ABSTRACT
Steroid-induced lipomatosis usually presents as a localized hypertrophy of the adipose tissue and seems more common than previously thought. Most patients develop this phenomenon after prolonged administration of moderate to high doses of oral corticosteroids. The localizations are numerous and determine the clinical presentation. Often asymptomatic, they can also be revealed by worrying symptoms usually due to a compressive syndrome. The most frequently reported localizations (spinal epidural, retro-orbital, mediastinal) are also the most clinically apparent. The cessation or reduction of steroid therapy, when medically possible, inconsistently results in the decrease or disappearance of the lipomatosis deposits. Computerized tomography or magnetic resonance imaging are the most helpful diagnostic means. Interestingly, these lipomatoses have rarely been reported in patients with Cushing disease. Their pathophysiology remains poorly elucidated and may imply an inhibition of the brown adipose tissue lipolysis.
Subject(s)
Glucocorticoids/adverse effects , Lipomatosis/chemically induced , Prednisone/adverse effects , Adult , Female , Humans , Lipomatosis/physiopathologyABSTRACT
A case of diencephalic dysregulation is reported during urological endoscopy following the intravenous administration of indigo carmine. It should be kept in mind that according to the literature, indigo carmine has severe side-effects on the cardiovascular system caused by vasoconstriction. Ergotamine-like effects of indigo carmine due to direct vasoconstriction with spasm of the cerebral arteries are discussed.
Subject(s)
Cystoscopy/methods , Hypothalamic Diseases/chemically induced , Indigo Carmine/adverse effects , Indoles/adverse effects , Aged , Aged, 80 and over , Cystoscopy/adverse effects , Humans , Indigo Carmine/administration & dosage , Injections, Intravenous , MaleABSTRACT
Very marked abnormalities of the complement system were discovered in two patients suffering from a lymphoid syndrome and an IgM 7S dysglobulinaemia. The abnormalities in the complement system were related to a deficiency in C1-estérase (C1 INH). Several findings suggest that such a deficiency is acquired, in particular the absence of any family history of angio-neurotic oedema and, above all, the detection of a marked fall in levels of the C1 fraction which does not exist in the congenital form of deficiency of the inhibitor. The IgM 7S immunoglobulins found in the serum of both patients are probably responsible for the abnormalities in the complement system observed. Such acquired deficiencies in C1 INH are extremely rare since only a few cases have been reported in the literaute, in particular two cases in patients with lymphosarcoma with a serum IgM 7S.
Subject(s)
Complement C1 Inactivator Proteins , Complement Inactivator Proteins , Dysgammaglobulinemia/complications , Esterases/antagonists & inhibitors , Immunoglobulin M , Immunologic Deficiency Syndromes/complications , Lymphatic Diseases/complications , Aged , Angioedema/etiology , Blood Protein Disorders/complications , Blood Protein Disorders/etiology , Complement C1/deficiency , Complement System Proteins/deficiency , Dysgammaglobulinemia/physiopathology , Female , Humans , Immunodiffusion , Immunoglobulin G/analysis , Immunoglobulin M/analysis , Middle AgedABSTRACT
The authors carried out long-term clinical and E.E.G. studies on 100 cases of acute drug poisoning. They made the following conclusions: - in unexplained coma, the E.E.G. can indicate toxic aetiology and may sometimes even suggest which drug is responsible, especially for certain chemical groups (barbiturates, phenothiasines, benzodiazepines); - the E.E.G. picture contributes a valuable indication of the depth of coma; the way in which it evolves affects the prognosis; - the effectiveness of therapy may be judged by monitoring cerebral electrical activity.
