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Biomedical subjects

P Cacoub

Publications and source records attributed to P Cacoub.

At least 253 records · Page 14Linked to original sources

[Hemolytic-uremic syndrome in adults].

Haemolytic uraemic syndrome is a rare condition easily diagnosed from biochemical data. Numerous forms consecutive to pregnancy, systemic diseases, carcinomas (notably mucin-secreting gastric adenocarcinoma), infections and medications have been described. The physiopathology of the syndrome, although more elaborate, is not entirely clear. The fundamental anatomical lesions (fibrin-platelet microthrombi) develop from vascular endothelial injuries. They persist and extend due to the non-functioning of physiological regulatory systems, in particular the coagulation-fibrinolysis system. In spite of frequently heavy and expensive treatments empirically applied, the course of the disease is generally unfavourable, with a mortality of about 50%.

Hemolytic-Uremic Syndrome↗

[Cyclosporin A].

Explore the source record for details and available documents.

Cyclosporins↗

[Microangiopathy and arterial hypertension in scleroderma and periarteritis nodosa].

The mechanisms of blood pressure regulation in periarteritis nodosa and systemic sclerodermia are discussed in the light of results of personal studies. Hypertension during PAN may be divided into two groups: hypertension related to renal microangiopathy responsible for stimulation of the renin-angiotensin-aldosterone system which often runs a severe course, sometimes accompanied by renal insufficiency and requiring treatment with beta-blocking agents or angiotensin conversion enzyme inhibitors; secondly, hypertension may not be linked to the renin-angiotensin-aldosterone system and the prognosis is then better. In systemic sclerodermia, a similar pattern may be found but it would also seem that the renin-angiotensin-aldosterone system may be stimulated in the absence of any hypertension. This rise in plasma renin activity and aldosterone preceding the onset of an acute sclerodermic renal episode has a very poor prognosis. Corticosteroid therapy may favour such a process. Other regulation mechanisms are also discussed: prostaglandins, bradykinin system.

Captopril↗

[Septicemia associated with the presence of a pacemaker with endocavitary electrode].

Septicaemia on endovenous pacemaker electrodes is infrequent and difficult to detect. We report the case of a 64-year old woman with a diagnosis of prolonged fever that dragged on for several months before infection of her pacemaker was considered, then confirmed. Repeated Staphylococcus epidermidis isolates from blood cultures were no longer regarded as contaminations, and transoesophageal echocardiography revealed the presence of a "mass" on her endocavitary electrode, which had not been visualized on several previous échocardiographies. Surgical removal of the electrode was soon required in view of multiple septic emboli despite a bacteriologically effective antibiotic therapy. The outcome is favourable after a 6-month follow-up. The authors review the diagnostic and therapeutic problems created by infections on electrosystolic exciting electrodes.

Aged↗

AL cardiac amyloidosis and arterial thromboembolic events.

OBJECTIVE: To study the prevalence and characteristics of arterial thromboembolic events (ATEE) in the course of AL amyloidosis. METHODS: We report the case of a non-anticoagulated patient with AL amyloidosis restrictive cardiomyopathy who developed acute lower limb ischaemia. We then prospectively determined the prevalence of ATEE in all patients with AL amyloidosis who were evaluated in our institution for autologous peripheral stem cell transplantation. RESULTS: Nine out of 15 non-anticoagulated patients (60%) developed ATEE: ischaemic stroke (3), transient cerebral ischaemic attack (2), multiple peripheral arterial emboli (1), bilateral iliac artery thrombosis (1), bilateral optic nerve ischaemia (1), and mesenteric ischaemia (1). Haemodynamic stasis seemed to play a leading role in the pathophysiology of ATEE, in that all patients were on sinus rhythm and only one had a thrombus on echocardiography. We identified possible contributing factors to ATEE occurrence: concomitant treatments with oestroprogestogen regimen, thalidomide, granulocyte-macrophage colony-stimulating factor (GM-CSF) and extracellular volume disturbances related to the cytapheresis procedure. CONCLUSION: We report on an unusual frequency of ATEE among patients with AL cardiac amyloidosis. Despite its theoretical risks, anticoagulation should be discussed for patients with amyloid cardiomyopathy.

Aged↗

[Polymyositis induced by tiopronine].

BACKGROUND: D-penicillamine-induced muscle disorders are well-known, tiopronine-induced disorders are less often reported. CASE REPORT: A 62-year-old patient, given tiopronine for rheumatoid arthritis, developed severe polymyositis with characteristic clinical and pathology features. The course was favorable after tiopronine withdrawal and substitution with methotrexate. DISCUSSION: Clinicians should be aware of the side-effects of tiopronine, particularly muscle disorders, and implement careful surveillance to achieve early diagnosis and appropriate therapy.

Amino Acids↗

Antiphosphatidylethanolamine antibody as the sole antiphospholipid antibody in systemic lupus erythematosus with thrombosis.

A previously healthy 34-year-old woman, was diagnosed as having systemic lupus erythematosus (SLE), with membranous glomerulopathy which improved rapidly. Neither lupus anticoagulant nor anticardiolipin antibodies were detected in her plasma. After three months of total remission, she developed a severe pulmonary thromboembolism for which no specific biological cause was found. Her plasma was analysed for different antiphospholipid antibodies: lupus anticoagulant and anticardiolipin antibodies were again negative. Using an ELISA prepared with either five different anionic phospholipids or zwitterionic phosphatidylethanolamine, solely an anti-phosphatidylethanolamine IgG was discovered in her plasma. In lupus patients, the presence of antiphospholipid antibodies is now well recognized as a high risk factor for repeated thrombosis and/or recurrent abortions. This case suggests that the presence of antiphosphatidylethanolamine antibody should be investigated in cases of unexplained thrombosis in SLE, where the usual clinical and biological investigations have failed to shed light.

Adult↗

Subacute bacterial endocarditis presenting as polymyalgia rheumatica or giant cell arteritis.

OBJECTIVE: To report on several patients with subacute bacterial endocarditis who were initially presumed, incorrectly, to have polymyalgia rheumatica or giant cell arteritis. METHODS: We report 3 cases of subacute streptococcal endocarditis mimicking giant cell arteritis in 2 cases and polymyalgia rheumatica in one. We reviewed the literature through Medline search of French and English-language articles published between 1966 and 2005 and found 5 similar cases. RESULTS: Shoulder and/or pelvic girdle pain was associated with neck or back pain in all patients. Scalp tenderness, bilateral jaw pain, amaurosis fugax were present in 2 patients. One patient had no fever. Two patients were treated with corticosteroids with initial good clinical response in one. Appropriate antibiotic therapy resulted in the rapid disappearance of rheumatic complaints in 2 patients and achieved a definitive cure of endocarditis in all cases. CONCLUSION: Rheumatologic symptoms may hinder the correct diagnosis of infective endocarditis in patients who present with a clinical picture suggesting polymyalgia rheumatica or giant cell arteritis. In such cases, blood cultures should be systematically drawn.

Adrenal Cortex Hormones↗

Malignant hypertension in antiphospholipid syndrome without overt lupus nephritis.

The antiphospholipid syndrome is usually defined by the association of a clinical manifestation (recurrent venous and/or arterial thrombosis, recurrent spontaneous miscarriages) and a biological abnormality (anticardiolipin antibody, lupus anticoagulant). We retrospectively analyzed the records of 5 patients (4 females, 1 male, aged 30 +/- 12 years) with antiphospholipid syndrome, primary (n = 1) or secondary to systemic lupus erythematosus (n = 4), who developed malignant systemic hypertension with renal insufficiency, in the absence of lupus nephritis. Before the episode of malignant hypertension, all patients had normal systemic blood pressure and renal function. During malignant hypertension the systolic pressure was 206 +/- 39 mmHg and the diastolic pressure 130 +/- 25 mmHg, peak serum creatinine was 204 +/- 95 mumol/l, daily proteinuria was 1.1 +/- 0.8 gr, and complement serum levels were normal in all patients. Renal angiography found normal proximal renal arteries. Renal biopsy showed ischaemic glomeruli without proliferative lesions (n = 5), focal intimal fibrosis either isolated (n = 3) or associated with thrombosis (n = 2) of the intrarenal vessels, and the absence of vasculitis. Immunofluorescence study did not reveal typical lupus deposits. Patients were treated with antihypertensive agents, increasing doses of prednisone (n = 3), and anticoagulant (n = 2) or anti-aggregant therapy (n = 1). After a mean follow-up of 6.8 +/- 5.2 years, 4 patients were still alive with normal blood pressure and renal function, whereas 1 patient died of a probable catastrophic antiphospholipid syndrome. Patients with antiphospholipid syndrome, primary or secondary to systemic lupus erythematosus, may develop malignant hypertension with renal insufficiency and intrarenal vascular lesions, in the absence of lupus nephritis.

Adolescent↗