Biomedical subjects

Nadia Belmatoug

Publications and source records attributed to Nadia Belmatoug.

11 recordsLinked to original sources

PubMed2006

Spinal tuberculosis: a longitudinal study with clinical, laboratory, and imaging outcomes.

OBJECTIVES: To study imaging changes associated with spinal tuberculosis (ST) over time and evaluate their association with clinical and laboratory data. METHODS: Between 1997 and 2004, patients with proven ST in our institution were prospectively enrolled and treated for 1 year. Clinical and laboratory data were collected at baseline and every 3 months. Computed tomography (CT) and magnetic resonance imaging (MRI) were performed at baseline. MRI was performed at least twice during treatment and at the end of treatment. RESULTS: Nineteen patients were enrolled; neurological signs were present at baseline in 14 patients (74%). Initial MRI/CT findings comprised (in percentages of patients) the following: paravertebral abscesses (100/100); intradiscal abscesses (47/0); and epidural abscesses (82/24) with spinal cord compression (64/18) or radicular compression (36/0). Edema of the vertebral body was observed on initial MRI in all the patients. Full follow-up data were available for 15 patients: all were cured with a mean follow-up of 25 months after the end of treatment. Weight gain was nearly maximal at 6 months, and pain relief was achieved within 9 months. C-reactive protein returned to normal after 3 months. On MRI, all epidural abscesses disappeared within 9 months; paravertebral abscesses disappeared after 3, 6, and 12 months in 45, 50, and 85% of patients, respectively. Vertebral body signal converted to a fatty signal in 75% of cases at 12 months. CONCLUSIONS: Significant imaging abnormalities can persist after successful treatment of ST. These findings suggest that MRI need not be repeated in patients with clinical and laboratory improvement.

Abscess↗

PubMed2006

Bone involvement in generalized crystal-storing histiocytosis.

The abnormal secretion of monoclonal immunoglobulins observed with monoclonal gammopathies and other clonal B cell dyscrasias can be responsible for a spectrum of deposition disorders. Crystal-storing histiocytosis (CSH) is a rare disease affecting patients with B cell dyscrasias and monoclonal gammopathies, characterized by the accumulation of histiocytes that have phagocytosed an abnormal crystalline immunoglobulin. We describe 2 cases of this rare disorder with multiorgan involvement and prominent bone involvement. Magnetic resonance imaging showed bone marrow infiltration and images of avascular necrosis. Bone specimen analysis gave histological proof of diffuse bone infiltration by the abnormal histiocytes. Bone involvement, which appears to be a specific feature of CSH, links this entity to other storage disorders, such as Gaucher disease. Because the accumulation of abnormal immunoglobulin-loaded histiocytes is clearly pivotal, CSH should be considered not only as an immunoglobulin deposition disease but also as a storage histiocytic disorder.

Aged↗

PubMed2005

Comparative study of postoperative and spontaneous pyogenic spondylodiscitis.

OBJECTIVES: Postoperative spondylodiscitis (POS) is poorly characterized, partly owing to its rarity. The aim of this prospective study was to compare the clinical, biological, bacteriological, and imaging features of postoperative and spontaneous spondylodiscitis (SS). METHODS: A multidisciplinary spondylodiscitis cohort follow-up study was conducted between February 1999 and June 2003 in a 500-bed teaching hospital. All patients hospitalized in internal medicine, orthopedic, and neurosurgery wards with a culture-proven diagnosis of pyogenic spondylodiscitis were included. Clinical and bacteriological data were collected. All patients underwent computed tomography and/or magnetic resonance imaging of the spine. RESULTS: Sixteen patients had SS and 7 patients had POS. Patients with POS tended to be younger (52 versus 69 years), with less frequent underlying diseases (29 versus 75%) and a more prolonged interval between symptom onset and diagnosis (16 versus 3.4 weeks) than patients with SS. Blood cultures were positive in 14 and 81% of cases in the POS and SS groups, respectively, and invasive diagnostic procedures were necessary in 86% of patients with POS and 19% of patients with SS ( P = 0.005). Staphylococci were the more frequent isolates in both groups but were more frequently coagulase-negative in POS patients than in patients with SS ( P = 0.01). Vertebral edema tended to be more frequent in POS and was located more posteriorly than in SS ( P = 0.023). CONCLUSIONS: POS is associated with specific clinical, microbiological, and imaging features possibly related to pathophysiologic characteristics. Knowledge of these characteristics should help reduce the current delay in the diagnosis of POS.

Adult↗

PubMed2005

[Acute pancreatitis revealing Behçet disease].

We report here a case of acute pancreatitis revealing Behcet's disease in an 18-year-old woman. Pancreatitis was due to ischemia secondary to severe abnormalities of the celiac trunk arteries with pseudo-aneurysms. The outcome was favourable after the administration of corticosteroids and cyclophosphamide. The patient did not experience relapse of pancreatitis 2 years after diagnosis.

Acute Disease↗

PubMed2005

Is idiopathic chronic pancreatitis an autoimmune disease?

BACKGROUND & AIMS: The proportion of patients with idiopathic chronic pancreatitis (ICP) that have an autoimmune origin is unknown. Three forms of ICP have been described: pseudotumoral, duct-destructive, and usual chronic pancreatitis. The aim of this study was to identify autoimmune stigmata in the 3 forms. METHODS: All patients who underwent exploration for ICP were included. The following data were recorded: examination by an internal medicine specialist, autoantibodies and immunoglobulin screening, and pancreatic duct imaging. RESULTS: Sixty patients were included (pseudotumoral, n = 11; duct-destructive, n = 27; usual, n = 22). There were no significant differences among the 3 types with regard to sex ratio, age, frequency of acute pancreatitis, or obstructive jaundice. Pancreatic calcifications were seen only in the usual form (81%; P = .0001). Autoimmune disease was present in 10 patients: ulcerative colitis in 5 patients, primary sclerosing cholangitis in 2 patients, and Sjögren's syndrome, Hashimoto's thyroiditis, and Graves' disease in 1 patient each. Autoimmune diseases were not more frequent in patients with pseudotumoral (36%) or duct-destructive (19%) forms than in those with the usual form (5%, P = .06). Immunoglobulin G4 levels were increased in 2 of 6 in the pseudotumoral, 1 of 9 in the duct-destructive, and 0 of 12 patients in the usual group. Combining clinical and biochemical autoimmune parameters, 24 patients (40%) had at least 1 autoimmune marker or disease. CONCLUSIONS: Clinical or biochemical autoimmune stigmata are present in 40% of patients with ICP. Autoimmune mechanisms may be frequent in idiopathic pancreatitis.

Adolescent↗

PubMed2003

[Epidemiologic, clinical, biological and therapeutic aspects of Gaucher disease].

GENERAL CHARACTERISTICS: Gaucher's disease is a genetic disease of autosomal recessive transmission due to a deficit in a lysosomal enzyme: beta-glucocerebrosidase. The disease is characterised by deposits of glucosylceramide in the cells of the liver, spleen and bone marrow. Acute or chronic neurological forms (type 2 and 3) account for only 5% of patients suffering from Gaucher's disease and are less frequent than the non-neurological forms (type 1). CLINICAL AND BIOCHEMICAL MANIFESTATIONS: Gaucher's disease is associated with spleno- or hepato-megalia, asthenia, bone complications (Erlenmeyer flask deformity, osteopenia and osteonecrosis), as well as with haematological (thrombopenia, anaemia) or biochemical abnormalities (increase in angiotensin-converting enzyme, ferritin, tartrate-resistant acid phosphatase and chitotriosidase). Central nervous system involvement is only found in the type 2 and 3. Diagnosis relies on measurement of beta-glucocerebrosidase activity in the circulating leukocytes. REGARDING TREATMENT: Treatment with enzyme replacement (imiglucerase: recombinant enzyme preparation) improves the haematological abnormalities, hepatosplenomegalia and quality of life in a matter of a few months. Regression of the bone disorders is usually observed only after 3-4 years of treatment. Recently, gene therapy trials have successfully been started.

Chromosome Aberrations↗

PubMed2003

Recurrent valvular replacement due to exacerbation of Behcet's disease by Streptococcus agalactiae infection.

Valvular heart complications in Behcet's disease are rarely reported. Moreover, the risk of dehiscence in postoperative valvular replacement is high in Behcet's disease. We report a case of recurrent aortic prosthetic dehiscence revealing Behcet's disease in a young woman. Each disease exacerbation was concomitant to a Streptococcus agalactiae infection. This infection appears to act as a trigger for Behcet's disease exacerbation. The patient was successfully treated with immunosuppression plus antibiotic therapy.

Journal Article↗

PubMed2003

Hypoparathyroidism preceding Riedel's thyroiditis.

We report the case of a woman who presented with primary hypoparathyroidism and who subsequently developed extensive Riedel's thyroiditis. To our knowledge, this is the first reported case of primary hypoparathyroidism preceding Riedel's thyroiditis. This observation suggests that Riedel's thyroiditis is part of a diffuse fibrotic process that may involve other organs, such as the parathyroid glands.

Journal Article↗

PubMed2002

Acute respiratory failure due to diaphragmatic weakness revealing a polymyositis.

Of the different respiratory disorders that complicate the course of polymyositis, diaphragmatic weakness is one that is seldom described and most often suspected rather than confirmed. We report a case of severe diaphragmatic weakness as a cause of acute respiratory failure revealing a polymyositis. The diaphragmatic involvement was proven by a very low esophageal pressure in response to cervical magnetic stimulation of the phrenic nerve. Corticosteroids and intravenous gammaglobulin, combined with mechanical ventilation, achieved a progressive recovery of diaphragmatic weakness.

Journal Article↗

PubMed2002

[Gaucher's disease ].

Gaucher disease is an uncommon autosomic recessive disorder. The disease is caused by a deficiency in the activity of the lysosomal enzyme glucocerebrosidase which is responsible for the degradation of glucosylceramide, résulting from the breakdown of red and white cell-membranes. In the absence of enzyme glucosylceramide accumulates in the lysosomes of macrophages. This accumulation leads to hepatomegaly, splenomegaly with subsequent haematologic abnormalities (leucopenia, anemia, thrombopenia) and bone manifestations. Three types of Gaucher disease are described: type 1 is the most common, type 2 and 3 are associated with neurologic symptoms. Macrophages are the likely cellular source of biochemical abnormalities: elevated blood level of ferritin, angiotensin converting enzyme, immunoglobulins and haemostasis abnormalities. Lysosomal perturbations lead to increased blood level of tartrate resistant acid phosphatase and chitotriosidase. Enzyme replacement therapy is available in France since 1991. In 2002, 136 patients are treated. The efficacy is overt on the asthenia, organomegaly and haematological manifestations. Bone pains disappear or decrease in intensity, however bone complications may be irreversible justifying treatment initiations before the appearance of lesions that may lead to serious functional impairment.

Biomarkers↗

PubMed2002

[French results of enzyme replacement therapy in Gaucher's disease].

Gaucher disease is an inborn recessive autosomal disease due to a partial deficiency of the lysosomal enzyme beta glucocerebrosidase. The deficient activity leads to accumulation of the lipid glucocerebroside in the liver, the spleen and bone marrow with concomitant anemia and thrombocytopenia. Patients with Gaucher disease have been classified in three types: type I is the more common, neurological manifestations occur in types II and III. Enzyme replacement therapy (ERT) with modified placental human glucocerebrosidase (ceredase) or recombinant glucocerebrosidase (cerezyme) is effective in most type I Gaucher disease and has become the current standard care administered to thousand of patients worldwide. ERT has obviated the need for bone marrow transplantation and virtually eliminated the need for splenectomy. We report here the French study including adults and children. ERT of 30 to 60 U/K every two weeks as starting dose was administrated to 108 patients with severe type I Gaucher disease. ERT fully reverse many of the manifestations of the disease. ERT regimen alleviated fatigue, and hematological and visceral signs and symptoms in nearly all severely-ill patients. Skeletal responses to treatment develop much more slowly than hematological or visceral responses. Studies in pediatrics show that the disease is more severe in children. These children should be treated early in the course of their disease to avoid irreparable damage. Hematological manifestation in type II cannot be reversed with enzyme replacement. In type III treatment can rarely reverse neurological deficit. Gaucher disease is also an excellent candidate for gene therapy.

Adult↗