Risk factors for maternal thromboembolism: obstetrical circumstances

We analyzed the statistical relationship described between the principal laboratory anomalies related to thrombophilia and obstetrical pathology and risk of maternal thromboembolism.     

Characterization of two hepatitis B virus populations isolated from a hepatitis B surface antigen-negative patient

In a study of surface antigen-negative, but weakly hepatitis B virus (HBV) DNA-positive, patients, we were able to amplify and clone whole HBV genomes from the serum of a cirrhotic patient. Sequencing showed that the patient harbored two different HBV populations, one of genotype A and the other of genotype D, with the genotype D genome apparently predominating. The surface antigen of the genotype A virus is heavily mutated, especially in the extracellular < determinant a > region, with several mutations that have not been previously described. The genotype D virus is a precore mutant. Both genomes possess the common A1762T-G1764A double mutation of the basal core promoter (BCP), and the genotype D virus is also mutated in the < TATA box > of the large surface antigen promoter. Biological characterization showed that the genotype A genome was fully replication-competent, whereas the genotype D genome replicated poorly. The small surface antigen of the genotype A virus was only very weakly recognized by commercial tests. The small surface antigen of the genotype D virus could be recognized by the tests, but it was mainly retained within transfected cells, probably because of an excess of large surface antigen. In conclusion, the cryptic nature of this double HBV infection is characterized by the predominance of the replication-deficient genotype D virus over the replication-competent genotype A virus.     

Increased body iron stores in elite road cyclists

BACKGROUND: One third of French elite road cyclists were found to have hyperferritinemia on antidoping control tests performed during the Tour de France in 1998. PURPOSE: This study was undertaken to determine whether hyperferritinemia corresponded to elevated body iron stores or not and, affirmatively, what were its mechanism, its clinical consequences, and its spontaneous course. METHODS: 83 elite road male cyclists presenting with hyperferritinemia, defined as serum ferritin level greater than 300 microg.L-1, were studied with respect to consumption of iron and other drugs, serum iron tests, HFE mutations, and hepatic iron concentration (HIC; N < 35 micromol.g-1 dry weight). RESULTS: All cyclists were asymptomatic and had normal physical and cardiac examination. Their median (range) serum ferritin, serum iron, and transferrin saturation levels were 504 microg.L-1 (306-1671), 20 micromol.L-1 (8.5-36.3), and 39% (20-76), respectively. HIC was increased in 24/27 up to 187 micromol.g-1. Allelic frequency of the H63D mutation was increased in cyclists when compared to controls (P = 0.04). However, iron tests did not differ according to HFE genotypes. Most cyclists (89%) had been supplemented with iron. The median iron supplementation was 25.5 g (range: 1.4-336) and correlated well (P = 0.002) with serum ferritin. Evolution of serum ferritin levels did not differ whether cyclists had been continuing iron supplementation or not. CONCLUSION: Hyperferritinemia in elite road cyclists accounted for increased body iron stores caused by and persisting after cessation of excessive iron supplementation. Even when mild, iron excess may expose to long-term complications and should be removed, at least at the time when professional cyclists retire. To prevent iatrogenic iron overload, supplementation with iron must be done according to serum ferritin follow-up and not either blindly or on the basis of serum iron determination only.     

Chemodectoma of the trachea.

The case history is described of a patient with lower tracheal chemodectoma who presented with haemoptysis. After conservative management for eight years she represented with airways obstruction. Preoperative tumour embolisation was followed by laser ablation, stenting, and radiotherapy.     

Effects of diclofenac on experimental streptococcal necrotizing fasciitis (NF) in rabbit

Abstract Aggravation of necrotizing fasciitis (NF) by the administration of non-steroidal antiinflammatory drugs (NSAIDs) has recently been suggested. A rabbit model of streptococcal NF was used to study the effects of parenteral administration of an NSAID on NF evolution and outcome. Of 16 rabbits inoculated with a Streptococcus pyogenes suspension together with staphylococcal alpha toxin, 8 were treated with two doses of 4 mg/kg diclofenac on day 1 after inoculation. Clinical, bacteriological and histological studies were performed until day 10. Under our experimental conditions, NSAID treatment significantly limited NF extension. A specific inverse relationship between the extent of inflammation and bacterial density in NF lesions was observed on day 1 after inoculation in the treated group suggesting that the greater severity of NF in humans treated with an NSAID could be due to the therapeutic delay induced by the misleading clinical effects of the NSAID, and not to inhibition of antibacterial defence. Received: 23 October 1997 / Received after revision: 23 June 1998 / Accepted: 30 July 1998     

Arteriosclerosis, vascular calcifications and cardiovascular disease in uremia

PURPOSE OF REVIEW: Arterial calcification in chronic kidney disease (CKD) is associated with increased cardiovascular risk. The mechanisms responsible for arterial calcification include alterations of mineral metabolism and expression of mineral-regulating proteins. RECENT FINDINGS: Arterial calcification is similar to bone formation, involving differentiation of vascular smooth muscle cells (VSMCs) into phenotypically distinct osteoblast-like cells. Elevated phosphate and/or calcium trigger a concentration-dependent increase of calcium precipitates in VSMC in vitro. The calcification is initiated by VSMC release of membrane-bound matrix vesicles and formation of apoptotic bodies. The presence of serum prevents these changes, indicating the presence of calcification inhibitors. Arterial calcification occurs in two sites: the tunica intima and tunica media. Intimal calcification is a marker of atherosclerotic disease and is associated with arterial stenotic lesions. Medial calcification influences outcome by promoting arterial stiffening whose principal consequences are left-ventricular hypertrophy and altered coronary perfusion. Aortic stiffness is an independent predictor of all-cause and cardiovascular mortality in CKD patients. Age, duration of dialysis, smoking and diabetes are risk factors for the development of arterial calcification in end-stage renal disease. Oversuppression of parathyroid hormone and low bone turnover potentiate the development of arterial calcification. SUMMARY: Arterial disease in CKD patients is characterized by extensive calcification. Evidence has accumulated pointing to the active and regulated nature of the calcification process. Elevated phosphate and calcium may stimulate sodium-dependent phosphate cotransport involving osteoblast-like changes in cellular gene expression. Arterial calcification is responsible for stiffening of the arteries with increased left-ventricular afterload and abnormal coronary perfusion as the principal clinical consequences.