Natural killer cytotoxic test in the presence of phytohemagglutinin distinguishes between patients in the early and late stages of human immunodeficiency virus infection.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to M Galli.
Explore the source record for details and available documents.
Laboratory parameters which are modified following administration of zidovudine are becoming increasingly useful in monitoring the efficacy of treatment of early stages of HIV-1 infection. The serum levels of soluble interleukin (sILR)-2 receptor, which have been reported to increase early in HIV-1 infection, were found to be significantly lower in 24 patients being treated with zidovudine than in 69 patients who were not treated, 28 of whom had CD4+ counts greater than 400 x 10(6)/l, and 41 less than 400 x 10(6)/l, respectively (P less than 0.0001). A prospective study group of 33 subjects treated with zidovudine demonstrated a decrease in sIL-2R during therapy (base values 2113 +/- 1131 versus 1444 +/- 728 after 90 days of therapy; P less than 0.0007). The reduction of sIL-2R was greater in those subjects were p24 antigen became negative during treatment. sIL-2R therefore seems to be a useful tool in the monitoring of therapy with zidovudine.
We describe two cases of prolonged postischemic ventricular dilatation during myocardial scintigraphy with 99mTc MIBI, the new perfusion tracer that has only negligible redistribution. Ventricular dilatation, caused by true chamber dilatation and/or subendocardial ischemia, was still present over two hours after the induced ischemic episode, suggesting a prolonged duration of such a commonly believed fleeting scintigraphic finding.
Explore the source record for details and available documents.
The purpose of the present study was to determine whether and to what extent mental stress can reproduce the perfusion defects that are known to be induced by exercise. Twenty-four patients with recent myocardial infarction (New York Heart Association functional class I) and evidence of ischemic response were evaluated by means of SESTAMIBI scintigraphy performed once after exercise and then again within 2 days after mental arithmetic. Baseline, exercise, and mental stress planar scintigrams were divided into 15 segments, and each segment was reviewed and scored on a scale of 0 to 3 by experienced observers using circumferential profile analysis. Conflicting scores were resolved by consensus. Electrocardiographic abnormalities were found in 15 of 24 patients during exercise and in none during mental arithmetic. Chest pain was experienced by five patients during exercise and by none during mental stress. Twenty patients showed reversible perfusion defects during mental stress. Of the 360 pooled scintigram segments, 99 evidenced uptake defects during exercise, and 48 of these showed the same defects during mental stress. Twenty of the remaining 51 of 99 segments were adjacent to segments showing reversible hypoperfusion, suggesting milder hypoperfusion in these segments during mental arithmetic than during exercise. Furthermore, 10 segments showed reversible defects only during mental stress such that seven of these occurred in areas adjacent to those that had shown exercise-induced reversible perfusion defects, two occurred in areas that had shown fixed SESTAMIBI defects during exercise, and one occurred in a segment that had shown completely normal uptake during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
In patients with coronary artery disease, radionuclide investigations have documented a high incidence of mental stress-induced myocardial ischemia in the absence of significant electrocardiographic changes and/or angina. To investigate the causes of the low electrocardiographic sensitivity, we recorded body surface maps during mental arithmetic in 22 normal volunteers and 37 postinfarction patients with residual exercise ischemia. Myocardial perfusion was studied with thallium-201 or technetium-99 (SESTAMIBI) planar scans. In 14 patients, body surface maps were also recorded during atrial pacing at the heart rate values achieved during mental stress. While taking the body surface maps, the area from J point to 80 msec after this point (ST-80) was analyzed by integral maps, difference maps, and departure maps (the difference between each patient's difference map and the mean difference map for normal subjects). The body surface mapping criteria for ischemia were a new negative area on the integral maps, a negative potential of more than 2 SD from mean normal values on the difference maps, and a negative departure index of more than 2. Scintigraphy showed asymptomatic myocardial hypoperfusion in 33 patients. Eight patients had significant ST segment depression. The ST-80 integral and difference maps identified 17 ischemic patients. Twenty-four patients presented abnormal departure maps. One patient presented ST depression and abnormal body surface maps without reversible tracer defect. In 14 of 14 patients, atrial pacing did not reproduce the body surface map abnormalities. The analyses of the other electrocardiographic variables showed that in patients with mental stress-induced perfusion defects, only changes of T apex-T offset (aT-eT) interval in Frank leads and changes of maximum negative potential value of aT-eT integral maps significantly differed from those of normal subjects. Our results confirm the low electrocardiographic sensitivity for detecting mental stress-induced myocardial hypoperfusion in postinfarction patients. ST analysis in the body surface map increases the information content of the electrocardiographic signal. T wave analysis appears to offer fewer diagnostic advantages.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The binding of affinity-purified anticardiolipin antibodies (ACA) to liposomes that contained cardiolipin or phosphatidylserine was investigated. ACA bound to these liposomes only in the presence of plasma or serum, which indicated a requirement for a plasma component. This component--referred to as aca-cofactor--was purified; its activity to support ACA binding to liposomes that contained cardiolipin was not destroyed by heat (10 min at 90 degrees C), but was greatly diminished on incubation with trypsin. aca-cofactor bound liposomes that contained negatively charged phospholipid but had no affinity for liposomes that contained neutral phospholipid (eg, phosphatidylcholine); this binding was independent of calcium ions. aca-cofactor was essential for ACA to bind to liposomes that contained cardiolipin or phosphatidylserine and, when coated on a microtitre plate in the absence of any phospholipid, aca-cofactor was an apparent antigen for ACA in an enzyme-linked immunosorbent assay. aca-cofactor is a single chain polypeptide with an apparent molecular weight of 50 kD (non-reduced), which increases to 70 kD upon reduction, and its properties closely resemble those of beta 2-glycoprotein I (apolipoprotein H).
T-lymphocyte subsets and serum immunoglobulins were assayed in 27 neonates and 12 infants younger than 6 months, all born to HIV-seropositive mothers. No differences in T-lymphocyte subsets between the 27 seropositive and 34 seronegative infants were found at birth. Twelve seroreverted and 14 infected children were followed. CD4+ cell counts were significantly lower in the latter at 3 and 24 months of age. Serum immunoglobulin levels and CD8+ percentages became higher in the infected group, starting from the sixth month, while CD4+ percentages and CD4+/CD8+ ratios became lower, starting from the twelfth month.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The effect of a single oral dose (50 mg) of captopril was studied in 12 hypertensive patients divided into 2 groups: 6 had a normal hemodynamic profile; the other 6 had NYHA class III or IV heart failure. Medical history and clinical and laboratory investigation showed that the heart failure was due exclusively to arterial hypertension. Mean arterial pressure (MAP), aldosterone, plasma renin activity (PRA) and atrial natriuretic factor (ANF) were followed for 4 hours after administration of captopril. MAP values showed a similar decrease in the 2 groups but the variations in the 3 hormones were much greater in the second group. This group showed higher basal levels of PRA, aldosterone and ANF; after stimulation PRA increased sharply preceded by a substantial decrease in aldosterone and ANF. To explain this phenomenon, the Authors propose that the liver of the patients with heart failure is unable to rapidly compensate the reduction in synthesis of angiotensin II caused by the drug with a corresponding increase in angiotensinogen production; the consequent sharp drop in plasma aldosterone would lead to a rise in renin production by the kidney. The arteriolar and venous vasodilatation induced by the ACE-inhibitor, would explain the drop in intra-atrial pressure with reduced plasma levels of ANF. The decrease in ANF could also be caused by the inhibition of the renin-angiotensin system of the heart leading to improved blood supply and hence myocardial contractility.
Severe thrombocytopenia (TP) accounted for 5.3% of cases in a consecutive series of 380 HIV-infected intravenous drug users (IVDUs) at presentation. Forty-one of 53 subjects with severe TP showed haemorrhages and were treated as follows: ten were splenectomized, 17 were given high-dose intravenous immunoglobulins (HDIg), and 10 received anti-Rh(D) immunoglobulins (anti-Rh Ig). Splenectomy induced a complete clinical response in all cases: four out of 10 patients maintained platelet counts greater than 100 x 10(9)/l. HDlg gave a good clinical response in all patients, but eight out of 17 suffered haemorrhages during the follow-up and recall treatments were necessary. Six out of 10 patients treated with anti-Rh lg maintained platelet counts greater than 30 x 10(9)/l, but in two cases the treatment was interrupted because of severe haemolysis. No patient progressed to overt AIDS during the follow-up. Splenectomized patients in particular did not show adjunctive risks of worsening of the HIV-related clinical picture. A platelet kinetic study performed in 20 patients with severe HIV-related TP suggests a possible role for platelet sequestration in TP of HIV-infected IVDUs, in which a liver involvement is very frequent.
Explore the source record for details and available documents.
Intravenous drug users (IVDUs) account for more than 64% of the total AIDS cases in Italy. The IVDUs' seropositivity rate is greater than 70% in Milan and greater than 50% in the main cities of Italy. The first evidence of seropositivity in this population dates back to 1979. In a cohort study performed in Milan the rate of progression to overt AIDS among IVDUs was 6% in 3 years (1984-1987). At presentation, more than 75% of the subjects had CD4+ cell counts higher than 400/mm3 (mean 631, median 528, mode 465). These values are significantly higher than those observed in the same population in New York, the only American city with HIV-infection spread comparable to that observed in Milan. The probability of having CD4+ cell counts lower than 400, 300, and 200/mm3 in relation to the length of follow-up was, respectively, 50, 40, and 2% after 36 months from presentation. At the same end point, subjects presenting less than 400 CD4+ cells at entry had 30% probability of falling under 200 cell/mm3. The pattern of CD4+ cells, as much as the low percentage of yearly progression to overt AIDS, is probably related to the recent, even if rapid, spread of infection among IVDUs in Italy. The clinical features of overt AIDS present some differences between IVDUs and other at-risk groups. Among U.S. IVDUs with AIDS, Kaposi's sarcoma is infrequent (2.9% vs 27.7% in homosexual men) while mycotic infections such as deep candidiasis and cryptococcosis are significantly more frequent. The same pattern has been observed in our case file in Milan: esophageal candidiasis represents the most frequent cause of diagnosis of overt AIDS. Mycotic infections, overall, are more frequent than in U.S. IVDUs. The increased rate of mycotic infections among IVDUs might be justified by altered functions of nonspecific immunity, such as PMNL killing and phagocytosis of Candida albicans spores, impaired in HIV-infected IVDUs, but generally normal in infected subjects belonging to the other at-risk groups.
Explore the source record for details and available documents.