High-dose intravenous immune globulin and acute renal failure.
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Acute Kidney Injury↗
Biomedical subjects
X Ferrer
Publications and source records attributed to X Ferrer.
[Myasthenic crisis after intravenous injection of iodine contrast product].
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Contrast Media↗
Effects of copper, iron and zinc on oedema formation induced by phospholipase A2.
1. Intradermal or subplantar injection of soluble snake venom phospholipase A2 (PLA2) evoked a brisk inflammatory response, with cutaneous vascular permeability increase and paw oedema. 2. These inflammatory processes are mainly the result of arachidonic acid cascade activation and mast cell degranulation. 3. Copper, iron and zinc have an inhibitory effect on vascular permeability increase and paw oedema induced by PLA2. 4. Copper and iron could have not only a direct effect on PLA2 but on enzymes of arachidonic acid cascade. 5. However, zinc have a moderate antiinflammatory activity. This effect could be the result to inhibit PLA2 induced mast cell degranulation.
Animals↗
[Autosomal dominant centronuclear myopathy].
In a family 6 members in 3 generations were affected by centronuclear myopathy (CNM) of autosomal dominant inheritance. The apparent onset was in the early forties and the disease progressed slowly. Limb weakness was predominant. Strabismus was present in 5 cases and calves hypertrophy in 3. Serum creatinine kinase was always within the normal range. In one case myotonic bursts were found at electromyography. In 2 cases brain stem auditory evoked potential studies demonstrated abnormal prolongation of interpeak latencies I-III and favoured subclinical nervous system involvement. Muscular biopsies showed typical features of centronuclear myopathy with 50 to 80% central nuclei. In two cases immunocytochemical labelling of dystrophin showed staining in the sarcoplasm in favour of an arrest in the morphogenesis of developing myofiber. Others families with autosomal dominant CNM in the literature and also some sporadic adult cases had similar clinical features.
Adult↗
PLA2-induced oedema in rat skin and histamine release in rat mast cells. Evidence for involvement of lysophospholipids in the mechanism of action.
Injection of phospholipase A2 (PLA2) in the rat skin produced a significant rise in oedema, which was inhibited by the simultaneous coinjection of aristolochic acid (100 micrograms), mepacrine (100 micrograms) and p-bromophenacyl bromide (10 micrograms). Indomethacin, nordihydroguaiaretic acid and WEB 2086 were without inhibitory effect on this model, whereas dexamethasone (5 mg/kg, p.o.) and coinjection of chlorpheniramine (20 micrograms) inhibited the oedema formation by more than 60%. Dose-dependent histamine release by rat peritoneal cells was induced by PLA2 and by lysophosphatidylserine and this effect could be antagonized by aristolochic acid and mepacrine. Apomorphine, previously reported to be an antagonist at lysophospholipid receptors, was able to inhibit the histamine release by mast cells as well as the oedema formation in rat skin. Taken all together, these results suggest that lysophospholipids, produced by the action of PLA2, are the mediators for the histamine release in rat peritoneal cells and could play an important role in the early oedema development in rat skin after PLA2 administration.
Animals↗
[Polymicrogyria and ulegyria. Diagnosis by magnetic resonance].
Three patients who had had epilepsy since the second decade of life were studied with cranial magnetic resonance (MR). Two patients had no antecedents of interest during pregnancy and the perinatal period and neurological examination was normal. The third patient had had dystocia and presented left hemiparesia since then, with normal intellectual development. None of the cases had any family history of neurological disease. Cranial magnetic resonance was performed in the three patients demonstrating polymicrogyria in two and ulegyria in the other, in addition to other lesions. The first patient presented an unilateral area of polymicrogyria related with a porencephalic cyst in the distal territory of the right sylvian artery and ipsilateral heterotopia of periventricular location. The second patient presented bilateral periventricular heterotopia, partial agenesis of the corpus callosum and an enlarged cisterna magna in addition to bilateral frontal-occipital polymicrogyria. Finally, ulegyria was observed in the third patient in the edges and neighboring regions of a right rolandic porencephalic cyst, as well as an enlarged cisterna magna.
Adult↗
Delayed onset movement disorders as a complication of central pontine myelinolysis.
This report describes a case of central pontine myelinolysis occurring after a rapid correction of profound hyponatremia. Delayed-onset generalized dystonia and choreoathetosis then appeared. A small pontine myelinolysis was demonstrated by magnetic resonance images, but striatal myelinolysis could not be established. Aspects of movement disorders associated with the osmotic demyelination syndrome are briefly reviewed and discussed.
Athetosis↗
Primary meningeal B lymphoma presenting as a subacute ascending polyradiculoneuropathy.
A subacute ascending polyradiculoneuropathy was the main feature of a primary meningeal B lymphoma in two patients. Tumour cells appeared in the CSF eight and six months respectively after the onset of the disease. Treatment by intrathecal methotrexate resulted in transient improvement.
Aged↗
[Hypokalemic paralysis disclosing vipoma].
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Aged↗
[Sensory neuropathy and subacute dysautonomia. Clinical and pathological study].
We report a case of severe subacute autonomic and sensory neuropathy in a 52 year-old man. Cerebrospinal fluid protein was 275 mg/dl. Electrophysiological data were consistent with an axonal sensory neuropathy. Nerve biopsy showed a severe decrease in myelinated fibers, and a less severe loss of unmyelinated fibers. No cause was found and recovery was almost complete over 4 years, with minimal persistent dysautonomia. This case and 4 similar reported cases are compared with pure dysautonomia and with sensorimotor dysautonomic neuropathy. The site of damage is discussed and it is suggested that these cases are axonal forms of inflammatory polyneuropathy.
Autonomic Nervous System Diseases↗
[Compliance with tuberculosis treatment in adults in Santiago, Chile].
A prospective study was conducted to estimate the current magnitude of adherence to short-course tuberculosis treatment, the degree of abandonment, the characteristics of treatment dropouts, and the causes of this abandonment. The study group was made up of tuberculosis patients over the age of 15 who received care at the Western and Southern Health Services of the Metropolitan Region of Santiago, Chile, between 1 October 1987 and 31 January 1988. The percentage abandoning treatment, calculated by the life table method, was 11.5. The profile of patients who dropped out of treatment was as follows: male, under 45 years of age, single, low level of education, no steady work, homeless, and alcoholic. In addition, an opinion survey on the variables associated with abandonment was conducted and it was concluded that the main ones were alcoholism and intolerance to tuberculosis drugs. Awareness of this profile makes it possible to take measures to prevent patients from abandoning treatment, as well as to educate and even hospitalize at the start of treatment those tuberculous patients exhibiting such a profile.
Adolescent↗
The influence of Calmette-Guérin bacillus immunization on the booster effect of tuberculin testing in healthy young adults.
The booster or enhancement effect of repeated tuberculin skin testing in Calmette-Guérin bacillus (BCG)-vaccinated young adults was studied in 208 first-year medical, nursing, and medical technology students in Santiago, Chile, where BCG vaccine is usually administered at birth and at 6 and 14 yr of age. Thirty-three students had no BCG scar, 62 had one scar, 71 had two scars, and 42 had three scars. The mean age for each group was 19 yr. All students were healthy and had no known exposure to tuberculosis or history of tuberculosis or other mycobacterioses. The size in millimeters of induration of the first tuberculin reaction (PPD1) was clearly correlated with the number of BCG scars: 2.3 +/- 4.6 for no scars; 6.7 +/- 6.7 for one scar; 10.9 +/- 5.9 for two scars, and 13.2 +/- 5.3 for three scars. The second tuberculin reaction (PPD2), performed 2 wk later on the contralateral forearm, showed a marked increase in reactivity. The increase in reaction size was most evident in students who had BCG scars but who were initially PPD negative (less than 10 mm). Smaller increases were observed in students without BCG scars, and also in those who had BCG scars but who were initially tuberculin positive (greater than or equal to 10 mm). The persistence of the booster effect was evaluated by performing PPD3 1 yr later. PPD1-negative students with BCG scars maintained the increased level of reactivity to PPD2 after 1 yr. An immunizing effect of tuberculin testing was suggested in 11 nonimmunized students who were initially PPD negative.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
[Hypothyroid neuropathy].
Two cases of polyneuropathy in patients with hypothyroidism are reported. In both cases, the polyneuropathy involved the lower limbs and was predominantly distal. It was sensorimotor in the first patient and purely sensory in the second one. Electrophysiological findings were consistent with an axonopathy. Symptoms and electrophysiological parameters improved with thyroid therapy. Neuropathy in such cases is probably related to the duration of hypothyroidism.
Aged↗
[Subacute familial thalamic atrophy. Memory disorders and complete insomnia].
Thalamic atrophy is rarely primitive. Selective atrophy of the dorso-medial and anterior thalamic nuclei has been reported in a few families. The clinical course is subacute. Symptoms and signs include sleep disorders and intellectual deficit. We report a new family with this uncommon disease and discuss its etiology.
Atrophy↗
[Choreo-acanthocytosis].
We report a case of choreo-acanthocytosis in a 33 year-old man with mild chorea of the limbs but no involuntary movements of the face, areflexia, epilepsy and personality changes. Acanthocytosis was 10-20% and creatine-phosphokinase levels were raised. Electrophysiological data were consistent with lower motor neurone dysfunction. Muscle biopsy revealed changes typical of neurogenic atrophy. Nerve biopsy showed a severe loss of large myelinated axons. Electron microscopic examination was in favour of primary axonal damage affecting mainly myelinated fibers and only slightly unmyelinated fibers.
Acanthocytes↗
Extensive cerebral calcification and retinal changes in pseudohypoparathyroidism.
The case of a 41-year-old woman with cerebral calcification of a rather unusual extent is reported. This condition was associated with mental deficiency, pseudohypoparathyroidism and Albright's hereditary osteodystrophy. Four years later hypothyroidism was diagnosed. Visual impairment and electroretinogram abnormality suggested a retinopathy involving mostly rods. Despite their rarity, pseudohypoparathyroidism and Albright's hereditary osteodystrophy are of major interest, since they represent the only human disease states in which G protein function has been found to be disrupted. The overall clinical picture was strongly suggestive of a genetic deficiency of a guanine nucleotide-binding protein, termed Gs. The putative involvement of another G protein, contained in rods and cones, transducin, in the pathogenesis of the retinopathy is discussed.
Adult↗
Multiple sclerosis: an overview.
Demyelinating lesions of MS are infiltrated by activated T-lymphocytes and macrophages with secretion of soluble factors. This results in the synthesis of oligoclonal immunoglobulin (IgG) by plasma cells. The activated T-lymphocytes migrate from the peripheral blood to the CNS. This hyperactive state is linked to a selective loss of the suppressor/inducer T-cell subset. Administration of a soluble factor--interferon gamma--enhances the immune response by promoting class II antigen expression on macrophages or astrocytes, resulting in a relapse. However, the reason for T-cell activation in peripheral blood is not known, nor is the antigen. Myelin basic protein (MBP) has been considered to be the target since MBP is able to induce chronic relapsing allergic encephalomyelitis (CRAE) in an animal model of MS. Yet other myelin antigens have succeeded in inducing CRAE in animal models, and anti-MBP antibodies have been found in healthy individuals. The possibility that the hyperimmune state results from a viral infection has not yet been proven. It is known that in Caucasians, a genetic susceptibility factor is linked to class II MHC. Using MRI it has been found that the presence of new plaques was not regularly correlated with relapses, which indicates that MS is an ongoing pathology process. Most drugs used in MS influence the immune response but have potential toxicity. Monoclonal antibodies offer the opportunity of specific targeting of T-cells and are promising for the future.
Animals↗