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Biomedical subjects

H Dechy

Publications and source records attributed to H Dechy.

At least 19 recordsLinked to original sources

Complete bilateral horizontal gaze paralysis disclosing multiple sclerosis.

Two women presented with bilateral internuclear ophthalmoplegia evolving in a few days to complete bilateral horizontal gaze paralysis. Convergence and vertical eye movements were normal. Cerebral MRI showed a few small white matter lesions in the lateral ventricle regions, and, at the brainstem level, a single, small, bilateral lesion affecting the posterior part of the medial pontine tegmentum and responsible for the clinical syndrome. The condition gradually improved in both patients, following a similar progression as at the onset: improvement first involved the adduction movements in both eyes, whereas bilateral abduction paresis still persisted for a few weeks, before complete recovery of eye movements. Bilateral damage to the medial longitudinal fasciculus and subsequent lateral extent of damage to the region of the two abducens emerging fibres may explain the clinical findings. In both cases, the cause was probably multiple sclerosis.

Adult↗

[Sulfasalazine neurotoxicity].

We report a case of seizures with acute encephalopathy in a female patient under sulfasalazine treatment for polyarthritis. Neurotoxicity secondary to sulfasalazine was suspected. This side effect has seldom been reported in the literature.

Acute Disease↗

[Temporal arteritis: a syndrome. From Horton's disease to periarteritis nodosa].

Four cases of histologically proven temporal arteritis presenting with atypical clinical, anatomical or evolutive features and raising nosological problems concerning the type of vasculitis involved are presented. In patients with temporal arteritis, some elements are suggestive of periarteritis nodosa. They include peripheral neurological lesions, renal or pleuro-pulmonary lesions and the histological appearance of the temporal artery. Diagnosing periarteritis nodosa in a case of temporal arteritis leads to a special therapeutic strategy.

Adrenal Cortex Hormones↗

[Behçet's diseases with multiple intracranial arterial aneurysms].

A case of multiple intracranial arterial aneurysms occurring in a 43 year-old patient with an 8-year history of Behcet's disease is reported. The diagnosis was based upon the past occurrence of polyarthritis, oral and scrotal aphthous ulcers and cutaneous hypersensitivity. There was a three year remission after a brief treatment with corticosteroids. At the end of this period, a left hemiplegia occurred. CT scan showed an infarction in the right middle cerebral artery territory. Angiography showed fusiform aneurysms of the intracranial right internal carotid, right anterior and middle cerebral arteries. The draining veins and sinuses were normal. Careful angiographic examination of visceral and peripheral arteries showed only bilateral retinal artery aneurysms. Large artery involvement is a rare complication of Behcet's disease, and a thorough review of the literature showed only one reported case of an intracranial aneurysm.

Adult↗

Alpha-fetoprotein in hepatitis superimposed on cirrhosis: a case of concomitant hepatitis B surface antigen and antibody associated with a major but transient increase in the alpha-fetoprotein level.

A 53-year-old man with hepatitis concurrent with cirrhosis was simultaneously positive for hepatitis B surface antigen and heterotypic anti HBs antibody. This could be explained by a state of tolerance, with chronic carrying of B virus (subtype a y w3), but would not preclude B virus (subtype d) reinfection, inducing the synthesis of specific anti-d antibodies. In the same patient, the very high level of 3460 ng/ml was reached for alpha-fetoprotein; this was transitory and returned to normal within 8 months; it was probably due to the acute hepatitis. Thus it appears that, even in cases of cirrhosis, a major rise in this marker does not absolutely imply the presence of hepatocellular carcinoma.

Acute Disease↗

[Horton's disease: a too often delayed diagnosis. Plea for an early biopsy of the temporal artery].

The diagnosis of temporal arteritis is made after a mean delay of four months. This delay is explained by the absence, in 50% of cases, of any clinical sign in the temporal area, the possible presence of alterations in liver function tests, and the frequency of anemia and loss of weight. These signs often suggest a mistaken diagnosis of hepatobiliary disease or cancer. The authors evaluate the cost of this delay in a personal series of 33 cases confirmed histologically. They recommend biopsy of the temporal artery in each patient aged more than 70 with a marked rise in erythrocyte sedimentation rate unexplained by an infectious disease or dysglobulinemia.

Aged↗

[Horton's disease: retrospective study of 33 cases and review of the literature].

Temporal arteritis is still often overlooked in 1982 as shown by the diagnostic delay reported in a retrospective review of 33 patients and in the series previously published in the medical literature. Clinical features to be especially kept in mind are the occasional nature of temporal signs, the pathognomonic value of jaw claudication and the existence of signs which may constitute a premonitory syndrome of blindness. The frequent rise in alkaline phosphatase levels is often misleading. In patients over 65 with an unexplained inflammatory syndrome, biopsy of both temporal arteries should be promptly performed, prior to the unpleasant and costly investigations designed to detect an occult carcinoma. Corticosteroids are still the best treatment of giant cell arteritis but the optimal initial dosage remains unknown as no data from randomized trials are available. Symptomatic relapses have been reported up to 10 years (5 years for ocular symptoms) after onset of the disease. Because of this protracted course, which makes adequate follow-up difficult to ensure, recovery rates from different series are at variance. The main side-effects of maintenance corticosteroid therapy in these elderly patients are osteoporosis, which warrants systematic countermeasures, and probably an increased rate of atheromatosis.

Adrenal Cortex Hormones↗