Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Schizophrenia and certain forms of idiopathic mental retardation may result from covert immune complex disease of the basal lamina of the choroid plexus, a process already known to cause covert transport dysfunction in similar structures of, for example, skin, bowel, kidney, and endocrines. Plexial attack could lead to cerebrospinal fluid contamination and then, via an "open" ependyma, to neurotransmitter dysfunction in the periventricular limbic brain. The immune complex mechanism implies polygenic induction, direct or autoimmune, of immune sensitivity to exogenous agents and is thus compatible with the genetic picture in schizophrenia. Candidate agents include viral coat peptides and cereal grain glutens. The glutens are known to cause immune complex skin and bowell disease variants, and some empirical evidence links them to schizophrenia. Only newer immunofluorescence methods can detect the pathology, which is otherwise silent. Systemic lupus erythematosus provides a model since it is a genetic immune complex disease strongly associated with schizophreniform psychoses, exhibits choroid plexial immunofluorescence but no central nervous system pathology by ordinary methods, and may be triggered by viruses.
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PMID:Covert transport dysfunction in the choroid plexus as a possible cause of schizophrenia. 4 42

Catatonia has generally been assumed by many physicians to be a subtype of schizophrenia. Numerous cases have been reported in the literature associating catatonia with other psychiatric and also medical illnesses. The present report describes a patient with Systemic Lupus Erythematosus (SLE) who presented in a catatonic state. A brief differential diagnosis of catatonia is also included.
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PMID:Catatonia and systemic lupus erythematosus. 90 61

A short text spoken by a patient with a supposed symptomatic schizophrenia in lupus erythematodes is analyzed by means of a structural interpretation. While the text appears schizophrenic, it is only the confusion and intermingling of five quite distinct textual levels which create this impression. These five levels are presented in three distinctive modes of narrative. (1) Deviation and periphrase: while psychopathologically these breaks in the narrative are deviations from the main thread of argument, stylistically they are periphrasic statements, all having identical structures. They are all related emotionally as well as thematically to the central subject of the text. Their informational quality is impaired by their density and their interlocked form. (2) Narrative: the text contains three meaningful and well-arranged stories. In one case a multilevel narrative structure is employed. Each story represents a response to the initial question. (3) Metalanguage: on a metatextual level, the patient repeatedly makes reference to her linguistic peculiarities. These statements coincide with objective evaluation. Delusions and misidentification of individuals and situations used in classical psychopathological diagnosis can be given a different meaning (in the sense used by Weinrich) if interpretation has deepened the knowledge of the text. In this case, the similarity to schizophrenic texts is only superficial. A more detailed analysis illustrates the difference from schizophrenia on every level.
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PMID:[Structural interpretation of a supposed symptomatic schizophrenia]. 103 17

Serum IgG and IgM antibodies to gangliosides GM1, GM2, GM3, AGM1, GD1a, GD1b and GT1b were determined in 210 patients with different degenerative and inflammatory disorders including motor neuron diseases, peripheral radiculopathies and neuropathies, multiple sclerosis and neuroborreliosis. No single disorder was associated specifically with ganglioside antibodies. No characteristic patterns of ganglioside antibodies were observed in any disease category. However, 32% of all patients had pathological antibody titres to at least one ganglioside. Four patients had pathological IgG and IgM titres for all gangliosides evaluated. They suffered from systemic lupus erythematosus [2], neuroborreliosis and schizophrenia, respectively. The results of this study indicate that the introduction of ganglioside antibody determination as a differential diagnostic test in clinical neurology is only helpful in a few patients with typical lower motor neuron syndromes.
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PMID:Ganglioside antibodies: a lack of diagnostic specificity and clinical utility? 144 74

This paper presents epidemiological data on the prevalence of 26 common (i.e., having a lifetime prevalence of more than 1 per 10(4) individuals in the population) multifactorial diseases in Hungary and estimates of detriment associated with them. The detriment is expressed using 3 indicators, namely years of lost life (LL), potentially impaired life (PIL) and actually impaired life (AIL). The total prevalence of these diseases in Hungary has been estimated to be about 6500 per 10(4) individuals in the population. This estimate is in agreement with published data for other parts of the world. On the basis of clinical severity, these diseases have been split into 3 groups, namely (1) very severe (schizophrenia, multiple sclerosis, epilepsy, acute myocardial infarction and related conditions, and systemic lupus erythematosus); (2) moderately severe and/or episodal or seasonal (15 entities including Graves' disease, diabetes mellitus, gout, affective psychoses, essential hypertension, peptic ulcers, asthma, etc.); and (3) less severe than those in the first 2 groups (varicose veins, allergic rhinitis, atopic dermatitis, Scheuermann disease and adolescent idiopathic scoliosis). The essential clinical and genetic aspects of these diseases are briefly discussed. With the exception of epilepsy, none of the diseases included in our list causes mortality between ages 0 and 19. However, they are among the leading causes of death between ages 20 and 69 and thereafter. A sizeable proportion of those with essential hypertension, diabetes mellitus, rheumatoid arthritis, etc. survive to 70 years and beyond, as do those with gout, glaucoma, allergic rhinitis, psoriasis, etc. Overall, about 16% of all deaths that occur in Hungary every year (all age groups) can be attributed to these diseases. The mean number of years of PIL covers a wide range (about 20-40, 12-70 and 40-60 for groups 1, 2 and 3, respectively), the overall mean being about 24 years. However, the nature and degree of impairment and the impact on the life quality of those afflicted differ for the different diseases. Likewise, the mean number of years of AIL (for which the interval between the mean age at premature retirement and mean age at death was used as a rough index) also spans a wide range from 16 to 45, and the overall mean is about 20 years. At the population level, the diseases considered in this paper cause about 2700 years of LL, 96,000 years of PIL and about 5800 years of AIL per 10(4) individuals in the population. Relative to Mendelian diseases as a whole, these multifactorial diseases are associated with much greater detriment (LL: 1.4 X; PIL: 30 X and AIL: 3.9 X).
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PMID:The load of genetic and partially genetic diseases in man. II. Some selected common multifactorial diseases: estimates of population prevalence and of detriment in terms of years of lost and impaired life. 305 77

The nature of the side effects produced by the antimalarials and a common moiety present in these drugs (spermidine) links the polyamines to both schizophrenia and depression. The raised incidence of psychosis in systemic lupus erythematosus and during pregnancy both associated with raised blood polyamine levels, makes the involvement of the polyamines in psychosis more likely.
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PMID:The side effects of antimalarial drugs indicates a polyamine involvement in both schizophrenia and depression. 406 32

Based on the apparent existence of a second (choroid plexial) blood-brain barrier offering a new brain attack mechanism on the periventricular primary personality brain (Rudin, 1980) and which may be breached to produce the schizophreniform psychosis characteristic of systemic lupus erythematosus (Rudin, 1981), we here assess the evidence that viruses and exogenous peptides, including especially the glutens of cereal grains, may be the primary triggers for schizophrenia. Schizophrenia would then be supposed to result as one expression of gene-determined combined transport organ dysfunction with underlying basal laminar immunopathy at the tissue level and possibly a prostaglandin disorder at the chemical and membrane level in turn, finally disrupting neurotransmission in the periventricular limbic system. We conclude that the evidence warrants test of the hypothesis, including a clinical trial under national auspices employing an elemental diet, plasmapheresis, immunosuppression together with an antiviral regimen.
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PMID:The choroid plexus and system disease in mental illness. III. The exogenous peptide hypothesis of mental illness. 611 83

Schizophrenia and certain idiopathic neuroses and retardations may be caused by polygenic sensitization to exogeneous peptide antigens or viruses causing a covert immune complex basal lamina disease of the choroid plexus. This organ has the general structure and disease susceptibility of many other transport organs but acts as a second blood--brain barrier putting at risk to contamination and dysfunction the periventricular primary personality (limbic) brain now thought to be centrally involved in schizophrenia. Genetic variability selects different antigens and different target organs so that a complex statistical structure of disease expression can result over the transport organ group as well as between this group and the endocrines and exocrines. This leads to the concept of intra- and intercombined system diseases all of which may have a covert biphasic (hyper-hypo) time course. To this extrinsic combinatorial complexity may be added an intrinsic or neural combinatorial complexity resulting from the fact that the choroid plexus is threaded throughout the limbic system and subject to spotty disease characteristic of many immunopathies. In this way a wide range of behavioral disorders may arise as well as mental retardations if the process occurs during development. In this paper we discuss basic mechanisms. In the next paper of the series we examine systemic lupus erythematosus, the prototypical "combined transport dysfunction," as a model for schizophrenia. In the last paper we search for specific exogeneous peptide triggers for schizophrenia viewed as one expression of combined transport organ dysfunction. We conclude that immunofluorescent and virological surveys should be conducted in all mental illnesses as well as clinical trials of interferon therapy and elemental diets.
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PMID:The choroid plexus and system disease in mental illness. I. A new brain attack mechanism via the second blood--brain barrier. 644 42

Carr et al. (1978) and Rudin (1979) independently suggested tat systemic lupus erythematosus (SLE) might provide a model for schizophrenia since SLE is strongly associated with schizophreniform psychoses and exhibits only a covert CNS pathology revealed by immunofluorescent immune complex deposits in the choroid plexus. To carry the concept forward we here examine SLE employing the ideas developed in the preceding paper (Rudin, 1980) indicating that the choroid plexus is part of a second blood-brain barrier guarding the periventricular primary personality brain, the limbic system, and that the choroid plexus is also but one of a set of "transport organs" sharing common vulnerability to covert basal lamina immune complex pathology. In this context both SLE and schizophrenia are viewed as expressions of combined transport dysfunction syndromes, resulting from polygenic-induced sensitivity to exogenous peptides or viruses causing basal laminar immune complex disease, but exhibiting differing statistical expressions over the transport organ group due to difference in genes which elicit different transport organ sensitivities to different exogenous viruses or peptide antigens. Immune disease processes are briefly reviewed.
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PMID:The choroid plexus and system disease in mental illness. II. Systemic lupus erythematosus: a combined transport dysfunction model for schizophrenia. 645 11

Fourteen male patients examined for a prolonged partial thromboplastin time were found to have the lupus anticoagulant. In contrast to previous reports, there was no increased incidence of false-positive results of serological tests for syphilis. In only two patients was systemic lupus erythematosus confirmed, although two additional patients had a positive result of a test for antinuclear antibody. Other clinical diagnoses included peripheral vascular disease, cardiac disease, pulmonary disease, and schizophrenia. Prothrombin times were distinctly abnormal in only two patients. Bleeding was rarely encountered in these patients, including ten who underwent surgical procedures or some type of hemostatic challenge. Thrombocytopenia was not associated with bleeding but was present in two patients who had thrombotic events.
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PMID:The lupus anticoagulant in 14 male patients. 681 13


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