Reversal of c-ANCA positive mesangiocapillary glomerulonephritis after removal of an infected cysto-atrial shunt.
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Antibodies, Antineutrophil Cytoplasmic↗
Biomedical subjects
F Bonnet
Publications and source records attributed to F Bonnet.
Adding clonidine to lidocaine for intravenous regional anesthesia prevents tourniquet pain.
UNLABELLED: Tourniquet pain often complicates the use of the pneumatic tourniquet during surgical procedures performed under IV regional anesthesia. Clonidine-containing local anesthetic solutions have better analgesic properties than plain solutions when used for spinal, epidural, or peripheral blocks. We tested the hypothesis that the addition of clonidine may improve the quality of IV regional anesthesia, especially tourniquet tolerance. Forty patients were allocated randomly in a double-blinded, randomized study to receive 40 mL of 0.5% lidocaine and either 1 mL of isotonic saline or clonidine (150 microg). A double-cuffed tourniquet was kept inflated until patients complained of pain, leading to release of the distal cuff. Pain at the tourniquet site, at the surgical site, and in the distal part of the arm was rated on a visual analog scale (VAS) and a verbal rating scale (VRS) every 15 min during tourniquet placement and every 15 min for 1 h after tourniquet deflation. Motor blockade, sedation, arterial pressure, and heart rate were also recorded. VAS and VRS scores were significantly lower in the clonidine group 30 and 45 min after tourniquet inflation. The tolerance for the distal tourniquet was also significantly longer in the clonidine group (median [range]: 22 [10-40] vs 10 [5-20] min; P < 0.05); motor blockade was comparable between the two groups. Pain was not different in the two groups after tourniquet release. The clonidine group experienced a higher degree of sedation. We conclude that clonidine improves tourniquet tolerance when added to a local anesthetic solution. IMPLICATIONS: A 150-microg dose of clonidine added to lidocaine improved tourniquet tolerance during IV regional anesthesia.
Adrenergic alpha-Agonists↗
Cardiac baroreflex during the postoperative period in patients with hypertension: effect of clonidine.
BACKGROUND: Patients with essential hypertension show altered baroreflex control of heart rate, and during the perioperative period they demonstrate increased circulatory instability. Clonidine has been shown to reduce perioperative circulatory instability. This study documents changes in measures of heart rate control after surgery in patients with essential hypertension and determines the effects of clonidine on postoperative heart rate control in these patients. METHODS: Using a randomized double-blind placebo-controlled design, 20 patients with essential hypertension (systolic pressure >160 mm Hg or diastolic pressure >95 mm Hg for > or =1 yr) were assigned to receive clonidine (or placebo), 6 microg/kg orally 120 min before anesthesia and 3 microg/kg intravenously over 60 min before the end of surgery. The spontaneous baroreflex ("sequence") technique and analysis of heart rate variability were used to quantify control of heart rate at baseline, before induction of anesthesia, and 1 and 3 h postoperatively. RESULTS: Baroreflex slope and heart rate variability were reduced postoperatively in patients given placebo but not those given clonidine. Clonidine resulted in greater postoperative baroreflex slope and power at all frequency ranges compared with placebo (4.9+/-2.9 vs. 2.2+/-2.1 ms/mm Hg for baroreflex slope, 354+/-685 vs. 30+/-37 ms2/Hz for high frequency variability). Clonidine also resulted in lower concentrations of catecholamine, decreased mean heart rate and blood pressure, and decreased perioperative tachycardia and hypertension. CONCLUSIONS: Patients with hypertension exhibit reduced heart rate control during the recovery period after elective surgery. Clonidine prevents this reduction in heart rate control. This may represent a basis for the improved circulatory stability seen with perioperative administration of clonidine.
Analgesics↗
Dissection of silencer elements in first intron controlling the human renin gene.
OBJECTIVE: A silencer within the renin first intron (intron A) was identified using Calu-6 cells, a pulmonary carcinoma cell line which produced renin. In the present study, a dissection of the first intron was performed to determine precisely the cis-regulatory elements involved in the silencer transcriptional effects. MATERIALS AND METHODS: Intron A was completely sequenced to characterize potential binding sites for known transcription factors. Partial portions of intron A were subcloned upstream the 892 bp of the renin promoter and transfected in different models of renin-producing cells: primary culture of human chorionic cells, human Calu-6 cells and mouse As4.1 cells. RESULTS: There is significant DNA homology (67%) between the 3' and 5' ends of the human and rat renin first intron. Several transcription factor binding sites identified in human first intron, but not in rat intron, do not contribute to the reported silencer activity. Transfections of renin/ luciferase constructs containing partial portions of first intron inserted upstream of the 892 bp in both renin-producing cells do not allow the precise characterization of cis-elements involved in the silencer effect. CONCLUSIONS: The silencer located renin intron A is cell specific. The integrity of the human first intron seems necessary for its repressor activity on renin proximal promoter in renin-producing cells.
Animals↗
Evaluation of new quantitative assays for diagnosis and monitoring of cytomegalovirus disease in human immunodeficiency virus-positive patients.
Cobas Amplicor CMV Monitor (CMM) and Quantiplex CMV bDNA 2.0 (CMV bDNA 2.0), two new standardized and quantitative assays for the detection of cytomegalovirus (CMV) DNA in plasma and peripheral blood leukocytes (PBLs), respectively, were compared to the CMV viremia assay, pp65 antigenemia assay, and the Amplicor CMV test (P-AMP). The CMV loads were measured in 384 samples from 58 human immunodeficiency virus (HIV) type 1-infected, CMV-seropositive subjects, including 13 with symptomatic CMV disease. The assays were highly concordant (agreement, 0.88 to 0.97) except when the CMV load was low. Quantitative results for plasma and PBLs were significantly correlated (Spearman rho = 0.92). For PBLs, positive results were obtained 125 days before symptomatic CMV disease by CMV bDNA 2.0 and 124 days by pp65 antigenemia assay, whereas they were obtained 46 days before symptomatic CMV disease by CMM and P-AMP. At the time of CMV disease diagnosis, the sensitivity, specificity, and positive and negative predictive values of CMV bDNA 2.0 were 92.3, 97.8, 92.3, and 97.8%, respectively, whereas they were 92.3, 93.3, 80, and 97. 8%, respectively, for the pp65 antigenemia assay; 84.6, 100, 100, and 95.7%, respectively, for CMM; and 76.9, 100, 100, and 93.8%, respectively, for P-AMP. Considering the entire follow-up, the sensitivity, specificity, and positive and negative predictive values of CMV bDNA 2.0 were 92.3, 73.3, 52.1, and 97.1%, respectively, whereas they were 100, 55.5, 39.4, and 100%, respectively, for the pp65 antigenemia assay; 92.3, 86.7, 66.7, and 97.5%, respectively, for CMM; and 84.6, 91.1, 73.3, and 95.3%, respectively, for P-AMP. Detection of CMV in plasma is technically easy and, despite its later positivity (i.e., later than in PBLs), can provide enough information sufficiently early so that HIV-infected patients can be effectively treated. In addition, these standardized quantitative assays accurately monitor the efficacy of anti-CMV treatment.
AIDS-Related Opportunistic Infections↗
Thrombocytopenia in critically ill surgical patients: a case-control study evaluating attributable mortality and transfusion requirements.
BACKGROUND: That thrombocytopenia results in increased mortality or transfusion requirements has not been confirmed by previous studies. We performed a case-control study in which 36 patients who developed severe thrombocytopenia of less than 50x109 platelets/l were carefully matched for the severity of underlying disease and other important variables. RESULTS: Seventeen (47%) thrombocytopenic patients died, versus 10 (28%) matched control patients who were not thrombocytopenic.Nine pairs had a discordant outcome, and in eight of these pairs the thrombocytopenic patient died (exact binomial probability 0.037). The estimated attributable mortality was 19.5% (95% confidence interval 3.2-35.8), and the estimated odds ratio was 2.7 (95% confidence interval 1.02-7.10). Thrombocytopenic patients had comparable values for severity of illness scores between day of admission and day of thrombocytopenia, in contrast with control patients who had a statistically significant decrease in severity of illness scores during the same period. Thirty (83%) of the thrombocytopenic patients required transfusion of blood products, versus 21 (58%) control patients (paired chi2 test 4.92, P < 0.04). The estimated attributable transfusion requirement was 25% (95% confidence interval 5.4-44.6), and the estimated odds ratio was 1.52 (95 confidence interval 1.05-2.20). CONCLUSION: The present study suggests that thrombocytopenia of less than 50 x 109 platelets/l may be a marker for more severe illness and increased risk of death, rather than causative, because a true causal relationship is not established. Thrombocytopenia also leads to an excess of blood product consumption.
Journal Article↗
Devic's neuromyelitis optica during pregnancy in a patient with systemic lupus erythematosus.
Neuropsychiatric forms of systemic lupus erythematosus (SLE) vary, most commonly consisting of seizures, psychiatric disturbances, or focal central nervous deficits. This is a new case of neuromyelitis optica or Devic's syndrome during the course of SLE. Few reports of this association exist in the literature. Our objective is to report this unique case of Devic's neuromyelitis optica during pregnancy in a patient with systemic lupus erythematosus. A 28-year-old woman had been diagnosed as having SLE with cutaneous and articular involvement in 1987 when she was 17 years old. She was treated with a synthetic antimalarial agent associated with corticosteroids. In 1994, during the fourth month of pregnancy, she had signs of transverse myelitis with a sensory level at T6 associated with an optic neuropathy suggesting a Devic's syndrome. The patient was managed by plasmapheresis sessions and intravenous corticosteroids. Transverse myelitis recurred postpartum and three years later at the same thoracic level. Management by bolus administration of a steroid and cyclophosphamide resulted in remission again. There have only been around a dozen reports in the literature of patients who had both Devic's neuromyelitis optica and SLE. Magnetic resonance imaging is contributive to diagnosis and therapeutic follow-up, showing spinal cord lesions with increased intensity on T2-weighted sequences. Although the clinical course of the present patient has been favourable so far, the prognosis of this neurologic disease is generally considered to be poor with elevated mortality.
Adrenal Cortex Hormones↗
Regulated phosphorylation of the RNA polymerase II C-terminal domain (CTD).
The largest subunit of RNA polymerase II has an intriguing feature in its carboxyl-terminal domain (CTD) that consists of multiple repeats of an evolutionary conserved motif of seven amino acids. CTD phosphorylation plays a pivotal role in controlling mRNA synthesis and maturation. In exponentially growing cells, the phosphate turnover on the CTD is fast; it is blocked by common inhibitors of transcription, such as 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole and actinomycin D. Transcription-independent changes in CTD phosphorylation are observed at critical developmental stages, such as meiosis and early development.
Animals↗
Human inter-alpha-trypsin inhibitor heavy chain H3 gene. Genomic organization, promoter analysis, and gene linkage.
To understand more about the human inter-alpha-trypsin inhibitor heavy chain H3 (ITIH3) expression and the relationship between this gene and the family of other ITI heavy chain genes, an analysis of the structure of the ITIH3 gene and its promoter region was performed. This gene is a single copy gene, 14 kilobase pair in length and consists of 22 exons. ITIH3 shares highly conserved exon size and intron-exon borders with other ITI heavy chain genes. We determined that the human ITIH1, ITIH3, and ITIH4 genes are closely linked within a 45-kilobase pair. They are arranged in the order of H1-H3-H4, with the ITIH4 gene transcribed in the opposite direction. A model for the evolution of the ITI heavy chain gene family is presented that involves multiple rounds of gene duplication plus inversion events. The minimum promoter region (-135 to +75) is identified in HepG2 cells. The transient transfection study in various cell lines indicates that the activity of the ITIH3 promoter is not liver-specific. DNase I footprinting, mobility shift assays, and cotransfection experiments reveal a functional CCAAT/enhancer-binding protein site (C/EBP, -1344 to -1305) which interacts with C/EBPalpha and C/EBPbeta factors. The latter factors control the transcription of the ITIH3 gene positively.
Alpha-Globulins↗
A novel distal enhancer confers chorionic expression on the human renin gene.
Renin catalyzes the rate-limiting step of the renin-angiotensin system, which regulates blood pressure and electrolyte homeostasis. To determine cell-specific human renin gene control elements, the transcriptional activity of promoter regions up to position -8876 was studied in renin-expressing cells. A positive regulatory region conferring approximately 57-fold higher transcriptional activity to the human renin gene promoter in chorionic cells was identified between nucleotides -5777 and -5552. It had the orientation-independent activity typical of classical enhancers. It also conferred approximately 59-fold higher transcriptional levels from the heterologous simian virus 40 (SV40) promoter in chorionic cells and approximately 6-fold higher transcriptional levels in Calu-6 and As4.1 cells, whereas no effect was measured in non-renin-expressing cells. DNase I footprinting showed that this enhancer contains three binding sites for chorionic cell nuclear extracts. Functional analysis suggested that the activity of the enhancer is regulated by differential mechanisms in the three renin-expressing cells involving a complex arrangement of AP-1 motifs binding cell-specific members of the basic leucine zipper family of transcription factors. Thus, our results demonstrate that this enhancer plays a key role in the expression of the human renin gene in the chorion and may also be involved in its regulated expression in other tissues.
Animals↗
Genomic organization of the human SPOCK gene and its chromosomal localization to 5q31.
SPOCK, previously identified as testican, is a modular proteoglycan that carries both chondroitin and heparan sulfate glycosaminoglycan side chains. The overall genomic organization has been established. The SPOCK gene spans at least 70 kb and is composed of 11 exons: the first half of the gene is dramatically expanded, but the second half is more compact. In situ hybridization and YAC mapping independently linked the SPOCK gene to 5q31, a region containing an impressive number of genes encoding growth factors, cytokines, and neurotransmitter and hormone receptors. The gene is located between the IL9 and the EGR1 genes, bordering the smallest commonly deleted region of chromosome 5.
Chromosome Banding↗
Calcium-dependent low renin syndrome in a diabetic patient with prostaglandin deficiency.
Calcium and prostaglandin are supposed to play a critical role in the renin-angiotensin aldosterone system. Calcium has been described as an inhibitory second messenger for renin exocytosis whereas vasodilatory prostaglandins, such as PGE2, are known to stimulate the production of renin. These factors are probably interrelated since calcium also enhances urinary prostaglandin release. We report the case of a 52 year-old diabetic patient treated with insulin injections with intestinal malabsorption leading to chronic hyperkalemia and hypocalcemia in whom a low renin syndrome and low levels of urinary prostaglandins were observed. The correction of the hypocalcemia was able to improve plasma renin as well as urinary prostaglandin levels. This observation suggests a prominent role played by calcium on the in vivo regulation of renin and prostaglandin release. These results illustrate the closed loop between plasma calcium level, urinary prostaglandins production and renin release.
Calcium↗
[Motor deficit of the lower limbs and urinary incontinence following peridural anesthesia].
Neurological complications of epidural anaesthesia are rare, but can be severe. We report the case of a 49-year-old man, with a history of non equilibrated diabetes, who experienced after an epidural anaesthesia for peripheral vascular surgery a polyneuropathy with muscle weakness of the lower extremities associated with a transient urinary incontinence. A spinal compression was excluded by computed tomography and magnetic resonance imaging. Electromyography showed an impaired nervous motor conduction. An aggravation of a pre-existing diabetic and alcoholic polyneuropathy, associated with possible spinal ischaemia of multifactorial origin could be the cause of these complications. This case emphasizes the importance, during preanesthetic assessment of candidates for epidural or spinal anaesthesia, to search for a possible unrecognized neuropathy at risk of aggravation by regional anaesthesia.
Alcoholism↗
[Total spinal anesthesia after posterior lumbar plexus block].
We report a case of total spinal anaesthesia which occurred after a lumbar plexus block using a posterior approach. After total hip arthroplasty under general anaesthesia, a lumbar plexus block was performed according to Winnie's landmarks at the L4 interspace using a nerve stimulator. Aspiration test for blood and spinal fluid were both negative, as well as a test dose of 3 mL lidocaine 2%-bupivacaine 0.5%. One minute after the injection of 27 mL of the same mixture, a complete anaesthetic block occurred with hypotension and loss of consciousness requiring intubation and controlled ventilation during 3h30, without sequelae. Lumbar plexus block using a posterior approach must be performed cautiously and a slow and fractionated injection of the full dose is recommended.
Aged↗
Immune thrombocytopenic purpura after recombinant hepatitis B vaccine: retrospective study of seven cases.
Recombinant hepatitis B vaccine is usually well tolerated. Clinical and laboratory test manifestations with immunologic mechanisms have nonetheless been described following use of this vaccine. We retrospectively report 7 cases of thrombocytopenia occurring within 3 months (7 weeks on the average) of 1 or following injections of recombinant hepatitis B vaccine. Four boys and 3 girls, average age 12 y, were involved. Three had a history of immune thrombocytopenic purpura. Four had haemorrhagic manifestations. The haemogram showed thrombocytopenia (24 x 10(9)/l on the average) without alterations of the other lines. Infectious and immune aetiologies were excluded in all cases. The course varied after treatment by corticosteroids, high-dose intravenous immunoglobulin, or both. After describing the different manifestations subsequent to recombinant hepatitis B vaccination, we discuss post-vaccinal thrombocytopenias (vaccines in question, mechanisms) and the reality of this entity.
Adolescent↗
Meta-analysis of the efficacy of extradural clonidine to relieve postoperative pain: an impossible task.
Clonidine, an alpha2 adrenoceptor agonist, has anti-hypertensive and anti-nociceptive effects. It is commonly used in association with local anaesthetics and opioids to enhance the quality and duration of extradural analgesia in the postoperative period, and to decrease the incidence of side effects. As a sole analgesic, it has seldom been used to relieve postoperative pain. The dose of extradural clonidine to achieve good pain relief without deleterious side effects remains undetermined. In order to address this problem, we performed a computer search via two well-known databases, Medline and Excerpta Medica, covering the period from 1985 to September 1997. One hundred and fifty-nine articles were retrieved of which 38 dealt with extradural clonidine and postoperative pain. All but 16 studies suffered from serious design flaws, such as lack of controls and/or randomization, or inadequate statistical analysis. The data from these studies were difficult to interpret because of the tremendous variation in variables, especially dose of clonidine, level of extradural injection, time of administration, type of anaesthesia, type of surgery, and reference and rescue drugs. The simultaneous extradural use of local anaesthetics and opioids further hindered data interpretation, and precluded any meta-analysis. Proposals for a standard study design are made to help comparison between studies involving extradural clonidine and postoperative pain.
Adrenergic alpha-Agonists↗
Sedation depends on the level of sensory block induced by spinal anaesthesia.
We have investigated the relationship between the extent of spinal block and occurrence of sedation. In a first series of 43 patients, the distribution of sedation score (measured on the Ramsey scale) was related to the extent of spinal block (pinprick). In a second series of 33 patients, the relationship between sedation score and spinal block persisted after injection of midazolam 1 mg. This study confirmed that high spinal block was associated with increased sedation.
Adolescent↗
Clonidine does not impair redistribution hypothermia after the induction of anesthesia.
UNLABELLED: Clonidine is commonly given for premedication, and it impairs normal thermoregulatory responses to warm and cold stimuli while depressing sympathetic tone. We studied the effect of premedication by clonidine on redistribution hypothermia induced by the induction of anesthesia. Sixteen ASA physical status I or II patients were randomly assigned to receive either clonidine 150 micrograms or a placebo. Anesthesia was induced 45 min later by thiopental, fentanyl, and vecuronium i.v. and was maintained by the administration of 0.6% isoflurane. We monitored central core (tympanic) temperature and skin surface temperatures at the forearm and the fingertip during the 2 h after the induction of anesthesia before surgery. We estimated skin blood flow at the level of the forearm by using laser Doppler during the same period. The core temperature decreased comparably in the two groups of patients, from 37.1 +/- 0.2 degrees C to 35.3 +/- 0.4 degrees C and from 37.1 +/- 0.2 degrees C to 35.5 +/- 0.3 degrees C in the clonidine and placebo groups, respectively. The forearm-fingertip surface temperature gradient decreased similarly in the two groups. There was no evidence of cutaneous vasoconstriction. The laser Doppler index at the fingertip increased similarly in the two groups, as did the forearm-fingertip temperature gradient. We conclude that premedication with clonidine does not significantly impair the profile of central hypothermia induced by heat redistribution after the induction of anesthesia. IMPLICATIONS: The induction of general anesthesia is associated with redistribution hypothermia. This study shows that premedication with oral clonidine does not worsen the decrease in core temperature resulting from general anesthesia.
Adrenergic alpha-Agonists↗