGB from January to December 2001 were reviewed. Of the 160 procedures, 143 were primary open cases, 14 were revisions from restrictive procedures, and 3 were laparoscopic cases. At 5 years, the body mass index and percentage of excess weight loss was available for 133 patients (83%) at office visits (n = 91, 68.4%), by telephone (n = 40, 30.1%), or by e-mail (n = 2, 1.5%).ResultsOf the 160 patients, 121 were women and 39 were men, with a mean age of 33.15 ± 10.0 years, percentage of ideal body weight of 195.7% ± 40.8%, and body mass index of 44.6 ± 9.3 kg/m². The mean hospital stay was 3 ± 1 days. One patient (.6%) died of a pulmonary embolus. Early complications included 3 cases (1.87%) of upper gastrointestinal bleeding and 4 gastric leaks (2.5%): 2 (1.36%) from primary cases and 2 (14.29%) from revisional cases. Late complications included 32 patients (20%) with incisional hernias, 20 (12.5%) with anemia, 14 (8.8%) with dumping, 4 (2.5%) with gastrojejunal stricture, 2 (1.25%) with intestinal obstruction, and 2 (1.25%) requiring silastic ring surgical removal. The 5-year follow-up data were available for 133 patients (83%). The mean body mass index in this group was 27 ± 5 kg/m², with a percentage of excess weight loss of 83% ± 18.3% at 5 years postoperatively.ConclusionThe results of our study have shown that SRVGB is an effective operation for promoting lasting weight loss, with acceptable mortality and complication rates.     

Phenotype delineation of ZNF462 related syndrome

Zinc finger protein 462 (ZNF462) is a relatively newly discovered vertebrate specific protein with known critical roles in embryonic development in animal models. Two case reports and a case series study have described the phenotype of 10 individuals with ZNF462 loss of function variants. Herein, we present 14 new individuals with loss of function variants to the previous studies to delineate the syndrome of loss of function in ZNF462. Collectively, these 24 individuals present with recurring phenotypes that define a multiple congenital anomaly syndrome. Most have some form of developmental delay (79%) and a minority has autism spectrum disorder (33%). Characteristic facial features include ptosis (83%), down slanting palpebral fissures (58%), exaggerated Cupid's bow/wide philtrum (54%), and arched eyebrows (50%). Metopic ridging or craniosynostosis was found in a third of study participants and feeding problems in half. Other phenotype characteristics include dysgenesis of the corpus callosum in 25% of individuals, hypotonia in half, and structural heart defects in 21%. Using facial analysis technology, a computer algorithm applying deep learning was able to accurately differentiate individuals with ZNF462 loss of function variants from individuals with Noonan syndrome and healthy controls. In summary, we describe a multiple congenital anomaly syndrome associated with haploinsufficiency of ZNF462 that has distinct clinical characteristics and facial features.     

Urodynamic Evaluation in Simultaneous Insulin-Dependent Diabetes Mellitus and End Stage Renal Disease

Purpose

We evaluated the urodynamic changes produced by insulin-dependent diabetes mellitus with end stage renal disease.

Materials and Methods

A urodynamic evaluation was performed on 51 young patients (mean age plus or minus standard deviation 35 plus/minus 6 years) with long-term diabetes mellitus (average 21 plus/minus 6 years) and end stage renal disease (86 percent on dialysis).

Results

The urodynamic study was abnormal in 84 percent of the patients. The bladder was hypersensitive in 39 percent and hyposensitive in 30 percent of the cases, and maximum vesical capacity was greater than 600 ml. in 33 percent. An acontractile detrusor was noted in 6 percent of the patients, while 4 percent had detrusor hyperreflexia and 35 percent had bladder outlet obstruction.

Conclusions

A high frequency of vesical alterations was observed, which were modified by association of progressive vesical dysfunction and diabetes mellitus. In diabetes mellitus dialysis protects against detrusor hypocontractility but predisposes the patients to have bladder obstruction.     

Study of the effect of changing glucose, insulin, and insulin-like growth factor-I levels on serum corticosteroid binding globulin in lean, obese, and obese subjects with glucose intolerance

We have previously described that serum corticosteroid binding globulin (CBG) concentrations are associated with insulin secretion. The present study was designed to evaluate the effects of changing insulin concentrations, both endogenous and after exogenous insulin administration, on circulating CBG levels in vivo. Serum CBG concentrations were measured during an insulin-modified frequently sampled intravenous (IV) glucose tolerance test (FSIVGT) in 14 lean and 19 obese otherwise healthy subjects with varying degrees of glucose tolerance. Acute insulin response to glucose (AIRg) correlated significantly with serum CBG concentrations at time 0 (r = -.38, P =.029), 22 minutes (r = -.41, P =.01), 50 minutes (r = -.41, P =.01), and 180 minutes (r = -.39, P =.02). Insulin sensitivity (S(I)) was not associated with serum CBG concentration at time 0 (r = -.16, P = not significant [NS]), but correlated significantly with CBG concentration at 22 minutes (r = -.41, P =.02) and 50 minutes (r = -.35, P =.048) of the FSIVGT. In lean subjects, serum CBG concentration decreased significantly after IV insulin from 37.9 +/- 5.4 to 35.4 +/- 3 mg/L (P =.02) and returned to basal levels thereafter. In contrast, obese, glucose-tolerant subjects had lower CBG levels than lean and obese glucose intolerant subjects (33.8 +/- 3.0 v 37.9 +/- 5.4 and 39.8 +/- 4.4 mg/L, respectively), and their serum CBG concentrations remained unchanged during FSIVGT. Mean serum-free insulin-like growth factor-I (IGF-I) concentrations steadily declined from 1.21 +/- 0.81 to 0.8 +/- 0.36 microg/L during the FSIVGT, and this effect was restricted to lean subjects. Basal serum-free IGF-I did not correlate with CBG levels at time 0, but correlated inversely with the serum CBG concentrations at 22 minutes (r = -.36, P =.04). Stepwise multivariant analysis showed that AIRg (P =.035) and S(I) (P =.046), but not free IGF-I levels, independently contributed to 28% of CBG variance at 22 minutes. These results suggest that insulin, but not IGF-I, constitutes an important negative regulator of CBG liver synthesis. Endogenous and exogenous insulin do not affect serum CBG concentrations in insulin-resistant obese subjects with preserved or decreased insulin secretion. Obese glucose-tolerant subjects are hypothesized to exhibit tonically inhibited serum CBG levels. In contrast, in lean subjects, the higher the insulin secretion the lower the serum CBG concentration. The mechanisms of this CBG inhibitory effect exerted by insulin and its implication on cortisol homeostasis and fat distribution in humans await further investigations.     

Participation of membrane adenylyl cyclase in heparin‐induced capacitation in cryopreserved bovine spermatozoa

The aim of this work was to study the participation of membrane adenylyl cyclase in heparin‐induced capacitation in cryopreserved bovine spermatozoa. Sperm suspensions were incubated in Tyrode's albumin lactate pyruvate medium in the presence of heparin (10 IU ml^?1) or forskolin (1–75 μm ), a well‐known membrane adenylyl cyclase activator. The participation of membrane adenylyl cyclase was confirmed using a specific inhibitor, 2′,5′‐dideoxyadenosine (6–25 μm ). Spermatozoa capacitated with forskolin (25 μm ) were incubated with bovine follicular fluid to evaluate their ability to undergo acrosome reaction. Capacitation percentages were determined by the fluorescence technique with chlortetracycline, and true acrosome reaction was determined by trypan blue and differential interferential contrast. The forskolin concentrations employed had no effect on progressive motility or sperm viability. Capacitation values induced by 25‐μm forskolin treatment (27.80 ± 2.59%) were significantly higher respect to the control (4.80 ± 1.30%). The inhibitor 2′,5′‐dideoxyadenosine prevented forskolin‐induced capacitation and significantly diminished capacitation induced by heparin. Follicular fluid induced physiological acrosome reaction in spermatozoa previously capacitated with 25‐μm forskolin (P < 0.05). Forskolin acts as a capacitation inducer and involves the participation of membrane adenylyl cyclase as part of the intracellular mechanisms that lead to capacitation in cryopreserved bovine spermatozoa.