Search PubMed⌕ Search

Biomedical subjects

R Gherardi

Publications and source records attributed to R Gherardi.

At least 55 records · Page 3Linked to original sources
PubMed1994

Zidovudine therapy and HIV encephalitis: a 10-year neuropathological survey.

OBJECTIVE: To assess the effect of zidovudine on productive HIV infection of the brain. DESIGN: To correlate the incidence of HIV-specific neuropathology with zidovudine therapy. PATIENTS: We examined 192 AIDS cases neuropathologically; 97 had never been treated with zidovudine, 72 had received zidovudine for over 3 months and until death, 23 had their treatment terminated more than 1 month before death. RESULTS: The incidence of HIV encephalitis/HIV leukoencephalopathy (HIVE/HIVL) and of multinucleated giant cells (MGC) was significantly lower in patients who had received zidovudine than in those who had never received zidovudine. The yearly incidence of HIVE/HIVL increased between 1982 and 1987 probably because of improved survival, and decreased between 1987 and 1990 although the percentage of patients treated with zidovudine increased. Since 1991 the incidence of HIVE/HIVL and of MGC increased slightly. The percentage of patients treated with zidovudine until death decreased and that of patients whose treatment was terminated increased concomitantly. In 1989 and 1990, most patients whose treatment was terminated had MGC and HIVE/HIVL. In 1991 and 1992 this incidence decreased markedly, coinciding with the introduction of dideoxyinosine therapy. CONCLUSION: Zidovudine treatment significantly reduces the occurrence of productive HIV infection of the brain in AIDS. Discontinuing zidovudine therapy may favour the occurrence of HIV encephalitis. Substitution therapy with dideoxyinosine also appears to protect against HIV-specific brain pathology.

AIDS Dementia Complex↗
PubMed1994

Hyperplastic pacinian corpuscles: an uncommonly encountered lesion of the hand.

The occurrence of hyperplastic pacinian corpuscles in the hand is rare, with only 13 cases reported in the literature. We describe such a case in a 70-year-old male who had worked as a locksmith for many years. A grape-like cluster of firm, rice-sized nodules was discovered in the subcutaneous tissue of the finger following a glass-induced injury. Histopathological findings revealed pacinian corpuscles to be increased in size and number. Individual corpuscles consisted of a central nerve fiber surrounded by 35 to 60 concentric lamellae (normal controls from other specimens: 13-15 lamellae). The external corpuscular diameter ranged from 1.8 to 3.2 mm (normal controls from other specimens: 1.6 mm). Immunohistochemistry showed positive staining with Leu 7 antibody and antiglial fibrillary acidic protein in the small nerves situated in the vicinity of the pacinian corpuscles, but not in the corpuscles themselves. The lesion reported here clearly differed from both neurofibroma with occasional pacinian differentiation and the so-called pacinian neurofibroma. There was no evidence of neurofibromatosis.

Aged↗
PubMed1994

Differential elevation of circulating interleukin-1 beta, tumor necrosis factor alpha, and interleukin-6 in AIDS-associated cachectic states.

Elevation of serum interleukin-1 beta (IL-1 beta) levels, and to a lesser degree tumor necrosis factor alpha levels, was found in cachectic human immunodeficiency virus (HIV)-infected African patients without concurrent opportunistic infection or neoplasia (HIV wasting syndrome). A heterogeneous pattern of elevations of cytokine levels, including mild elevations of IL-1 beta and pronounced elevations of IL-6 levels, was found in other cachectic states.

Acquired Immunodeficiency Syndrome↗
PubMed1994

Acute rhabdomyolysis in patients infected by human immunodeficiency virus.

To delineate the spectrum of rhabdomyolysis associated with human immunodeficiency virus (HIV) infection, we reviewed the clinical and pathologic data from nine HIV-infected individuals with acute rhabdomyolysis, and pooled data with those of 11 previously reported cases. Patients with rhabdomyolysis were at all stages of HIV infection and could be classified into three groups: (1) HIV-associated rhabdomyolysis (7 of 20), including rhabdomyolysis in primary HIV infection, recurrent rhabdomyolysis, and isolated rhabdomyolysis; (2) rhabdomyolysis induced by drugs (6 of 20), including didanosine; and (3) rhabdomyolysis at the end stage of acquired immunodeficiency syndrome (7 of 20), including opportunistic infections of muscle and rhabdomyolysis without a definite cause. Because prognosis, in part, depends on the cause of rhabdomyolysis, recognition of drug-induced or opportunistic infectious muscle disorders is required.

Acute Disease↗
PubMed1994

Optimal handling of blood samples for routine measurement of lactate and pyruvate.

Blood lactate and pyruvate are of critical importance for the diagnosis of mitochondrial diseases. To determine guidelines for adequate blood pyruvate and lactate determinations, intraindividual studies were carried out on 10 subjects, and the influences of venostasis, delay before deproteinization, and pH in the pyruvate assay were analyzed. Delays of 1 hour or more before deproteinization of samples induced major elevations of lactate-pyruvate ratios. The lactate-pyruvate ratio correlated positively with pH in the pyruvate assay, and inadequate pH appeared as a largely underestimated cause of misleading results, while venostasis was a minor source of errors.

Adult↗
PubMed1994

Thalidomide neuropathy incidence and clinico-electrophysiologic findings in 42 patients.

BACKGROUND AND DESIGN: Thalidomide therapy was shown to be effective in numerous dermatologic diseases. As reliable methods of contraception are now available, neurotoxicity has become the most important side effect limiting the use of thalidomide. The incidence of this neuropathy and its relationship to thalidomide doses are still matters of debate. In a retrospective study, we reviewed the files of 42 patients who had received thalidomide between 1987 and 1992 for various dermatologic diseases. The incidence and the conditions of occurrence of the neuropathy were analyzed. RESULTS: Evidence of a thalidomide-induced neuropathy was present in nine patients (21%), who had both clinical and electrophysiologic typical abnormalities. Twelve other patients (28%), however, presented with isolated clinical or electrophysiologic signs. Thus, the diagnosis of thalidomide neuropathy could not be affirmed. The occurrence of the neuropathy did not appear to be related to the daily dose nor to the duration of treatment. The highest risk of developing a thalidomide neuropathy was found in female and elderly patients. Two monozygotic twin sisters, who received thalidomide for Behçet's disease, both developed a neuropathy. CONCLUSIONS: These data suggest that the incidence of thalidomide neuropathy may be between 21% and 50%. Individual susceptibilities with possible genetic predisposition seem to be more important than daily dose and duration of thalidomide therapy.

Adult↗
PubMed1993

Cytochrome c oxidase reaction improves histopathological assessment of zidovudine myopathy.

Zidovudine can induce a mitochondrial myopathy with ragged-red fibers and partial cytochrome c oxidase deficiency. In an attempt to improve histological assessment of zidovudine myopathy, we evaluated cytochrome c oxidase histochemical reaction in the muscle of 10 patients with biopsy-proven zidovudine myopathy (Group 1), 10 myopathic zidovudine receivers without typical histopathological features of zidovudine myopathy (Group 2), and 10 human immunodeficiency virus (HIV)-infected patients not treated by zidovudine who had an immunohistological profile of HIV-associated myopathy or other neuromuscular disorders (Group 3). Among zidovudine receivers, cytochrome c oxidase deficiency was found in 10 of 10 patients from Group 1 and 7 of 10 from Group 2. No cytochrome c oxidase deficiency was observed in patients not treated by zidovudine. When present, cytochrome c oxidase-negative fibers accounted for 2 to 28% of fibers, and there was no difference for the number of cytochrome c oxidase-negative fibers between Group 1 and Group 2. Most patients with cytochrome c oxidase deficiency that could be evaluated clinically after muscle biopsy improved after withdrawal of zidovudine (5 of 7 in Group 1, 5 of 5 in Group 2). Patients who did not improve had an HIV-associated myopathy concurrently with zidovudine myopathy. We conclude that cytochrome c oxidase reaction may be used as a reliable marker of zidovudine mitochondrial toxicity in HIV-infected patients with muscular symptoms.

Acquired Immunodeficiency Syndrome↗
PubMed1993

The spectrum of vasculitis in human immunodeficiency virus-infected patients. A clinicopathologic evaluation.

OBJECTIVE: To delineate the different types of inflammatory vascular diseases (IVD) occurring in patients with human immunodeficiency virus (HIV) infection. METHODS: Muscle, nerve, or skin biopsy specimens from 148 symptomatic HIV-infected individuals were reviewed, and subgroups of vasculitis were identified using the American College of Rheumatology (ACR) 1990 clinicopathologic criteria for the classification of vasculitis. RESULTS: IVD was documented in 34 patients (23%) and included necrotizing arteritis (3 patients), non-necrotizing arteritis (1 patient), neutrophilic IVD (7 patients), mononuclear IVD (17 patients), and other small vessel inflammatory changes (6 patients). According to the ACR criteria, 11 patients could be classified as having a distinct category of vasculitis, including polyarteritis nodosa (4 patients), Henoch-Schönlein purpura (1 patient), and drug-induced hypersensitivity vasculitis (6 patients), and 23 were classified in the group "other vasculitis, type unspecified." One patient had hepatitis B virus surface antigenemia, 2 had cryoglobulinemia, and 2 were coinfected by human T lymphotropic virus type I. Cytomegalovirus inclusions and antigens were found in endothelial cells in 1 patient. HIV antigens and genome were detected in perivascular cells of 2 of the 3 patients with necrotizing arteritis; in 1, HIV-like particles were seen by electron microscopy. Immune deposits were found in small vessel walls in 5 skin biopsy samples showing small vessel vasculitis and in the muscle of the 3 patients with necrotizing arteritis. CONCLUSION: A wide range of inflammatory vascular diseases may occur in HIV-infected individuals. Vascular inflammation appears multifactorial and may result from HIV-induced immunologic abnormalities and exposure to a variety of xenoantigens, such as HIV itself, other infectious agents, and drugs.

Adult↗
PubMed1993

Tubular aggregates and partial cytochrome c oxidase deficiency in skeletal muscle of patients with AIDS treated with zidovudine.

We report on two patients, who had myalgias while receiving long-term zidovudine treatment for an HIV infection, in whom muscle biopsy findings included a partial cytochrome c oxidase (CCO) deficiency, a feature of zidovudine myopathy, and tubular aggregates, a finding hitherto unreported in HIV-infected patients. The CCO deficit was observed in 28% and 24% of muscle fibers, respectively. Tubular aggregates were the prominent histopathological feature in patient 1, and were detected by systematic electron microscopy in patient 2. Inflammation and myonecrosis were not detected. In patient 1, the typical mitochondrial and myofibrillar changes of zidovudine myopathy were present and 12% of fibers showed tubular aggregates. The aggregates were not stained at CCO reaction, and 96% of myofibers enclosing tubular aggregates showed a decreased CCO activity. This suggested more than a chance association between mitochondrial dysfunction and the formation of tubular aggregates. We conclude that tubular aggregates are detected in some patients treated by zidovudine, and that the finding could be related to the long-term administration of the drug.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Long-lasting postmortem viability of human immunodeficiency virus: a potential risk in forensic medicine practice.

To determine the time from death when an autopsy could be carried out without any risk of contamination by human immunodeficiency virus (HIV), we cultured HIV from serial samples of blood and liquid effusion, collected as long as possible alter death from refrigerated dead bodies of HIV-infected patients. Samples were cocultivated with stimulated normal human lymphocytes and viral replication was assessed by p24 HIV1 antigen ELISA determination and by reverse transcriptase HIV1 and HIV2 activity microassay. Viable HIV was isolated from blood obtained 16.5 days postmortem, from pleural liquid effusion obtained 13.8 days postmortem, and from pericardial liquid effusion obtained 15.5 days postmortem. Viral replication was in evidence in at least one sample from all nine patients of the study. The present study did not allow us to determine a time from death when an autopsy could be carried out without any risk of contamination by HIV. We conclude that postponement of autopsies does not eliminate occupational risk of contamination by HIV.

Adult↗
PubMed1993

Successful treatment of HIV-related vasculitis with peripheral neuropathy with short-term steroids followed by the association of zidovudine and plasmapheresis.

OBJECTIVE: treatment of HIV-related vasculitis, avoiding prolonged immunosuppressive therapy. DESIGN: prospective pilot study of HIV-related neurological vasculitis. PATIENTS: two HIV-infected patients with histologically proven vasculitis. INTERVENTION: short-term corticosteroid followed by zidovudine combined with plasmapheresis. MAIN OUTCOME MEASURES: clinical, biological, immunological and electromyographic evaluation. RESULTS: complete neurological recovery. CONCLUSION: excellent tolerance and efficacy of combined zidovudine and plasmapheresis therapy in peripheral neurological HIV-related vasculitis.

AIDS-Related Opportunistic Infections↗
PubMed1993

Peripheral neuropathies after arthropod stings not due to Lyme disease: a report of five cases and review of the literature.

Five patients developed neurologic symptoms a few hours to 2 months after being stung by a non-hooking arthropod with immediate cutaneous reaction. The patients had no clinical or serologic evidence for Lyme borreliosis and rickettsial disease. Clinical and electrophysiologic findings were consistent with a mixed axonal and demyelinating mononeuropathy, a monomelic multiple mononeuropathy, a mononeuropathy multiplex, a radiculoneuritis, and a distal symmetric polyneuropathy. Muscle and nerve biopsies showed lymphoplasmacytic small-vessel vasculitis in all patients, and wallerian degeneration in three. These patients, and 17 others from the literature, indicate a spectrum of peripheral neuropathies occurring after insect and spider stings.

Adolescent↗