Biomedical subjects
Publications and source records attributed to P Bigel.
Immotile cilia syndrome was diagnosed in a 10 year-old boy presenting with Kartagener syndrome: chronic otitis, sinusitis, recurrent respiratory disease and situs inversus. Electronmicroscopic examination of biopsies of the nasal mucosa showed the lack of interne dynein arms, explaining the immotile cilia syndrome in that boy.
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Peripheral blood T lymphocytes were studied in 24 untreated patients with renal adenocarcinoma, 80 per cent of whom had local extension of the tumor. T lymphocytes were evaluated with the total and the active rosette assays, and were further submitted to stimulation by a range of phytohemagglutinin concentrations in vitro. Controls were healthy volunteers tested on the same days as the patients. Total E-rosette forming cells were slightly decreased but the difference compared to controls was not significant. Active rosettes were normal. When present lymphocytopenia affected total E-rosette forming cells. The mean of the log-converted stimulation indexes was reduced significantly in the patient group only when a suboptimal concentration of phytohemagglutinin was used. Total E-rosette forming cells returned to normal 3 weeks postoperatively but lymphocyte reactivity did not improve and active rosette forming cells remained within normal range. Thus, only minor abnormalities of T lymphocytes were disclosed in this study, suggesting functional alterations rather than depletion. Our study confirms that a cancer operation may act as immunotherapy.
Autologous rosette-forming T lymphocytes were enumerated in periphal blood of patients with established alcoholic cirrhosis and compared with T lymphocytes forming rosettes with sheep red blood cells (total and 'active' rosette-forming cells; RFC). Decreased autologous RFC was the most frequent T lymphocyte abnormality observed in 43 patients and was shown to occur even in patients with normal total and 'active' RFC. No correlation was found between autologous RFC and total or 'active' RFC. Skin anergy to 2,4-dinitrochlorobenzene was noted in 44% of the patients tested. Autologous RFC did not correlate with delayed cutaneous hypersensitivity to 2,4-dinitrochlorobenzene.
Looking for an early immune defect assay in non metastatic (MO) squamous cell lung carcinoma, 48 untreated patients were tested at the time of diagnosis for peripheral blood "active" rosette-forming T lymphocytes, delayed cutaneous hypersensitivity to recall antigens and skin reactivity to phytohemagglutinin (PHA). 32 patients had a resectable tumour (group 1) and 16 patients had a loco-regional extension which made the tumour inoperable (group 2). No significant difference (p greater than 0.05) was observed between any of the two groups of patients and normal controls nor between group 1 and 2 for "active" rosettes and skin tests to recall antigens. However, skin reaction to PHA was significantly impaired in patients of both groups compared to normal age-matched controls whatever the dose of PHA (4 microgram and 10 microgram). The number of unreactive patients in group 2 was higher than in group 1, but the difference was not significant (p greater than 0.05). It is concluded that skin reactivity to PHA is an useful and easy assay for cell-mediated immunity deficiency in early squamous cell lung carcinoma, whereas "active" rosettes are not altered.
There is increasing evidence in the literature for persistent deficiency in cell-mediated immunity (CMI) in Hodgkin's diseases during apparent remissions after discontinuation of the treatment. Patients were followed for 6 months to 2 years after all treatments were stopped. There was a high percentage (41.6) of subjects with skin anergy to seven recall antigens, a highly significant (p less than 0,0001) decrease, as compared with controls, in total and active E rosettes independently from the number of lymphocytes, and a highly significant diminution of T-lymphocyte in vitro reactivity to various doses of phyto haemagglutinine (PHA). There was no difference between the patients tested between 6 months and 1 year and those tested more than 2 years after treatment. No correlation between skin tests and active rosettes was found in this series. Finally, the CMI deficiency is some what different in patients on remission and in untreated patients.
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Sister chromatid exchanges (SCEs) were studied in peripheral human leukocytes from 16 patients with balanced translocations or with unbalanced karyotypes, and from 4 controls. No difference was seen between these two groups of people in the mean number of SCEs per cell, or in the total number of SCEs observed for each pair of autosomes involved in the translocations studied. With this last number no difference from the expected number of SCEs, if one supposes that SCEs follow a random distribution, was seen.
Human red blood cells of the Bombay type which lack ABH group substances can bind to allogeneic lymphocytes just as well as erythrocytes of any other type. A much lower percentage of auto-rosettes between erythrocytes and lymphocytes from the Bombay donor was observed, a result which may be due at least partially to some T lymphocyte defect in the Bombay donor.
The percentage of E-rosettes and active E-rosettes was determined in untreated patients with Hodgkin's disease. All patients had numbers of peripheral blood lymphocytes within the normal range (1,200-5,000 lymphocytes/cu mm). The mean percentage of E-rosettes was significantly lower in the patients (55 +/- 15.7) as compared to normal controls (63 +/- 6.7). No difference in the percentage of active E-rosettes was found (36.6 +/- 8.6 in controls versus 40.3 +/- 10.8 in patients).
Glanzmann's thrombasthenia begins in infancy. The most important clinical signs are cutaneous and mucous hemorraghes (purpura, epistaxis, bleeding gums, menorraghia after puberty). The disease proceedes by alternate periods of activity and remission, the frequency and severity of which decrease with age. Death occurred during any of the attachs. Our 10 cases (7 girls, 3 boys) were in 5 "Manouche" gypsies sibships, interrelated by consanguineous marriages. Genetic studies demonstrated that the disease was inherited in the autosomal recessive pattern. The detection of heterozygotes is now possible with an antibody which appeared in a thrombasthenic patient. This antibody agglutinated the normal platelets, but not the ones of thrombasthenic patients. In heterozygotes the agglutinating effects is intermediate between the homozygote and normal.
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A method of interpretation of the lymphocyte transformation test is described which results on the basis of statistical evaluation. With this method good results were received in cases of drug induced side effects of type I according to Gell and Coombs. The investigations on 61 patients have shown that differneces between the clinical findings and lymphocyte transformation tests are rare. They are mainly in relation to false-positive reactions of the lymphocyte transformation test in Penicillin allergy.
Sera containing cold lymphocytotoxins were studied in the presence of lymphocytes from neonates, pregnant women, blood donors and old people and the degree of positivity varied according to the lymphocyte population investigated: a strongly positive response to lymphocytes from neonates and pregnant women, a weaker response to lymphocytes from old people and a very weak response to chronic leukemic lymphocytes. Cold lymphocytotoxins seem to be a supplementary method of demonstrating a difference in lymphocytic behavior.