[Aspects of mitotic pathology due to sulfonamides].
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Biomedical subjects
Publications and source records attributed to L Minoli.
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Seven cases of Pneumocystis carinii pneumonia (PCP) (two in 1988, three in 1989, one in 1990 and one in 1991) have been observed in a group of 241 heart transplant recipients transplanted in Pavia, Italy, from November 1985 through December 1991. Median time to onset of symptoms was 100 days after transplantation (range 59-333 days). Diagnosis was achieved in all patients by cytological examination of bronchoalveolar lavage (BAL) fluid and/or transbronchial biopsy. Clinical and roentgenographic features were remarkably similar in all PCP-affected heart transplant recipients. A dry, persistent hacking cough associated with dyspnoea was consistently observed. Fever ranged from 37.6 to 39.4 degrees C, median leukocyte count and median arterial oxygen saturation (SaO2) values were 7,300/mm3 (range 3,000-16,000/mm3) and 61% (range 49.3-93%), respectively. Median CD4+ count at the onset of symptoms was 211/mm3 (range 28-739/mm3). The only patient experiencing a recurrence of PCP had a CD4+ cell count of 28/mm3 at the end of treatment with trimethoprim-sulfamethoxazole (TMP-SMX). In all patients human cytomegalovirus was isolated from BAL fluids; however, treatment with TMP-SMX alone (20 mg/kg/day of TMP) was consistently followed by a complete recovery.
Authors report the results of the isoenzyme analysis of strains of Entamoeba histolytica isolated from international travellers. This recently developed method allows the detection of pathogenic strains by evaluating the electrophoretic mobility of cytoplasmic enzymes and was proved to be more reliable and quickly feasible than previous ones. The experience reported refers to three strains isolated from travellers coming from Ecuador, Brazil and Indonesia, respectively; the zymodeme XIX (in accordance with the Sargeaunt's classification) was identified in all the three cases. This zymodeme has been first detected in 1981 and should currently be considered rare; moreover, it has never been previously reported from the Americas.
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Infectious complications are an important cause of morbidity and mortality in heart transplantation. In this report we describe their incidence in the Italian Heart Transplantation Program and their relationship to induction immunosuppressive protocols used. A total of 662 heart transplantations in 651 patients had been performed by March 1, 1990, in 10 Italian centers, with a follow-up of 12,022 patient-months. Actuarial survival at 54 months was 80%. There were 115 deaths, 28 as a result of infection (24%); 30 were perioperative. Mortality from infection was 15% in the first 30 postoperative days and 35% thereafter. During follow-up, 256 life-threatening infectious episodes occurred in 180 patients, for a mean of 1.42 infections/patient. Of these episodes, 28 (10.9%) were lethal. The rate at 54 months, excluding perioperative deaths, was 0.021 episodes/patient-month, with a mean of 0.39 infections/patient in the 651-patient series. At 6 months, 72% of patients were free from infection. This value did not change significantly during subsequent follow-up. Bacterial infections were most frequent (49.2%); fungal (10.5%) and protozoan (5.9%) infections had the worst outcome (lethality 26% and 20%, respectively). A primary cytomegalovirus infection was observed in 23 cases (12 mismatches). Lung involvement (99 episodes) and bacterial sepsis (47 episodes) were most common. Eighty episodes of infection (31.2%) were preceded by a supplementary treatment for rejection with steroid pulses (69%), prednisone boost (20%), or cytolytic therapy (11%). Treatment had preceded the infection by less than 15 days in 55% of cases.(ABSTRACT TRUNCATED AT 250 WORDS)
One hundred twenty-four patients underwent heart transplantation over a 3-year period. All patients were monitored for human cytomegalovirus (CMV) infection if at risk for primary CMV infection or in the presence of CMV-related symptoms. Rapid diagnosis of CMV infection relied on virus isolation and identification or viral antigen detection by using monoclonal antibodies to CMV immediate early or early antigens. In addition, "in situ" hybridization was used to detect viral DNA in tissue samples. Specimens examined included peripheral blood polymorphonuclear cells for CMV viremia and antigenemia determination, together with the most appropriate clinical samples when organ involvement was suspected. There was a 100% (6/6 patients) incidence of primary CMV infection in seronegative recipients of hearts from seropositive donors, whereas no CMV infection occurred in the three seronegative recipients receiving a transplant heart from CMV-negative donors. CMV hyperimmunoglobulin prophylaxis did not prevent primary CMV infection. Five of the six patients with primary CMV infection were symptomatic. In addition, 15 patients (13%) had symptomatic recurrent CMV infection. The most frequent symptoms associated with CMV infection (either primary or recurrent) were fever (19 patients) and pneumonia (eight patients). CMV viremia was detected in 17 patients either before or concomitantly with the appearance of fever. CMV was isolated from bronchoalveolar lavage in all cases with pneumonia; however, another pathogen was associated with CMV and appeared to be the major cause of pneumonia in 75% of these patients (6/8). Twelve patients (five with primary and seven with recurrent CMV infections) were treated with ganciclovir.(ABSTRACT TRUNCATED AT 250 WORDS)
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Infection by Human Immunodeficiency Virus (HIV) is the recognized cause of the Acquired Immunodeficiency Syndrome (AIDS) and related syndromes, all characterized by a devastating and progressive impairment of immunity. What ensues is the onset of opportunistic infections, neoplasms, both central and peripheral nervous system alterations and other conditions as well. Current therapeutic options, either with antiretroviral and anti-infective drugs, are only credited to prolong survival while not assuring definite cure. A significant improvement in the clinical management of these patients could be anticipated only after a better understanding of HIV life-cycle and its pathogenetic mechanisms.
In this paper we review our experience with HIV-related thrombocytopenic purpura (TP) in 24 patients seen from October, 1985 through April, 1988: the median follow-up was 16 months (range 3-32). All patients belonged to risk groups for AIDS and intravenous drug abusers represented 83% of the entire cohort. The male/female ratio was 4, and most of the patients were Walter Reed stage 3. The mean value of platelets at diagnosis was 33 x 10(9)/liter (range 6-120), and half of the patients had severe thrombocytopenia with hemorrhagic symptoms. Anemia and/or neutropenia were concomitant with TP in 21% and 17% of cases; four cases had pancytopenia. Marrow pictures showed megakaryocytic hyperplasia in 68% of cases; myelodysplasia or hypoplasia were observed in 14% and 18% of patients, respectively; lymphoid aggregates were present in two cases. Antiplatelet antibodies and circulating immune complexes were detected in 40% and 50% of cases, and the mean T4/T8 ratio was 0.9 (range 0.4-1.8). Half of the patients did not require specific therapy due to lack of bleeding; however no spontaneous reversions to normal platelet values occurred. The response to steroids and to immunoglobulins (either high-dose or anti-D) was good but temporary, and required maintenance therapy. The 2-year actuarial risk of evolution into overt AIDS was 30%, with a crude rate of 4 cases over 365 person-months at risk. The events which determined AIDS were opportunistic infections in two cases, Kaposi's sarcoma and malignant lymphoma in the other two. A comparison with the features of idiopathic TP is made and hypotheses regarding the pathogenetic mechanisms are discussed.
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