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Biomedical subjects

S Leibowitz

Publications and source records attributed to S Leibowitz.

At least 19 recordsLinked to original sources
PubMed1995

Appropriate response to pneumococcal vaccine in celiac sprue.

Hyposplenism as a complication of celiac sprue confers an increased risk of pneumococcal sepsis, but such patients do not routinely receive pneumococcal vaccine despite reports of overwhelming pneumococcal sepsis. Because antibody response in these patients has not been previously assessed, we measured pre- and postvaccination levels in 10 patients with documented sprue. All demonstrated appropriate acute antibody responses to a polyvalent pneumococcal vaccine. Vaccination of all patients with celiac sprue seems appropriate.

Adult↗
PubMed1992

Sural nerve biopsies in Guillain-Barre syndrome: axonal degeneration and macrophage-associated demyelination and absence of cytomegalovirus genome.

T-cell infiltration was detected by immunohistochemistry in only 2 of 10 sural nerve biopsies from patients with Guillain-Barré syndrome (GBS). The number of endoneurial macrophages, identified by the monoclonal antibody MAC 387, was increased, compared with the number in 10 cases of axonal neuropathy. Macrophage-associated demyelination was identified in 7 and axonal degeneration in 8 cases. Cytomegalovirus (CMV) genome was not detected with the polymerase chain reaction.

Adult↗
PubMed1991

Sarcoid neuropathy.

In a case of subacute sensory and motor polyneuropathy associated with sarcoidosis, multiple epineurial and endoneurial granulomas were demonstrated in a sural nerve. Neighbouring nerve fibres were displaced by the granulomas and some were undergoing axonal degeneration. Ultrastructural and teased fibre studies showed axonal atrophy and degeneration with secondary demyelination. Histochemical studies indicated the presence of HLA-DR antigen on epithelioid cells in the granulomas. A non-specific inflammatory process in the nerve does not cause significant primary demyelination.

Aged↗
PubMed1991

The clinical spectrum of peripheral neuropathies associated with benign monoclonal IgM, IgG and IgA paraproteinaemia. Comparative clinical, immunological and nerve biopsy findings.

Observations have been made on a consecutive series of 62 patients with peripheral neuropathy associated with benign monoclonal paraproteinaemia. The paraprotein class was IgM in 46 cases, IgG in 11 and IgA in 5. Although showing variations between patients, the clinical picture was similar for those with either IgM or IgG paraproteins, usually consisting of a late-onset, slowly progressive, distal sensorimotor demyelinating polyneuropathy, often with tremor and ataxia as prominent features. Tremor was slightly more common in patients with IgM paraproteins, in whom there was a male preponderance. The patients with both paraprotein classes were indistinguishable clinically and electrophysiologically from chronic idiopathic demyelinating polyneuropathy. In the 5 patients with an IgA paraprotein, there was a distal sensorimotor neuropathy in 4 which was demyelinating in 1. In 1 there was proximal demyelinating motor neuropathy. Immunoglobulin deposition on myelin was observed only in the patients with IgM paraproteinaemia, more commonly with a kappa light chain. No deposition of immunoglobulin in the endoneurium was seen. IgM deposits on the perineurium are a feature of normal nerve and were present in all cases. Widely spaced myelin was confined to cases with IgM paraproteins in which immunoglobulin deposition was detected on myelin. The response to treatment could not be assessed systematically but, in general, the patients with IgG and IgA paraproteins responded more satisfactorily (to corticosteroids, cytotoxic drugs, or plasma exchange) than did those with an IgM paraprotein.

Adult↗
PubMed1991

A clinicopathological study of the Guillain-Barré syndrome. Nine cases and literature review.

The postmortem findings are reported from 9 cases of the Guillain-Barré syndrome with survival between 10 days and 1 yr. In 8 cases there was multifocal loss of myelin throughout the peripheral nervous system with relative preservation of axons. In 1 case there was predominant loss of axons. Inflammatory mononuclear cell infiltration was present in the peripheral nervous system of all cases except 1 case surviving a year. The extent and severity of cell infiltration was variable, usually being less prominent than in previous reports, and sometimes sparing nerves in which myelin destruction was severe. Vesicular dissolution of myelin noted by electron microscopy was considered to be a postmortem artefact. In cases examined within 30 days after the onset, immunohistochemical studies with monoclonal antibodies identified more leucocytes (PD7/2B11+) and T cells (UCHL1+) in the endoneurium than in cases examined later or control cases. These findings and recent single case reports indicate that the pathology of the Guillian-Barré syndrome is variable. This variability may reflect differences in pathogenesis, with greater cell-mediated immunity in some cases and greater antibody targeted macrophage-mediated demyelination in others.

Adolescent↗
PubMed1989

Peripheral neuropathy associated with Castleman's disease.

Four patients with polyneuropathy complicating the plasma cell variant of Castleman's disease (angiofollicular lymph node hyperplasia) are described. The neuropathy was predominantly motor and severely disabling. Vasculopathy, papilloedema, organomegaly, endocrinopathy, oedema and paraproteinaemia were variably present in these patients. Sural nerve biopsy showed changes of both demyelination and axonal loss. Capillary proliferation and endothelial hypertrophy in the epineurium and endoneurium, similar to that seen in affected lymph nodes, suggested that a diffuse vasculopathy may contribute to the neuropathy. Serum antibody activity against a variety of neural antigen preparations was not detected in any of the patients. Two untreated patients died. Substantial improvement in the neuropathy occurred in the two patients treated with cyclophosphamide and prednisolone.

Adult↗
PubMed1989

Creating a smoke-free environment in a medical center: an overview.

Beth Israel Medical Center committed itself to a smoke-free environment on May 7, 1987 after seven months of careful study by a policy determination committee and, thereafter, seven months of meticulous planning for its announcement and implementation. The policy rests on two premises: passive smoking is harmful to nonsmokers; a medical center "employer," above all others, has a special, impelling obligation to shield persons in its environs from such exposure. The impetus came from the medical staff. The policy acceptance and commitment had the combined approval of the medical staff, administration, and trustees. The ban applies to all who serve, are served in, or otherwise visit the Center. Care was taken to prepare all staff and patients for the stringent policy effective May 7, 1987. Its medical basis was made clear. Support was arranged for smokers who were interested. Response in the first year and a half has been increasing acceptance, which reflects careful preparation as well as in depth support from the medical staff. Problems are met with discussion and reasoning, not punitively.

Academic Medical Centers↗
PubMed1988

A prospective study of acute idiopathic neuropathy. III. Immunological studies.

The immune responses of 100 patients who presented with an acute idiopathic neuropathy were compared with those of age and sex matched controls. Blood lymphocytes and their subsets were counted with a fluorescent activated cell sorter. CD8+ (putative suppressor) lymphocytes were significantly reduced in the first week of the disease but total lymphocytes, total T and CD4+ (putative helper) cells were not altered. This reduction depended on the nature of the preceding infection. Serum complement C3 and C4 concentrations remained normal and immune complexes were rarely detected with a C1q binding assay. Complement-fixing antibodies to human peripheral nerve antigens were discovered in the serum of 7% of patients but only 1% of controls. Complement-fixing antibodies to galactocerebroside were not discovered in any sera. Enzyme-linked immunoassays detected increased antibody responses to galactocerebroside but none at all to human P2 myelin protein in the patient sera. Forty microliter of serum from five patients injected into the sciatic nerves of rats did not induce significantly more demyelination than the serum from control patients. It is concluded that auto-immune responses can only be detected by these techniques in a small minority of patients with acute idiopathic neuropathy.

Adolescent↗
PubMed1984

The binding of human IgM paraprotein from cases of polyneuropathy associated with benign monoclonal gammopathy to specific neurons of the rodent brain.

Human sera from patients with IgM paraproteinaemia were screened for IgM binding to frozen sections of the rat cerebellum by the indirect immunoperoxidase procedure. Out of 18 patients with a benign IgM gammopathy and associated demyelinating polyneuropathy (PPN), 17 showed binding to the surface of specific neurons, i.e. those of the deep cerebellar nuclei and the intermediate cell of Lugaro. Examination of other regions of the mouse brain suggests that the reactivity is restricted to cells of certain nuclei of the sensory-motor system. The use of F(ab)2 and monoclonal anti-idiotype antibodies demonstrate that the binding involves the antigen binding sites of the paraprotein. This reactivity indicates that some neurons have on their surface an antigen having an hapten in common with human myelin-associated glycoprotein (MAG) and the pi granules of human Schwann cells and furthermore is an additional serological characteristic of this group of patients. In addition 3 sera from the PPN group stained a particulate component in the cytoplasm of all medium-sized and large neurons. A similar staining was found with 7 out of 52 other unselected IgM paraproteinaemias.

Animals↗
PubMed1984

Immune responses to myelin antigens in Guillain-Barré syndrome.

Antibodies to nerve antigens were sought in the sera of 17 patients with acute Guillain-Barré syndrome (GBS), 11 with chronic relapsing demyelinating poly-radiculoneuropathy (CRP), 20 with other neuropathies (ON), 15 with other neurological diseases (OND) and 19 normal subjects. Complement-fixing antibodies to a suspension of human peripheral nerve tissue were identified in only 2 patients with GBS and 1 with chronic progressive neuropathy. Five GBS sera gave complement fixation reactions with rabbit sciatic nerve. The sera were also tested for galactocerebroside (Gal-C) binding activity using a solid phase assay. The range of values in all groups was the same, although the mean values for patients with GBS, ON and OND were higher than those of normal subjects. In a radioimmunoassay for antibodies to bovine P2 slightly more radiolabelled antigen was precipitated by the GBS group of sera than by sera from the other groups, but only one serum from the GBS and another from the CRP patients precipitated more than 10% of the label. Addition of bovine P2 to cultures of peripheral blood mononuclear cells from 11 patients with GBS did not cause significant stimulation. Immunoassay for antibody to myelin basic protein (MBP) showed an increased proportion of sera with low binding activity in the GBS and CRP groups. The results suggest that humoral immune responses to potentially neuritogenic antigens are found with marginally increased frequency in patients with GBS and CRP.

Adolescent↗
PubMed1983

IgM paraproteins with immunological specificity for a Schwann cell component and peripheral nerve myelin in patients with polyneuropathy.

The sera of 9 patients with benign IgM paraproteinaemia and chronic sensorimotor neuropathy were tested for reactivity to human peripheral nerves by the indirect immunoperoxidase method. They reacted in very high titre (10(-3)-10(-6) with a cytoplasmic Schwann cell component, and to lesser degree, with peripheral nerve myelin (10(0)-10(-3). The Schwann cell staining was in the form of perinuclear cytoplasmic granules and was only seen with adult nerve. The distribution of the antigen was similar to that of the metachromatically staining Pi-granules of Reich, which accumulate in the peripheral nerves with age. Specific activity was present in the IgM and F(ab)2 fractions and could be absorbed out with peripheral nerve tissue, but not with liver. Reactivity is not a simple function of the IgM level, since many IgM paraproteins do not react. The antibody is species specific and binds to human, but not to any component of rabbit, rat or guinea pig sciatic nerves. Antigenicity is removed by pretreatment of the nerve with chloroform-methanol or periodate, but not protease or trypsin. Reactivity is restored, after periodate treatment, by exposure to sodium borohydride. It is suggested that some IgM paraproteins have a specificity for a myelin glycolipid or glycoprotein, which normally accumulates in the Pi-granules of the Schwann cell cytoplasm as a function of age.

Humans↗
PubMed1981

Immunogenicity of human amniotic epithelial cells after transplantation into volunteers.

Human amniotic epithelial cells do not express on their surfaces HLA-A, B, C, and DR antigens, or beta 2-microglobulin. In vitro these cells synthesise the enzymes lacking in patients with selected enzymatic deficiencies: the survival of a transplanted monolayer of human amniotic epithelial cells was therefore investigated in seven volunteers. None of the volunteers showed clinical signs of acute rejection, and amniotic epithelial cells were demonstrated by biopsy up to 7 weeks after implantation. HLA antibodies were not detected in samples of serum from four volunteers thoroughly investigated, and there was no in-vitro lymphocyte reaction to the amniotic cells in two of them. The results suggest that acute immune rejection does not occur after the transplantation of human amniotic epithelial cells.

Adult↗
PubMed1981

The behaviour of immature and mature rats exposed prenatally to anti-ganglioside antibodies.

Three behavioural experiments were carried out in rats born to mothers injected with anti-ganglioside antibodies between days 16 and 19 of their pregnancies. Immature animals were slower to habituate to an open-field arena and took longer to learn sequence maze when no cues were provided than did offspring of mothers who had received normal serum. The latter difference disappeared when the way through the maze was cued. In a third experiment mature rats, exposed prenatally to the antibody, showed superior adaptation on a visual discrimination task compared to their controls. It was concluded that antiganglioside modifies sensory rather than motor mechanisms in the rat.

Age Factors↗
PubMed1981

Immune responses in experimental allergic neuritis.

The antibody and cell mediated immune responses were investigated in inbred Lewis rats with experimental allergic neuritis (EAN) induced by either P2, a protein purified from the bovine cauda equina nerve roots, or whole bovine nerve root myelin. In the P2 immunised animals both antibodies to P2 detected by radioimmunoassay and cell-mediated immunity to P2 assayed by skin testing appeared before the onset of EAN and persisted during and after the disease. In the myelin immunised animals the antibody titres were lower and somewhat delayed and the skin tests became negative at the height of the disease. Complement-fixing antibodies to galactocerebroside, which have been implicated in the production of demyelination under some circumstances, could not be detected in the serum after immunisation with either P2 or myelin. EAN was transferred passively with lymph node cells from rats immunised with either P2 or myelin although anti-P2 antibodies could not be detected in the serum of recipients with EAN. The results favour a cell-mediated immune response to P2 as the most important pathogenetic mechanism in EAN induced wtih whole myelin in the rat.

Animals↗
PubMed1980

EAE, EAN and galactocerebroside sera bind to oligodendrocytes and Schwann cells.

Sera from rabbits with EAN induced by sensitization with galactocerebroside (GalC-EAN) bound to the surface of Schwann cells and oligodendrocytes in rat nervous system dispersion cultures. Sera from rabbits with bovine femoral nerve-induced EAN (FN-EAN) bound to Schwann cells, oligodendroglia and occasional fibroblasts. Sera from animals with bovine spinal cord-induced EAE (SC-EAE) bound to these cells and to some astrocytes as well. Absorption of the capacity to bind to oligodendroglia and Schwann cells suggests that GalC is the major, if not the only surface antigen on these two cell types to which these sera bind. The capacity of GalC-EAN, SC-EAE, and FN-EAN sera to bind to the surface of the cells responsible for myelin synthesis in both PNS and CNS correlates with the ability of these sera to cause both PNS and CNS demyelination in vitro and PNS demyelination in vivo.

Animals↗
PubMed1980

Behavioural changes in adult rats following administration of antibodies again brain gangliosides.

Mature rats, previously trained in a standard two-lever chamber, were injected with antibodies against ganglioside and the effect was evaluated in a series of different behavioural tests. Compared with the controls, the injected rats showed transient differences in their response to stimuli. The apparent counter-intuitive superiority of the treated animals over the controls is discussed with reference to other experimental studies performed in young rats, and to discrete pathological human conditions associated with the presence of brain antibodies.

Animals↗