Antibodies to human platelet antigens form a significant proportion of platelet antibodies detected in Indian patients with refractoriness to platelet transfusions.

BACKGROUND: The transfusion of platelets is an important therapeutic strategy in bleeding patients with thrombocytopenia. However, some chronically transfused patients fail to achieve the appropriate platelet count increment following transfusion due to the presence of platelet alloantibodies. OBJECTIVES: The aims of this research were to study the prevalence of platelet alloimmunisation and to characterise the platelet-reactive (PR) antibodies in haematology patients refractory to platelet transfusions in an Indian setting. PATIENTS AND METHODS: A total of 80 patients with a prior history of multiple transfusions (minimum of five cellular transfusions) were included in the study if they did not achieve an adequate corrected count increment within 24 h of the platelet transfusion. Patients with non-immunological causes of platelet refractoriness were excluded from the study. The test was performed on a blood sample of 4 mL of Ethylenediaminetetraacetic acid (EDTA) blood sample in which plasma was separated and stored at -80 °C and underwent batch testing in PAK-2LE. RESULTS: The overall prevalence of platelet alloimmunisation in our study was 60%. Of the 48 patients who were detected to have platelet antibodies, the combination of anti-human leucocyte antigen (HLA) and platelet-specific (PS) antibodies together constituted the majority of 54·2%. The overall prevalence of anti-HLA antibodies was 51·25% and of PS antibodies was 41·25% in the total study population of 80. CONCLUSION: The overall prevalence of PS antibodies in our study was greater than that reported by other groups in India and other countries. This needs to be considered, particularly in the management of patients refractory to platelet transfusions, where HLA-matched platelets constitute current best practice.

Valvular dysfunction in antiphospholipid syndrome: prevalence, clinical features, and treatment.

Valvular abnormalities develop in 36% and 35% of patients with primary antiphospholipid syndrome (PAPS) and with systemic lupus erythematosus (SLE) respectively, and in 48% of patients with SLE and antiphospholipid antibodies (aPL). Valvulopathy includes leaflet thickening, vegetations, regurgitation, and stenosis. A literature survey shows that significant morbidity from valvular dysfunction, mostly mitral regurgitation leading to congestive heart failure, occurs in 4% and 6% of SLE and PAPS patients, respectively. The pathogenesis of valvulopathy may involve interaction of aPL with antigens on the valve surface, resulting in valvulitis. Current therapy includes symptomatic measures and valve replacement. A novel approach for symptomatic antiphospholipid syndrome (APS) related valvulopathy involves treatment with systemic corticosteroid. We describe four such patients and their dramatic clinical and hemodynamic response to treatment with prednisone when symptomatic measures failed.

Polyarteritis nodosa and drug abuse: is there a connection?

Drug abuse has been controversially linked to polyarteritis nodosa. A 28-year-old man with a history of drug abuse with inhaled heroin presented with an enigmatic illness consisting of refractory fever, bilateral pleural effusions, migratory polyarthritis, and a leukaemoid reaction. An abdominal angiography confirmed the diagnosis of polyarteritis nodosa, and treatment with both prednisone and cyclophosphamide resulted in significant clinical and laboratory improvement.

Salmonella mycotic aneurysm of the aortic arch: case report and review.

Salmonella mycotic aneurysms of the thoracic aorta are exceedingly rare. We describe what we believe is only the third reported case involving the aortic arch. The patient was treated with surgical intervention and a prolonged course of antibiotics, which resulted in long-term survival. We review 13 previously reported cases of salmonella mycotic aneurysms of the thoracic aorta. The overall outcome was abysmal, with 10 of 13 patients dying within 1 month after the diagnosis was made. We discuss the pathogenesis, clinical presentation, diagnostic approach, and management (including surgical intervention and duration of antibiotic therapy) of this condition on the basis of the findings in these cases.

A prospective randomized trial of intravenous magnesium versus intravenous propranolol in acute myocardial infarction.

A total of 266 patients entered into a study comparing the effect of intravenous magnesium and propranolol following acute myocardial infarction. Of these, 97 were able to receive either drug and were therefore randomized into the magnesium (n = 51) or propranolol group (n = 46). 88 patients were unable to receive propranolol and formed a third group (NR) while a further 81 patients could not receive either drug and formed a fourth group (N). The study showed that intravenous magnesium was as effective in preventing potentially lethal arrhythmias as propranolol and could be given to some 70 per cent of such patients whereas propranolol could only be given to 36 per cent.

Long-term follow-up after acute myocardial infarction in patients randomized to treatment with intravenous magnesium or intravenous propranolol in the acute phase.

Ninety-five patients with acute myocardial infarction were followed up for 6 months to 3 years (mean 25.4 months) in a preliminary study to compare the effects of intravenous magnesium (49 patients) with that of intravenous propranolol (44 patients) given immediately after admission to the intensive care unit. There were four cardiac deaths in the propranolol group and no deaths in the magnesium group (P < 0.046) and 27 per cent of patients who received propranolol subsequently developed cardiac failure as opposed to 12 per cent of those who had received magnesium (P < 0.04). Intravenous magnesium given in the early stages of myocardial infarction reduces the subsequent cardiac death rate possibly by reducing infarct size.

Progression and regression of coronary artery disease in one year. Quantitative angiographic assessment in patients with stable angina pectoris.

The rate of progression of coronary artery stenoses (CAS) is not clear. Spontaneous regression may also occur. Seventy-one CAS in 25 patients who were enrolled in a study of the effects of chromium on CAS were analysed. Coronary angiography was performed in multiple views and patients randomised to chromium or placebo treatment. Videodensitometric quantitative analysis was performed using a Vanguard XR70 Analyzer. After 1 year all patients were recatheterised. Corresponding frames from identical views were analysed. CAS were assessed with the observers blinded to the initial study results. No differences were found between chromium or placebo and the results have been combined. There was no overall progression of CAS as assessed by % area stenosis (p = 0.65), % diameter stenosis (p = 0.19), stenotic area (p = 0.87), or stenotic diameter (p = 0.99). However, 20% of individual lesions progressed, while 10% regressed, and 70% remained the same. These changes must be taken into account in studies of interventions which may modify the course of coronary atherosclerosis, and if coronary by-pass surgery is to be performed with a 1 year delay after angiography.

An unusual case of Q fever endocarditis.

We describe a patient with unusual features of Q fever endocarditis. The unusual features of this case were the presence of an abscess surrounding the involved aortic valve and the appearance of circulating anticoagulants in the patient's serum.

Brucellosis with nephrotic syndrome, nephritis and IgA nephropathy.

A patient with systemic brucellosis due to Brucella melitensis had severe renal involvement. Clinical features included hypertension, macroscopic haematuria, massive proteinuria of 10 g per 24 hours and azotaemia. Following treatment with antibiotics, the azotaemia resolved and proteinuria decreased to less than 0.5 g per 24 hours, but microscopic haematuria and hypertension persisted. Renal biopsy during recovery revealed IgA nephropathy with minimal mesangial changes, suggesting a causal relation between brucellosis and IgA nephropathy with a reversible nephrotic syndrome.

Serum and mononuclear cell potassium, magnesium, sodium and calcium in pregnancy and labour and their relation to uterine muscle contraction.

Thirty women in their third trimester of pregnancy (37-42 weeks), 40 women during and 72 h after labour and 18 non-pregnant controls were studied for changes in serum and mononuclear cell cation content, and their relationship to cervical effacement and intensity of pain as measured by plasma beta endorphin concentrations during labour. Serum magnesium fell from 0.95 +/- 0.01 (mean +/- SEM) to 0.84 +/- 0.02 mmol/litre at late pregnancy and further to 0.76 +/- 0.01 during labour (P < 0.001); serum potassium fell from 4.25 +/- 0.05 to 3.79 +/- 0.06 mmol/litre (P < 0.0001) during labour; and serum calcium fell from 2.40 +/- 0.02 to 2.28 +/- 0.01 mmol/litre at late pregnancy (P < 0.001) and further to 2.25 +/- 0.02 mmol/litre during labour (P < 0.001). Mononuclear cell magnesium content rose from 4.5 +/- 0.3 to 5.6 +/- 0.04 fmol/cell (P < 0.02); potassium content rose from 37.7 +/- 2.0 to 50.9 +/- 3.0 fmol/cell (P < 0.001); and calcium content rose from 4.4 +/- 0.4 to 7.6 +/- 1.1 fmol/cell (P < 0.105). On the other hand, mononuclear cell sodium content fell from 7.2 +/- 0.5 to 3.8 +/- 0.3 fmol/cell (P < 0.001). Plasma beta endorphin concentrations increased with increasing degrees of effacement, as did intracellular Na, whereas intracellular Mg and K showed an inverse trend. A significant correlation was found between intracellular cation and beta endorphin levels (r = -0.98, Mg; -0.99, K; 0.83, Na). These changes are probably due either to intercompartmental cation shifts or possibly to endometrial ischaemia and damage during labour.

The effects of chromium supplementation on serum glucose and lipids in patients with and without non-insulin-dependent diabetes.

Seventy-six patients with established atherosclerotic disease were treated daily with either 250 micrograms of chromium orally as chromium chloride or a placebo for a period of 7 to 16 months (mean, 11.1 months). Serum chromium increased from 2.69 +/- 0.09 to 12.12 +/- 0.77 nmol/L (mean +/- SE, P less than .005). Serum triglycerides were lower (1.68 +/- 0.11 and 2.10 +/- 0.14 nmol/L, respectively; P less than .02) in the chromium-treated patients than in the patients who received placebo, and serum high-density lipoprotein (HDL) increased (from 0.94 +/- 0.05 to 1.14 +/- 0.07 mmol/L, P less than .005) in the patients who received chromium. There was no change in serum cholesterol or blood glucose during the study.

Effects of hydrochlorothiazide, diltiazem and enalapril on mononuclear cell sodium and magnesium levels in systemic hypertension.

Sixteen patients (mean age 68 years) with mild to moderate hypertension were treated with either diltiazem or hydrochlorothiazide for 6 weeks, followed by enalapril for a further 6 weeks. A second group of 40 patients (mean age 71 years) was treated with either hydrochlorothiazide or enalapril for 12 weeks; nonresponders received both drugs for 8 weeks. Treatment with hydrochlorothiazide or enalapril resulted in a lowering of systolic and diastolic blood pressures, but diastolic pressure was lower in patients treated with enalapril (89 +/- 2 and 82 +/- 2 mm Hg, respectively; p less than 0.05). Treatment with diltiazem resulted in a decrease in diastolic pressure only. Treatment with hydrochlorothiazide resulted in a 17% decrease in serum potassium (p less than 0.05), which returned to normal when enalapril was substituted. Hydrochlorothiazide also produced a 23% decrease in mononuclear cell sodium content at 4 weeks (p less than 0.01), with a further 15% decrease at 12 weeks (p less than 0.05). Mononuclear cell potassium and magnesium also decreased at 12 weeks by 18 and 16%, respectively (p less than 0.05). All these effects were reversed when enalapril was substituted. A similar pattern of events was seen with diltiazem, which was again reversed with enalapril. Finally, there was no relation between changes in mononuclear cell sodium or other cation content and changes in blood pressure.

Serum and intracellular electrolytes in patients with and without pain.

The effect of acute stress, with and without pain, on serum and mononuclear cell cation content was studied in 205 healthy women in their last trimester of pregnancy or during normal labour, in patients with acute medical conditions in which pain was or was not present, in acute surgical conditions, and immediately prior to elective surgery. In all subjects there was a fall in serum sodium, potassium, magnesium and calcium concentrations during stress, with an apparent shift into the intracellular space. An inverse correlation was present between the severity of pain and the fall in serum cations.

The rise of serum creatinine levels during labor.

Serum creatinine, blood urea nitrogen and creatine phosphokinase were measured in 32 women during the last 3 weeks of pregnancy and, in a further 39 women, during and after labor. The serum creatinine increased from 61.9 +/- 0.9 to 69.8 +/- 1.8 mumol/l (mean +/- SEM) (P less than 0.05) in the third stage of labor and returned to normal by 72 h after delivery. The muscle creatine phosphokinase increased from 54 +/- 7 to 77 +/- 9.9 units (P less than 0.05) during the third stage and remained high (87 +/- 13.3 units) 72 h later. We conclude that these changes are due to muscle contraction and injury during delivery.

Chromium and cholesterol-induced atherosclerosis in rabbits.

Thirty-three rabbits on a cholesterol-enriched diet were randomized into 6 groups and treated with daily injections of either water, 20 micrograms of potassium chromate or 1, 5, 10 or 20 micrograms of chromium chloride, respectively, for 135 days with a 2- to 10-fold increase in serum chromium. There was a marked reduction in the percentage of aortic intimal surface covered by plaque, in aortic weight and cholesterol content in the treated animals. Rabbits treated with 20 micrograms of chromium chloride showed a better response than those treated with either 10 or 20 micrograms of potassium chromate.

The relationship between beta-endorphin levels and uterine muscle contractions during labor.

Plasma beta-endorphin (BE) levels (8.6 +/- 0.8 pmol/l) (mean +/- SE) were lower in the third trimester than in non-pregnant controls (14.8 +/- 1.1 pmol/l) (P less than 0.001), increased during labor, to 29.3 +/- 4.4 pmol/l (P less than 0.005) and decreased, 72 h after delivery, to 3.5 +/- 0.4 pmol/l (P less than 0.001). BE levels were found to correlate significantly with uterine muscle contraction (r = 0.966, P less than 0.05) and with cervical effacement (r = 0.974, P less than 0.05) during labor.

A routine method for the measurement of the sodium, potassium, magnesium and calcium content of human lymphocytes.

We describe a rapid, single-step procedure for the isolation of human lymphocytes from whole blood, suitable for a routine clinical laboratory. Lymphocyte content of sodium, potassium, magnesium and calcium were measured simultaneously in a group of controls and found to fall within expected ranges. Expression of results per mg protein produced less inter-individual variation than per unit cell. In order to examine another, physiologically different but normal population, women during pregnancy were also studied. The cation content of lymphocytes expressed per mg protein was significantly lower than for controls due to a 44% increase in protein content per cell.

Continuous intravenous infusion of magnesium sulfate after acute myocardial infarction.

Two hundred and fifty patients admitted with acute myocardial infarction were treated with a continuous infusion of magnesium sulfate for 24 h (a total of 46 mmol of elemental magnesium). Only 1 patient had ventricular fibrillation; no patient had sustained ventricular tachycardia requiring cardioversion. Twenty-five patients had short runs of non-sustained ventricular tachycardia and did not need cardioversion. In 6 further patients, the infusion had to be discontinued because of a drop in blood pressure. The in-hospital mortality for the group was 3.4%.

Treatment of patients with acute myocardial infarction with intravenous magnesium.

Acute myocardial infarction (AMI) accounts for a large number of deaths annually. The major cause of early deaths is ventricular fibrillation. During the past few years, intravenous magnesium has been instituted as a therapy for AMI. This report reviews the latter literature and discusses the potential mechanisms whereby intravenous Mg is beneficial in AMI. Intravenous Mg is a safe and inexpensive drug whose use reduces the incidence of arrhythmias, infarct size and early mortality following AMI.