[Study of left ventricular systole in myocardial infarction].
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Biomedical subjects
Publications and source records attributed to M Covic.
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Patients admitted in dialysis centers are at greatest risk to achieve blood-borne infections. One of the most frequent is the cytomegalovirus infection, acquired from transfused blood products. The aim of our study was to determine the prevalence of IgG anti-CMV in patients on dialysis at the "C. I. Parhon" Hospital from Iaşi (Romania). In addition, the role of non-invasive samples (saliva and capillary blood) for such epidemiological studies was determined. ELISA Wellcome anti-CMV IgG was used for identification of specific antibodies in serum, capillary blood, saliva. The prevalence of anti-CMV IgG in the group of study was higher than that established in general populations and 79.06% saliva specimens and 93.76% of capillary blood samples were positive. To establish the specificity, sensitivity and predictive values of Wellcome anti-CMV when non-invasive samples are used, we compared the results obtained by testing saliva and capillary blood to those obtained by testing serum. We may conclude that the non-invasive samples are useful for CMV-infection surveillance in risk groups.
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Post-rifampicin (RMP) acute renal failure (ARF) is a complication seldom recognized of the antiTB treatment worldwide. The renal failure which occurs especially after intermittent administration of RMP is most frequent due to acute interstitial nephritis by allergic mechanism. In our study we found very few cases of acute tubular necrosis or glomerular lesions revealed by rapidly progressive glomerulo-nephritis or nephrotic syndrome. The renal lesions, accompanied by anuria and usually needing hemodialysis, were associated to auto-immune hemolytic anemia, trombocytopenia, hepatic failure and gastro-intestinal disturbances. The authors review their experience (60 cases), representing about half of the cases published worldwide. The main causes of this high prevalence of post-RMP ARF in Romania are discussed: intermittent twice-a-week RMP treatment, high incidence of TB, lack of compliance to treatment, possible contribution of some by-substances in RMP capsule. We described the clinic, biology and evolution of this dangerous and underestimated entity. We compared our experience with the published data, discussing the etiology and pathogenesis, trying to design the fine portrait of this ailment.
The paper presents the case of a 43 year old female patient with multi-malformations syndrome (facio-auriculo-vertebral syndrome), distinguished by alterations of the skeleton, face, sensorial organs and the heart. The syndrome is dominant at young ages and scarce at adults, and the explanation of the favorable evolution could be the lack of severe visceral or central nervous system involvement. The peculiar anomalies of this case are: asymmetric face, epibulbar dermoid, dysplastic ears, auricular tags, conductive and sensorineural deafness, fusion of vertebrae, hemivertebrae, ventricular septal defect.
Renal bone disease represents one of the major complications of end-stage renal disease, accounting for the numerous and various changes at bone level, determined by abnormal calcium and phosphorus homeostasis and by changes in calcitriol and PTH synthesis. PTH represents as well a major uraemic toxin, exerting profound systemic effects, particularly at the cardiovascular level. PTH synthesis is mainly controlled by changes in calcium-phosphorus balance and calcitriol production by the kidneys. Several others factors are important in the development of secondary hyperparathyroidism: acidosis, autonomisation of PTH secretion and peripheral (target-organ) resistance to PTH actions. Although bone biopsy represents the definitive diagnostic test to differentiate between osteitis fibrosa, low-turnover bone disease and bone involvement unrelated to disturbed calcium metabolism (i.e. beta 2-microglobulin-related amyloidosis), plasma intact PTH generally exhibits a reasonably good relation with bone histology parameters. Moreover serum bone-specific alkaline phosphatase isoenzyme, serum pyridinoline and the novel serum markers for bone turnover are highly specific and correlate with bone histomorphometry parameters, so that, preventive and therapeutic strategies should be re-evaluated based solely on biochemical parameters.
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Renal bone disease represents one of the major complications of end-stage renal disease, accounting for the numerous and various changes at bone level, determined by abnormal calcium and phosphorus homeostasis and by changes in calcitriol and PTH synthesis. PTH represents as well a major uraemic toxin, exerting profound systemic effects, particularly at the cardiovascular level. PTH synthesis is mainly controlled by changes in calcium-phosphorus balance and calcitriol production by the kidneys. Several others factors are important in the development of secondary hyperparathyroidism: acidosis, autonomisation of PTH secretion and peripheral (target-organ) resistance to PTH actions. Although bone biopsy represents the definitive diagnostic test to differentiate between osteitis fibrosa, low-turnover bone disease and bone involvement unrelated to disturbed calcium metabolism (i.e. beta 2-microglobulin-related amyloidosis), plasma intact PTH generally exhibits a reasonably good relation with bone histology parameters. Moreover serum bone-specific alkaline phosphatase isoenzyme, serum pyridinoline and the novel serum markers for bone turnover are highly specific and correlate with bone histomorphometry parameters, so that, preventive and therapeutic strategies should be re-evaluated based solely on biochemical parameters.
Hereditary predisposition is a common trait of many cancers. 15 to 20 percent of all cancers occur in individuals who have inherited a single gene alteration being members of families where multiple persons carry a high risk of developing cancer. Other than these so-called high penetrance genes which confer elevated risks of cancer development, there are many other genes that generate less dramatic but clinically important risks of cancer, often only if associated to specific exposures.
UNLABELLED: The aims of the study were to describe the clinical, pathological and biological features of membranous GN and to prospectively evaluate the relationships between individual negative prognostic factors--type of therapy and outcome. Between 1993-1998, 13/150 (8.7%) consecutive patients with renal biopsy had membranous GN (M = 62%, age = 42.5 +/- 14.5 years). Main (major) findings in these patients were: asymptomatic proteinuria--23.1%, heavy proteinuria (> 10 g/day)--33.3%, microscopic hematuria--53.8%, increased plasma creatinine levels--33.3%, hypertension--23.1% cases. 60% of the patients with nephrotic proteinuria had an underlying cause (infection, malignancy, immune-mediated systemic diseases). 40% of the patients with nephrotic proteinuria had 0 or less than 2 negative prognostic factors (without any of the recognized severe morphological changes). The following differentiated treatment protocols were applied: no treatment for asymptomatic proteinuria (group A), i.v. methyl-prednisolone boluses + prednisone 1 mg/kgc/day 3 months for those patients with few negative prognostic factors (group B), and steroids (as above) + cyclophosphamide (2 mg/kgc/day 3 months) or the Ponticelli regime in patients with important risk factors (group C). Outcome after a median follow-up period of 24 months was: complete remission in all cases from groups A + B (with only one exception were the underlying cause was breast malignancy); in group C in 75% of the subjects a complete or partial remission (proteinuria < 1 g/day) was obtained. Only one case progressed to chronic renal failure. There were no secondary effects from corticoids or immunosuppressive therapy. CONCLUSIONS: In membranous GN treatment should be tailored to the presence and type of negative prognostic factors. Even in high-risk patients combined steroids and immunosuppressive therapy determines a favorable outcome in 75% of the cases, without severe adverse effects.
Diabetic nephropathy (DN) is the most important cause of increased morbidity and mortality in patients with diabetes mellitus. Moreover DN is associated with a high risk for cardiovascular complications and progression of renal failure. It is known that there is a cumulative risk of development of DN represented by genetic factors, glycaemic factors, hypertension, alterations in the lipid metabolism, smoking. Functionally, it is represented by increased glomerular filtration rate (silent phase) and renal hypertrophy, increased the urinary albumin excretion rate, increased blood pressure and decline in glomerular filtration rate (end phase). Biochemical DN induced the alterations in lipid metabolism (increased the serum concentrations of triglicerides, VLDL, LDL), alterations in glycaemic metabolism (blood glucose, glycated hemoglobin, glycated albumin). The correlations between clinical and biochemical aspects are developed in this reference.
Cardiovascular disease is the main cause of death in end-stage renal failure treated by hemodialysis or peritoneal dialysis. Though reduced in renal transplant recipients compared to the dialysis population, an excess cardiovascular mortality is still present after transplantation. The authors are reviewing the main data on mortality in the renal transplant population, focusing on major risk factors: hypertension, left ventricular hypertrophy. Chronic immunosuppression is also discussed in this context, as a major determinant of blood pressure elevation after renal transplantation. The presence of these factors and the extent of cardiac and vascular abnormalities in the dialytic patient are closely related to outcomes in the post-transplant period. It is thus mandatory to approach and minimize all these in the dialytic and even predialytic period of chronic renal failure in order to reduce renal transplant mortality in patients with functioning grafts.
Integrity maintenance of the genome is crucial. Human DNA is vulnerable to damage arising from both endogenous and exogenous sources. Different DNA repair pathways counteract these potentially mutagenic accidents: damage reversal by methylguanine methyl transferase (MGMT), base nucleotide repair (BER), nucleotide excision repair (NER), mismatch repair (MMR) and repair of strand breaks. In some cases, DNA damage is not repaired but is instead bypassed by specialized DNA polymerases. The existence of human diseases associated with defects in DNA repair illustrates the importance of this process of quality control. Many of these human diseases have an increased susceptibility to cancer.
The infertility is a important health problem, affecting about 10-15% of couples. The important role of genetic factors in pathogenesis of infertility is now increasingly recognized and our knowledge in this field are improved each day. For these reasons we review the most important genetic causes of infertility. In this paper we analyse the genetic implications in gonadal and postgonadal infertility. Gonadal infertility affects both sexes and are characterised by hypergonadotrophic hypogonadism. Gonadal infertility is produced by chromosomal or monogenic mutations. Chromosomal causes are represented by gonosomal aneuploidy and structural chromosomal abnormalities. The monogenic disorders are consequences of a recessive mutations of hormone, hormonal receptor or enzymes genes. Postgonadal infertility is present in men and is the result of some obstructive disorders.