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R Gherardi

Publications and source records attributed to R Gherardi.

At least 73 records · Page 4Linked to original sources
PubMed1992

Skeletal muscle toxoplasmosis in patients with acquired immunodeficiency syndrome: a clinical and pathological study.

The present article describes the clinical and pathological findings in 5 human immunodeficiency virus (HIV)-infected patients with muscle toxoplasmosis. The patients had marked lymphopenia (5/5), with less than five CD4+ cells/mm3 (3/3), when they developed fever (5/5), and multiorgan failure (5/5), including diffuse encephalitis, pneumonia, pancytopenia, and myopathy. Muscle involvement included weakness and wasting (4/5), myalgias (3/5), and high serum creatine kinase levels (3/3). Serology for toxoplasmosis showed high IgG titers in 3 patients (3/4). Anti-Toxoplasma therapy resulted in complete recovery in 2 patients. Muscle toxoplasmosis was detected by biopsy (3/5) or postmortem evaluation (2/5), and was identified using immunocytochemistry and electron microscopy. Toxoplasma cysts were detected in 0.5 to 4% of muscle fibers close to or remote from necrotic fibers and inflammatory infiltrates. Muscle fibers strongly expressed the major histocompatibility complex class I antigen (2/2) as in polymyositis. We suggest that Toxoplasma gondii should be sought by muscle biopsy in patients who have acquired immunodeficiency syndrome with fever, encephalitis, multiorgan dysfunction, and elevated serum creatine kinase levels of obscure origin.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Early brain changes in HIV infection: neuropathological study of 11 HIV seropositive, non-AIDS cases.

We examined 11 brains of human immunodeficiency virus (HIV) seropositive cases who died from unnatural causes (10 intravenous drug abusers who died from heroin overdose and 1 homosexual dead from a gunshot injury); 10 brains of HIV seronegative heroin addicts who died from overdose and 1 seronegative drug abuser who died from gunshot injury served as controls. Complete postmortem examination did not show evidence of acquired immune deficiency syndrome (AIDS) or AIDS related complex. Terminal changes including nerve cell ischemia, edema and diffuse vascular congestion were observed in all cases. Perivascular pigment deposition with macrophages was a constant finding in drug addicts and was probably related to chronic intravenous injection. In contrast, cerebral vasculitis was significantly more frequent and marked in HIV seropositive cases and was often associated with lymphocytic meningitis. Granular ependymitis, myelin pallor with reactive astrocytosis and microglial proliferation were also more frequent and more severe in HIV seropositive cases. Immunocytochemistry was negative for HIV antigens. Our study further supports the view that early central nervous system changes occur in HIV infection.

Adolescent↗
PubMed1992

Cardiac monitoring during medical management of cocaine body packers.

The cardiac risk of cocaine body packing was studied by means of continuous ECG monitoring in 13 cocaine body-packers during spontaneous elimination. The packages were all well manufactured bundles (McCarron type 2) not susceptible to spontaneous breakage. At the beginning of the Holter study, packages were still present in the bowel of twelve patients (range: 2 to 196). The mean time of Holter recording was 46 h (range 16 h to 75 h). Ten patients eliminated all their packages during the time of Holter recording. No ECG modifications were recorded for all of the patients in regard to usually admitted standard requirements of the American Heart Association. While initial cardiac frequencies were within the normal range, a significant decrease of pulse rates was associated with the elimination of bundles. We conclude that the McCarron type 2 cocaine body-packers are not in impending danger of cardiac acute events allowing a non-surgical management of these individuals.

Adult↗
PubMed1991

[Medical secrecy].

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Confidentiality↗
PubMed1991

Zidovudine myopathy: a distinctive disorder associated with mitochondrial dysfunction.

Muscle biopsy specimens were obtained from 48 human immunodeficiency virus-infected patients suffering from various neuromuscular symptoms. Microscopic examination by conventional and electron microscopy revealed a characteristic structural myopathy associated with mitochondrial changes in 13 patients, all of whom had received long-term zidovudine therapy. The mean cumulative dose they had received (498 +/- 145 gm) was significantly higher than that of the other 14 zidovudine recipients of the study. They suffered from a progressive, usually painful, proximal myopathy with pronounced wasting, normal-to-moderately elevated creatine kinase levels, and a myopathic electromyographic pattern. The condition usually improved after withdrawal of the drug. Assay of mitochondrial enzymes, including succinate-cytochrome c reductase, cytochrome c oxidase, and citrate synthase, showed a decline in respiratory chain capacity. Southern blot analysis of mitochondrial DNA showed no abnormality. It is likely that mitochondrial dysfunction, probably resulting from drug-induced inhibition of the mitochondrial DNA polymerase, is implicated in the pathogenesis of this complication of zidovudine therapy.

Adult↗
PubMed1991

Muscle mitochondrial DNA in encephalomyopathy and ragged red fibres: a Southern blot analysis and literature review.

Various mitochondrial DNA abnormalities have been described in patients with encephalomyopathies. We performed Southern blot analysis of skeletal muscle mitochondrial DNA in nine adult patients with clinical features and ragged red fibres suggesting mitochondrial dysfunction. Two patients with encephalomyopathy and two with the MERRF syndrome (myoclonus epilepsy with ragged red fibres) had the normal PvuII restriction pattern of muscle mitochondrial DNA. In contrast, mitochondrial DNA deletion was observed in two of six patients with ophthalmoplegia. One suffered from typical Kearns-Sayre syndrome and the other from isolated external ophthalmoplegia. None of these patients had affected relatives. The detection of mitochondrial DNA deletion in external ophthalmoplegia and their site and size support previously reported data.

Blotting, Southern↗
PubMed1991

Ischaemic myelopathy secondary to disseminated intravascular coagulation in AIDS.

A 39-year-old patient with AIDS presented with a rapidly progressive myelopathy with a partial Brown-Séquard syndrome. He died, 9 weeks after onset of the first neurological signs, from diffuse encephalopathy. Neuropathological examination revealed multiple, usually small, frequently haemorrhagic, infarcts or various ages and numerous fibrin thrombi in medium and small penetrating vessels and capillaries of the brain and spinal cord, characteristic of disseminated intravascular coagulation. There were no inflammatory changes. Immunohistochemical studies for human immunodeficiency virus, cytomegalovirus, varicella zoster virus, herpes simplex virus type 1 and type 2 were negative. Ischaemic spinal cord lesions due to disseminated intravascular coagulation may represent an unusual cause of focal, non-inflammatory, non-tumoral, myelopathic syndrome in AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Increased growth of myoblasts from hypertrophic muscles in syringomyelia.

Proliferation and differentiation of myoblasts from hypertrophic muscles were studied "in vitro" in two cases of syringomyelia with muscle hypertrophy (MH). Their myoblast growth was compared with that of muscle cells sampled on the contralateral side in the same patients and in control subjects. The effect of a circulating factor was tested using patient sera in place of fetal calf and horse sera. The results showed that MH cells were morphologically abnormal (giant and granular). MH myoblasts proliferated more rapidly than contralateral and normal myoblasts, their fusion was accelerated and the resulting myotubes synthesized higher levels of protein. MH sera increased these effects. Serum factors are therefore likely to be involved in "in vivo" muscle hypertrophy. These findings suggest that the pathogenesis of muscle hypertrophy in syringomyelia involves acquired abnormalities due to molecules released in response to neural lesions.

Adult↗
PubMed1991

Partial cytochrome c oxidase deficiency and cytoplasmic bodies in patients with zidovudine myopathy.

A histochemical study of cytochrome c oxidase (CCO) was performed in the muscles from eight patients with full-blown zidovudine myopathy. All patients had ragged-red fibres (total cumulative count: 160) and myofilamentous changes, that predominated in type 1 fibres and included diffuse or punch-out myofibrillar loss (75 affected fibres) and constant cytoplasmic body formation (106 affected fibres). Inflammatory infiltrates were present in four out of eight patients. A partial CCO deficiency (22-47% of fibres; both types 1 and 2 affected) was detected in all cases, and contrasted with the normal or increased succinate dehydrogenase activity observed in most fibres. Among CCO-deficient fibres, 71% were normal on trichrome, but all ragged-red fibres were CCO-negative. Myofilamentous changes were restricted to CCO-deficient fibres. The present study strongly supports the idea that mitochondrial toxicity is the specific mechanism of zidovudine myopathy.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Multifocal multinucleated giant cell myelitis in an AIDS patient.

A 19-year-old male intravenous drug abuser, was admitted to hospital with a one-week history of lower limb weakness and urinary retention. He was known to have been HIV-seropositive for 3 years and had been treated for cerebral toxoplasmosis. Neurological examination confirmed flaccid paraparesis with weak ankle jerks and bilateral extensor plantar responses. There was no obvious sensory deficit. Neurological examination was otherwise normal. CSF contained 63 mg/dl protein and 10 leucocytes/mm3. Myelography was normal. He died 1 month later from septic peritonitis. Neuropathological examination showed chronic lesions of toxoplasmosis in brain. Small necrotic foci with myelin loss, proliferation of microglia, macrophages and multinucleated giant cells (MGC) were disseminated in the whole spinal cord, mostly in the white matter, but the brain was spared. Immunohistochemistry demonstrated p24 and p17 HIV antigens in macrophages, MGC and microglial cells. These lesions resemble those of so called 'multifocal giant cell encephalitis'. The present case demonstrates that HIV-related multifocal inflammatory changes may be restricted to the spinal cord and may be a cause of myelopathy in AIDS patients.

Acquired Immunodeficiency Syndrome↗
PubMed1991

[Neuropathologic study of 135 adult cases of acquired immunodeficiency syndrome (AIDS)].

The central nervous system was examined in 135 adult AIDS patients who died between August 1982 and December 1990. Twenty two brains showed non-diagnostic changes including microglial nodules, discrete myelin pallor with reactive astrocytosis, mineralization of blood vessels and granular ependymitis. In 105 brains with specific changes, toxoplasmosis was the most frequent finding (55 cases) manifested by multifocal necrotic lesions or diffuse pseudo-encephalitic process. Other opportunists included cytomegalovirus (21 case), progressive multifocal leukoencephalopathy (1 cases), cryptococcosis (6 cases), mycobacterium avium intracellulaire (2 cases), varicella-zoster virus (2 cases), aspergillosis (1 case) and multiple bacterial microabscesses (1 case). Multinucleated giant cells were found in 52 cases. In 40 cases, they were widely disseminated throughout the brain and in 39 cases, they were associated with diffuse or multifocal white matter changes. Fifteen cases had a cerebral lymphoma, 9 hepatic encephalopathy, 1 centropontine myelinolysis and 1 focal pontine leukoencephalopathy. Three cases had a cerebral haemorrhage due to disseminated intravascular coagulation, antithrombin therapy and amyloid angiopathy. Spinal changes in 13 cases included vacuolar myelopathy (7 cases), HIV myelitis (1 case) and ganglio-radiculitis (1 cases), cytomegalovirus myelo-radiculitis (1 case) secondary spread from a lymphoma (1 case) and spinal infarcts due to disseminated intravascular coagulation (1 case). These lesions were frequently atypical and various combinations of all these pathologies were encountered in the same brain, sometimes in the same area and occasionally in the same cell. Chronological variations in the incidence of some complications could be related to changes in treatment.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Spinal cord lesions in the acquired immune deficiency syndrome (AIDS).

Spinal cord involvement in AIDS is not uncommon. Different types of lesions corresponding to varying pathogenetic mechanisms have been reported. Vacuolar myelopathy is the most frequently found. The symptoms and pathological changes resemble those of subacute combined degeneration; however, cobalamine or folate levels have always been found normal. Its frequent association with the multi-nucleated giant cells characteristic of HIV encephalitis makes it likely that the virus plays a role in its pathogenesis. Cytomegalovirus may be responsible for acute myeloradiculitis involving the spinal roots of the cauda equina and inferior part of the spinal cord. In cases of Herpes simplex virus myelitis has been reported; they are usually associated with cytomegalovirus infection and are due to herpes simplex virus type II. Secondary spread from systemic lymphomas may involve the subarachnoid space of the cord and the spinal roots. Compression of the spinal cord by epidural lymphomatous masses has also been described. Spinal infarcts may be secondary to acute or chronic vasculitis or to less specific vascular processes such as disseminated intravascular coagulation.

Acquired Immunodeficiency Syndrome↗