[Secretan's syndrome: myth or pathomimia?]. / Le syndrome de Secrétan : mythe ou pathomimie ?

UNLABELLED: Secretan's syndrome is a rare condition involving generally trauma-induced hard edema of the dorsal aspect of the hand. The cause is poorly understood but factitious trauma is often suspected. CASE REPORT: A 42-year-old woman presented with a fortuitous edema on the back of the right hand. The minimally depressible edema was associated with moderately intense mechanical pain. Routine laboratory tests were normal. An extensive imaging work-up (bone x-ray of the hand and wrist, bone scintigraphy, computed tomography phlebography, lymphoscintigraphy, magnetic resonance imaging) was equally non-contributive. The diagnosis of self-inflected trauma was suggested by the atypical nature of the edema, the absence of any organic disorder on the tests performed, and the patient's attitude concerning her disease. In this clinical context, the diagnosis of Secretan's syndrome was retained. Outcome was compatible, with secondary development of complex regional pain syndrome. DISCUSSION: Three forms of Secretan's syndrome have been recently described: benign; hyperplastic; and mixed. The cause remains poorly defined. Certain authors report that it is most likely related to pathomimia. Treatment can combine physiotherapy and psychological counseling. CONCLUSION: Secretan's syndrome is a poorly-understood and rarely-described condition that may be underdiagnosed. Physicians specialized in vascular medicine should be aware of this syndrome and its difficult diagnosis by elimination.

Low persistence of the induced mutant phenotype in Chinese hamster cells.

We have analysed the recovery of individual CHO-derived mutants during the generations immediately following their induction. This characteristic, which we call persistence, was measured by propagating mutagenized cultures in non-selective medium after subdivision into many very small populations, each containing either zero or one mutant. The recovery of most hypoxanthine phosphoribosyltransferase (hprt)-deficient mutants induced by ethyl methanesulphonate was low, and we have previously shown that this was usually due to an apparent rapid loss of the mutant phenotype with continued culture in non-selective medium (Bradley, 1980). A minority of about 15% manifest high persistence. We now show that most adenine phosphoribosyltransferase (aprt)-deficient mutants and some ouabain-resistant mutants had low persistence. Mutants induced by UV irradiation also generally exhibited low persistence but those induced by X-irradiation had significantly higher persistence than what was seen among EMS-induced mutants. Among various sublines of CHO cells which were tested for persistence of induced mutants, only one group consistently yielded mutants of high persistence. These were lines which carried glucose-6-phosphate dehydrogenase mutations which themselves had been originally induced by EMS.

Increased persistence of induced mutants of Chinese hamster cells by 12-O-tetradecanoylphorbol-13-acetate.

Hypoxanthine phosphoribosyltransferase deficient mutants of Chinese hamster ovary cells induced by ethyl methanesulfonate usually do not maintain their phenotype during growth in non-selective medium immediately following the induction. This phenomenon, called poor "persistence" of the induced mutation, is in most cases unrelated to growth rate but results from establishment of contact with wild type cells (Bradley, W. E. C. Exp. Cell Res., 129: 251, 1980). We report here that 12-O-tetradecanoylphorbol-13-acetate, a strong tumor promoter, increases the persistence of these mutants.

Familial hyperbilirubinemia in Friedreich's ataxia.

The combined metabolic stresses of fasting and the intravenous injection of 50 mg nicotinic acid in Friedreich's ataxia resulted in the delineation of two sub-groups of responses. High bilirubin ataxics maintained abnormally elevated levels of bilirubin, while normal bilirubin ataxics behaved like the normal control group. It is postulated that this finding infers the possible linkage of the gene for Friedreich's ataxia and that for Gilbert's disease.