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J Moindrot

Publications and source records attributed to J Moindrot.

6 recordsLinked to original sources
PubMed1990

[Pseudomyasthenic pre-Basedow ophthalmoplegia].

A 67-year old woman presented with isolated and bilateral external ophthalmoplegia of the myasthenic type following a subacute course and resistant to anticholesterinases and corticosteroids. A biological hyperthyroidism with immunological markers was discovered. An intensive care of corticosteroids was partially effective, but fatal bone marrow aplasia attributed to carbimazole developed. Pure ophthalmoplegia without local signs of inflammation may be the sole manifestation of dysthyroid orbitopathy.

Aged↗
PubMed1976

[Multiple sclerosis with reduced and with normal levels of complement in the blood. Clinical and genetic correlation].

The authors describe the results of immunological assay of complement factors C3, C4 (the usual path of activation of complement) and of B factor (the alternate path of activation) in 61 multiple sclerosis patients not receiving corticoids, 52 normal controls and 217 patients with other neurological disorders. Hypocomplementaemia (fall in factor C3 related to a fall in total haemolytic activity) was found in 29.5 p. 100 of the patients not on corticotherapy at the first assay, and in 36 p. 100 of the patients when repeated assays were carried out. Hypocomplementaemia is significantly more frequent in multiple sclerosis than in the normal population (0 p. 100) and in neurological patients (9.6 p. 100). In 13.1 p. 100 of the multiple sclerosis patients there was a decrease in B factor: 50.3 p. 100 of the multiple sclerosis patients exhibited no quantitative abnormality of the main factors of complement (normocomplementary multiple sclerosis). The group of multiple sclerosis patients with hypocomplementaemia was characterized by the incidence of other abnormalities in the complement system: cleavage of the C3 factor and a fall in B factor in 60 p. 100 of the cases. A more frequent increase in IgE and measles antibodies was found also while the normocomplementary multiple sclerosis patients more frequently had higher levels of IgA. Genetically, the group with hypocomplementaemia is related to a significant increase in the incidence of the HL-A W18 group while the normocomplementary multiple sclerosis patients appear closely related to the HL-A7 group. Familial investigations show that hypocomplementaemia is usually present in the ascendents and collaterals and that it seems to be transmitted with the HL-A haplotypes. Four families gave evidence of transmission with the W18 group. This transmission sometimes occurs together with transmission of an increase in IgE and/or of measles antibodies. In two pedigrees, one of the ascendents carried in his serum an activator of the alternate path of complement. There does not appear to be any prognostic difference between the two groups. In multiple sclerosis with hypocomplementaemia, the facts suggest a complex immunological abnormality, transmitted genetically to the subject and existing prior to the illness, comprising both elements of deficient and excessive immune response. The recognized presence of a gene of immunological reactivity and of genes of synthesis of complement on the 6th chromosome, in proximity with genes of histocompatability (HL-A and M.L.C.) provides a theoretical basis for this supposition.

Adult↗
PubMedDate not supplied

[Selective study of sulfate and glucuronide conjugates of urinary MHPG in nervous depression. Peripheral and central influences].

The determination of urinary MHPG (3-methoxy-4-hydroxyphenyl glycol) has been extensively performed to confirm the noradrenergic hypothesis of some depressions. However, owing to the double origin, central and peripheral, of this norepinephrine metabolite, the validity of total MHPG assay as an index of central noradrenergic activity may be challenged. MHPG exists in human urine in two conjugated forms, at equal amounts: sulfate and glucuronide. A number of arguments suggest that MHPG sulfate and MHPG glucuronide respectively reflect central and peripheral norepinephrine metabolism. In this work, we have selectively estimated both MHPG conjugates in 24 h-urine samples of 36 severely depressed women in view to assess the extent and frequency of central or/and peripheral norepinephrine dysfunction. On the basis of MHPG sulfate and glucuronide values, we conclude that in the examined population (6 endogenous, 19 neurotic, 11 reactive depressions) about 80% of patients exhibited a central NE functional deficit, and many of them had also a diminished sympathetic activity. Clinical symptoms related to psychic factors (melancholia) or associated to sympathetic activity changes (anxiety, retardation) respectively alter sulfate or glucuronide MHPG excretion. These data altogether validate the concept of the independent origin of the two MHPG conjugated and show that their selective assay is able to provide a more satisfactory reflection of the psychobiological state in depressed patients than total MHPG determination.

Adult↗