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K N Chengappa

Publications and source records attributed to K N Chengappa.

54 records · Page 3Linked to original sources
PubMed1994

Differences in serum interleukin-6 (IL-6) between healthy dextral and non-dextral subjects.

Serum interleukin-6 (IL-6) was measured in picograms/ml pg/ml using an immunoassay (ELISA) in healthy individuals (n = 148), of whom 128 were classified as dextral and 20 as non-dextral, as per a laterality questionnaire. Only 3 (15%) non-dextral individuals had serum IL-6 levels above the lower limit of the assay sensitivity as compared to 59 (46%) of dextral individuals (P < 0.013). There were no significant correlations between previously determined mitogen stimulated interleukin-2 production and autoantibodies in a subset of the same individuals. While this data does not provide casual information, it adds to the evidence of the asymmetric regulation of immune functions by the cerebral hemispheres.

Adult↗
PubMed1994

An association between anti-hippocampal antibody concentration and lymphocyte production of IL-2 in patients with schizophrenia.

Serum concentrations of anti-hippocampal antibodies and in vitro production of the lymphokine interleukin-2 (IL-2) in response to phytohaemagglutinin (PHA) stimulation were determined using an enzyme immunoassay in 49 schizophrenic patients and 41 healthy controls. Decrease in IL-2 production, a finding frequently associated with many autoimmune diseases, was associated with an elevation in anti-hippocampal antibody optical density (AHA-OD) in schizophrenic patients. Although some control subjects had elevated antibody levels, this elevation was not associated with decreased IL-2 production. Low IL-2 production is well known to be a state marker associated with active autoimmune disease. We suggest that production of hippocampal antibody is a trait marker of vulnerability to autoimmune diseases. Thus, our finding of low IL-2 production in patients with high concentrations of hippocampal antibody is compatible with the possibility that such patients have an ongoing autoimmune process.

Adult↗
PubMed1994

The prevalence of akathisia in patients receiving stable doses of clozapine.

BACKGROUND: Akathisia is a common side effect of traditional neuroleptic drugs and is associated with medication refusal and impulsive behavior. While our previous experience indicates that clozapine is effective in treating persistent akathisia, two controlled studies indicate vastly different prevalence rates of akathisia (7% vs. 40%) in patients receiving clozapine. METHOD: We used the Barnes Rating Scale for Drug-Induced Akathisia to estimate the prevalence of akathisia in patients receiving stable doses of clozapine alone (N = 29) in a state hospital. Measurements were also made of manifest psychopathology (Brief Psychiatric Rating Scale) and tardive dyskinesia (Abnormal Involuntary Movement Scale). RESULTS: Two patients (6.8%) receiving clozapine were rated as having akathisia. Only 4 (28.6%) of the 14 subjects with a history of moderate-to-severe tardive dyskinesia on traditional neuroleptic drugs continued to show current evidence of tardive dyskinesia, and in 10 patients (71.4%) there was no evidence of the syndrome (p < .002). In the 4 subjects with tardive dyskinesia there was amelioration to a milder form of the syndrome. There were no new cases of tardive dyskinesia among clozapine-treated subjects. CONCLUSION: These data support the low prevalence of akathisia in patients receiving stable doses of clozapine monotherapy. There is further support that clozapine has an ameliorating effect on tardive dyskinesia associated with traditional neuroleptic drugs. These and other data indicate the need for a controlled trial of clozapine in patients experiencing persistent and disabling akathisia on traditional neuroleptic drugs.

Adult↗
PubMed1993

Autoimmunity in schizophrenia: a review of recent findings.

The pathophysiology of psychotic and other symptoms in schizophrenia remains a mystery despite decades of research. Even though it has been suspected for many years that autoimmune mechanisms may play a role in the pathophysiology of schizophrenia, firm evidence for this hypothesis has been lacking. Our studies, over the last 10 years, have revealed that a subgroup of schizophrenics have several significant immunological abnormalities, including increased prevalence of autoimmune diseases and of antinuclear antibodies (ANA) and anticytoplasmic antibodies (ACA), decreased lymphocyte interleukin-2 (IL-2) production, increased serum IL-2 receptor concentration, increased serum IL-6 concentration, and an association with HLA antigens. These findings are characteristic of autoimmune diseases such as systemic lupus erythematosus (SLE), rheumatoid arthritis and insulin-dependent diabetes mellitus. We also found that some schizophrenics have antibodies to hippocampal antigens (AHA) in their serum, together with lowered IL-2 production. None of the above findings can be interpreted as definitely confirming the role of autoimmunity in schizophrenia. Nevertheless, taken together, the recent evidence points towards the existence of a subgroup of schizophrenics who have immunological findings consistent with that hypothesis. Further studies directed at finding the brain antigens targeted by the immune system in these patients, and longitudinal studies correlating clinical and immune changes over time, are needed.

Autoimmune Diseases↗
PubMed1992

The prevalence of autoantibodies among right and left handed schizophrenic patients and control subjects.

Sera from schizophrenic patients (n = 186) and healthy control subjects (n = 346) were tested for the presence of seven common autoantibodies by standard immunological methods. The association between handedness and autoantibodies was tested in a multi-way contingency table using a log-linear model. For men, but not women, nondextrals (patients and controls) were twice as likely to test positive for autoantibodies than dextrals (p = 0.0002). Although more women (33%) than men (24%) tested positive for autoantibodies, handedness was not a distinguishing factor among women. These data suggest that sinistrality and gender are associated with autoantibodies in a subgroup of schizophrenic patients and healthy control subjects.

Adult↗
PubMed1992

Non-right sidedness: an association with lower IL-2 production.

Using a laterality questionnaire, 138 normal healthy individuals were classified as right-sided and 25 as non-right sided. Interleukin-2 (IL-2) was generated from whole blood obtained from these subjects using mitogen (PHA) stimulation. IL-2 was quantitated in picograms/ml using an enzyme immunoassay (ELISA). Additionally, sera from these subjects were tested for 7 autoantibodies by standard serological methods. As compared to right sided subjects, non-right sided individuals had significantly lower IL-2 production. Non-right sided individuals with autoantibodies had significantly lower IL-2 production than right sided subjects with or without autoantibodies, but did not differ significantly from their non-right sided counterparts without autoantibodies. These data support the increasing evidence for the differential and lateralized regulation of immune functions by the right and left cerebral regions.

Adult↗
PubMed1992

Altered interleukin-2 production in schizophrenia: association between clinical state and autoantibody production.

Mitogen-stimulated interleukin-2 (IL-2) production was measured in 122 patients who met Research Diagnostic Criteria for schizophrenia and 98 normal control subjects. The presence of autoantibodies against seven common antigens was also determined. There was no relationship between the presence of circulating autoantibodies and IL-2 production in control subjects. In patients, however, autoantibody-positive, acutely ill patients had significantly lower IL-2 production as compared with other patients and control subjects. Never-medicated patients showed the same trends for decreased IL-2 production in association with autoantibodies. These data suggest that decreased IL-2 production is associated with acute illness in schizophrenic patients who produce autoantibodies, a trait known to be associated with increased vulnerability to autoimmune disease.

Adult↗
PubMed1992

Left-handed first-episode, neuroleptic-naive schizophrenic patients have a higher prevalence of autoantibodies.

Using standard immunological techniques, sera from first-episode, neuroleptic-naive schizophrenic patients (n = 51) and age, race and sex matched healthy controls (n = 51) were screened for seven common autoantibodies. Significantly more left-handed (67%) than right-handed (23%) schizophrenic patients had autoantibodies (p = 0.011). Left-handed schizophrenic patients were six times more likely than right-handed patients or controls and four times more likely than left-handed controls to test positive for autoantibodies (p = 0.012). These data suggest that disease and sinistrality contribute to the excess of autoantibodies in schizophrenia.

Adult↗
PubMed1992

Elevated IgG anti-histone antibodies in a subgroup of medicated schizophrenic patients.

A total of 57 schizophrenic patients (of which 17 were first-episode, neuroleptic naive) and 76 healthy controls were screened for anti-histone IgG antibodies using an enzyme immunoassay (ELISA). All patients had significantly higher anti-histone antibody titers than controls (t = 3.1, p less than 0.003). Previously medicated patients had significantly higher titers than neuroleptic-naive first episode patients (t = 2.87, p less than 0.006). This study suggests that neuroleptic medications are associated with anti-histone antibodies.

Adult↗
PubMed1992

Should chronic treatment-refractory akathisia be an indication for the use of clozapine in schizophrenic patients?

BACKGROUND: Clozapine, an atypical neuroleptic, is an effective medication in a subgroup of schizophrenic patients who have either failed to respond to the typical neuroleptics or experienced intolerable side effects such as neuroleptic malignant syndrome and disabling tardive dyskinesia. Its efficacy for persistent and disabling akathisia is less clear. Akathisia, especially the chronic and disabling form, can be a treatment dilemma for the clinician and the patient. METHOD: We describe three representative case illustrations of schizophrenic patients who had severe, persistent treatment-resistant akathisia. Two of them had refractory psychoses and the third had multiple disabling side effects during treatment with typical neuroleptics. Two had tardive dyskinesia. These patients were treated with clozapine while other neuroleptics were discontinued. RESULTS: During a 2-year follow-up, these patients made impressive social and vocational strides coinciding with a fairly rapid remission of akathisia (under 3 months) and a lesser though notable improvement in the psychoses. Tardive dyskinesia also remitted, though over a period of 6 to 12 months. CONCLUSION: Our experience leads us to suggest a trial of clozapine in a subgroup of schizophrenic patients, who in addition to refractory psychoses have persistent disabling akathisia. However, given the risk of agranulocytosis with clozapine, we suggest that the usual treatment strategies for akathisia be tried before clozapine is initiated in the approved manner. Future controlled trials of clozapine that specifically investigate persistent akathisia may answer this question more conclusively.

Adult↗
PubMed1992

Emergence of obsessive compulsive symptoms during treatment with clozapine.

BACKGROUND: Clozapine differs from other currently available antipsychotics in its prominent serotonin blockade. We explore the relationship between clozapine and obsessive compulsive symptoms, which have been linked to deficient serotonin. METHOD: We reviewed our experience in treating 49 chronic schizophrenic patients with clozapine. RESULTS: Five patients were identified who experienced either de novo obsessive compulsive symptoms or exacerbation of preexistent symptoms. Clinical details are provided for each case. CONCLUSION: Clozapine may produce or unmask obsessive compulsive symptoms. This may reflect a variation on the normal course of clinical improvement, or may more specifically result from clozapine's atypical pattern of CNS receptor antagonism. Further attention to this issue is warranted.

Adult↗