Bone density and microarchitecture in hepatitis C and HIV-coinfected postmenopausal minority women.

We found that HIV+/HCV+ women had 7-8% lower areal bone mineral density (aBMD) by dual-energy x-ray absorptiometry (DXA) at the spine, hip, and radius (p < 0.01) and 5-7% lower volumetric BMD (vBMD) by central quantitative computed tomography (cQCT) at the spine and hip (p < 0.05). These data suggest that true deficits in vBMD may contribute to bone fragility and excess fractures reported in HIV+/HCV+ women. INTRODUCTION: aBMD by DXA is lower in persons coinfected with HIV and HCV (HIV+/HCV+) than with HIV monoinfection (HIV+). However, weight is often also lower with HCV infection, and measurement of aBMD by DXA can be confounded by adiposity; we aimed to determine whether true vBMD is also lower in HIV+/HCV+ coinfection. METHODS: We measured aBMD of the lumbar spine (LS), total hip (TH), femoral neck (FN), and ultradistal radius (UDR) by DXA and vBMD of the spine and hip by cQCT and of the distal radius and tibia by high-resolution peripheral QCT (HRpQCT) in 37 HIV+/HCV+ and 119 HIV+ postmenopausal women. Groups were compared using Student's t tests with covariate adjustment by multiple regression analysis. RESULTS: HIV+/HCV+ and HIV+ women were of similar age and race/ethnicity. HIV+/HCV+ women had lower body mass index (BMI) and trunk fat and were more likely to smoke and less likely to have a history of AIDS. In HIV+/HCV+ women, aBMD by DXA was 7-8% lower at the LS, TH, and UDR (p < 0.01). Similarly, vBMD by cQCT was 5-7% lower at the LS and TH (p < 0.05). Between-group differences in LS aBMD and vBMD remained significant after adjustment for BMI, smoking, and AIDS history. Tibial total vBMD by HRpQCT was 10% lower in HIV+/HCV+ women. CONCLUSION: HIV+/HCV+ postmenopausal women had significantly lower spine aBMD and vBMD. These deficits in vBMD may contribute to bone fragility and excess fractures reported in HIV+/HCV+ women.

Vancomycin-resistant Enterococcus faecium meningitis successfully managed with linezolid: case report and review of the literature.

Enterococci cause serious illness in immunocompromised patients and severely ill, hospitalized patients. Resistance to vancomycin has increased in frequency during the past few years. Limited therapeutic options are available for vancomycin-resistant enterococcal infections and the optimum therapy has not been established. We report a case of nosocomial vancomycin-resistant Enterococcus faecium meningitis in the setting of hyperinfection with Strongyloides stercoralis that was successfully treated with linezolid. We also review the previously reported cases of vancomycin-resistant E. faecium meningitis.

Magnesium orotate in myocardial and neuronal protection.

The nervous tissue and the myocardium have in common many denominators, such as: the inability to renew to substitute the severely damaged or dead cells, the role of the membrane electric activity, the presence of similar systems for antioxidation protection, which are obviously involved in pathologic events a.s.o. Aggressive factors mainly act by free radicals injury and increase in cytosolic calcium level. Magnesium orotate molecule includes two synergic protective components: orotic acid and magnesium. Moreover, the orotic acid behaves as a transporter, carrying magnesium into the cells. The antioxidation protective effect of the orotic acid is mainly due to the pirimidinic bases that favor and increased synthesis of enzymes which act as free radical scavengers. The cell antioxidation protective system is dramatically impaired following heavy aggressions such as the ischemia-reperfusion process. Magnesium orotate improves the survival of cells situated within the perinecrotic areas as well as of the cells secondarily damaged during the so-called "second wind".

Study of serum ceruloplasmin and of the copper/zinc ratio in cardiovascular diseases.

The serum copper and zinc concentration, the Cu/Zn ratio and ceruloplasmin activity have been studied in 400 subjects divided into 4 groups of study: 50 normal subjects (controls), 100 patients with ischemic heart disease, 100 subjects with myocardial infarction in the past history and 150 patients with acute myocardial infarction. It was observed that in normal subjects the Cu/Zn ratio is about 1, in acute myocardial infarction it reaches 2.5 but it returns to normal during convalescence. In the patients with ischemic heart disease the ratio decreases to 0.8 and in the subjects with infarction in the past history it is about 1.6 (almost normal). The variation of these ratio is due to the serum zinc concentration which in ischemic heart disease presents values over the upper normal limit and in acute myocardial infarction below the lower normal limit. In the subjects with acute infarction ceruloplasmin (copper depending enzyme) the activity was observed to be inversely proportional to the Cu/Zn ratio in the first 4 days after the onset of the disease. The quick normalization of one or of both parameters is a sign of positive evolution of the disease.

[Hereditary angioedema due to C1-esterase inhibitor deficiency]. / Angioedemul ereditar prin deficit de inhibitor al C1-esterazei.

The paper presents a case of family oedema by shortage of C1-esterase inhibitor, characterized by appearance at an early age (8 months), participation in some attacks of nasal mucous membrane, with nasal obstruction and sinusal manifestations and also the abnormally long period, up to 9 days, of some localized oedemas. The crises were absent during pregnancy. The study of four generations of the family showed the predominantly hereditary character of the genetic transmission. Two cases in which the disease apparently "overleapt" a generation, as clinical manifestations, were presented.

Hereditary angioedema due to deficit of C1 esterase inhibitor.

A case of familial angioedema due to deficit of C1 esterase inhibitor is presented. The case had the following peculiarities: onset at a very early age (8 months); involvement, in some attacks, of the nasal mucosa with nasal obstruction and sinusitis manifestations; unusually long duration (as long as 9 days) of some of the localized edema. The absence of attacks during pregnancy was noted. The family study over 4 generations illustrated the dominant hereditary character of genetical transmission. Attention is drawn on two cases in the family in which the disease apparently skipped one generation from the point of view of clinical signs.

Recent data on mitral valve prolapse and magnesium deficit.

Idiopathic mitral valve prolapse (IMVP) is a widespread disease. IMVP may be latent, but most patients describe a great variety of symptoms. The clinical pictures of IMVP and of latent tetany are superimposed with regard to Mg deficit. IMVP appears as a late complication of latent tetany due to magnesium deficit (LTMD). The Mg deficit has various causes: insufficient Mg intake (especially during slimming diets), and depletion of Mg provoked by stress, coffee excess, corticosteroids or catecholamine excess. The high prevalence in women is mainly due to the ovarian hormones. Constitutional factors such as the HLA Bw35 antigen and the behavioural type A favour Mg depletion. The HLA-Bw35-positive individuals show a lower level of tissue Mg. In the development of the valvular lesion there are some other associated factors apart from Mg deficit which alter collagen metabolism: ascorbic acid deficit, febrile illnesses, corticosteroid excess. Symptomatology is dominated by the latent tetany syndrome. Palpitations and precordial pain are the most frequent cardiac symptoms. The click and mid-late systolic murmer do not appear in all IMVP cases. In clinical investigation the following tests are indispensable: echocardiogram, electrocardiogram, evaluation of plasma and erythrocyte Mg, calcaemia and calciuria. In particular cases more sophisticated studies are necessary. Therapy based on Mg should be applied consistently and for long periods of time. Mg therapy results in the control of latent tetany as well as in morphologic recovery. The administration of Mg in LT prevents the development of IMVP.

The biology of the myocardium in chronic hypoxia. Note I. Myocardial lesions in experimental chronic heart failure.

The biology of the myocardium was studied in chronic heart failure, especially in the course of compensatory hypertrophy induced experimentally by partial stenosis of the aorta for 10 months and the administration of large isoproterenol doses for 7 months. In the stage of acute aggression, varied disseminated ultrastructural lesions are predominant, with the decrease of energy reserves, hydroelectrolytic and ECG perturbations. In the stage of ultrastructural compensatory hypertrophy, there is a prevalence of normal myocytes or others presenting regenerative aspects next to progressive fibrosis reflected biochemically by return to almost normal values, with certain oscillations due to the presence of some lesional foci, also recorded on the ECG tracings. The question of the pathogenesis and prognosis of these lesions is discussed.

Considerations on the pathogenesis of mitral valve prolapse.

Forty patients (11 males and 29 females) with mitral valve prolapse (MVP) were investigated clinically as well as by echocardiographic, phonomechanocardiographic, radiologic, electroencephalographic, electromyographic, psychologic and biologic examinations. Hypomagnesemia was found statistically significant and is assumed to have an important etiopathogenic role particularly in causing the rhythm and neuropsychic disturbances in MVP. A case in which MVP appeared after a prolonged treatment with prednisone, is presented.

Electrocardiographic alteration induced by accidental hypothermia.

Electrocardiographic alterations during hypothermia are studied and a case is reported presenting a very marked J wave which disappeared when the patient recovered his normal temperature.

Morphophysiological studies in experimental myocardial stress induced by isoproterenol. Note II. The myocardioprotector effect of magnesium ascorbate.

The efficiency of magnesium ascorbate, a new Romanian cardioprotector drug, was studied in guinea pigs and Wistar rats, both normal and with scurvy, within the framework of morphophysiological investigations of the pathogenesis of myocardial disease induced by large doses of beta-adrenergic substances of the isoproterenol type. The preventively treated animals presented only disseminated myocardial ultrastructural lesions within reversible limits. Biochemically, as compared with controls, a return to normal levels of ATP and Mg2+ and a decrease in the uptake of 45CaCl2 by the myocardium were observed. The pharmacological mechanisms of action of magnesium ascorbate are discussed.

Morphophysiological studies in experimental myocardial aggressions with isoproterenol. Note I. Morphological aspects.

The morphopathogenesis of lesions induced by high doses of isoproterenol injected for 1-7 days and 1-3 months is dynamically studied in groups of Wistar rats and guinea pigs. The disseminated myocardial necroses induced were of a hypoxic nature. By cicatricial substitutions, lesions of cardiosclerosis similar to those observed in pheochromocytoma cases were obtained.

Hepatitis and renal tubular acidosis after anesthesia with methoxyflurane.

A 69-year-old man operated for acute cholecystitis under methoxyflurane anesthesia developed postoperatively a hepatic insufficiency syndrome and renal tubular acidosis. Massive bleeding appeared during surgery which lasted for six hours. Postoperative evolution under supportive therapy was favourable. Complete recovery was confirmed by repeated controls performed over a period of one year after surgery.

Serum myoglobin in the diagnosis of acute myocardial infarction.

Serum myoglobin (Mgl) level was studied by the method of passive hemagglutination inhibition in 128 patients of whom 65 with acute myocardial infarction, 27 with unstable angina and 36 with various diseases as well as in 197 apparently normal subjects. The immunologic determination of serum myoglobin by the passive hemagglutination inhibition reaction was proved useful in the diagnosis of acute myocardial infarction (AMI) since in 95.3% of the cases myoglobin was found present in the serum in concentrations of 100-4.800 ng/ml depending on the moment of blood collection and the severity of infarction. The passive hemagglutination inhibition reaction for the determination of serum Mgl is superior to the biochemical tests (transaminases) both by the proportion of positive results obtained (95.3% by the Mgl test as compared with 73.8% by the transaminase test) and by its precocity, Mgl appearing in the serum within the first 1-2 hrs after onset of infarction. In the cases of AMI with negative or uninterpretable biochemical tests and/or ECG, serum Mgl determination can be decisive for the diagnosis. The presence of serum Mgl in 37.5% of the cases with intermediary syndrome (unstable angina) suggests the existence of some microfoci of myocardial necrosis undetectable by the usual biochemical or electric methods. Serum Mgl determination by the passive hemagglutination inhibition reaction is a relatively simple method, rapid (the results are obtained 1-2 hrs after blood collection) and practical since it can be performed in any laboratory with the usual equipment.