Microangiopathic Hæmolytic Anæmia and the Pathogenesis of Malignant Hypertension

Linton, A. L.; Hutchison, H. E.; Gavras, Haralambos; Lawson, D. H.; Gleadle, R. I.; Lever, A. F.; Macadam, R. F.; McNicol, G. P.; Robertson, J. I. S.

doi:10.1016/s0140-6736(69)92221-1

Cited by 98 publications

(24 citation statements)

References 44 publications

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“…Classical HUS presents typically a few days after the onset of an acute diarrheal "prodromal" illness which is often bloody and shows remarkable similarities clinicopathologically (156) and radiologically (5,88,159,170) (86), the prodrome is nondiarrheal and may consist of upper or lower respiratory tract symptoms, fever, and vomiting. The other much less common types of HUS include a childhood form that is inherited (75) and adult forms that occur in association with pregnancy (29,172), oral contraceptive use (13,87), malignant hypertension (11,105), and various chronic illnesses (42,51).…”

Section: Hemorrhagic Colitismentioning

confidence: 99%

“…The factor VIII molecule, or complex, consists of a low-MW portion which has the factor VIII anticoagulant activity and a high-MW component referred to as factor VIII-related antigen ( Another manifestation of HUS is a microangiopathic hemolytic anemia characterized by the presence of fragmented erythrocytes (11,105). The damaged erythrocytes are removed from the circulation by the reticuloendothelial system.…”

Section: Colonization and Multiplicationmentioning

confidence: 99%

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Infection by verocytotoxin-producing Escherichia coli

1989

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Verocytotoxin (VT)-producing Escherichia coli (VTEC) are a newly recognized group of enteric pathogens which are increasingly being recognized as common causes of diarrhea in some geographic settings. Outbreak studies indicate that most patients with VTEC infection develop mild uncomplicated diarrhea. However, a significant risk of two serious and potentially life-threatening complications, hemorrhagic colitis and the hemolytic uremic syndrome, makes VTEC infection a public health problem of serious concern. The main reservoirs of VTEC appear to be the intestinal tracts of animals, and foods of animal (especially bovine) origin are probably the principal sources for human infection. The term VT refers to a family of subunit exotoxins with high biological activity. Individual VTEC strains elaborate one or both of at least two serologically distinct, bacteriophage-mediated VTs (VT1 and VT2) which are closely related to Shiga toxin and are thus also referred to as Shiga-like toxins. The holotoxins bind to cells, via their B subunits, to a specific receptor which is probably the glycolipid, globotriosyl ceramide (Gb3). Binding is followed by internalization of the A subunit, which, after it is proteolytically nicked and reduced to the A1 fragment, inhibits protein synthesis in mammalian cells by inactivating 60S ribosomal subunits through selective structural modification of 28S ribosomal ribonucleic acid. The mechanism of VTEC diarrhea is still controversial, and the relative roles of locally acting VT and "attaching and effacing adherence" of VTEC to the mucosa have yet to be resolved. There is increasing evidence that hemolytic uremic syndrome and possibly hemorrhagic colitis result from the systemic action of VT on vascular endothelial cells. The role of antitoxic immunity in preventing the systemic complications of VTEC infection is being explored. Antibiotics appear to be contraindicated in the treatment of VTEC infection. The most common VTEC serotype associated with human disease is O157:H7, but over 50 different VT-positive O:H serotypes have now been identified. The best strategies for diagnosing human VTEC infection include testing for the presence of free VT in fecal filtrates and examining fecal cultures for VTEC by means of deoxyribonucleic acid probes that specify genes encoding VT1 and VT2. Both methods are currently confined to specialized laboratories and await commercial development for wider use. In the meantime, most laboratories should continue to screen for the most common human VTEC serotype, O157:H7, using a sorbitol-containing MacConkey medium.

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Section: Hemorrhagic Colitismentioning

confidence: 99%

Section: Colonization and Multiplicationmentioning

confidence: 99%

Infection by verocytotoxin-producing Escherichia coli

1989

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“…If hypertension is not controlled, the regenerative process continues and the lumen of the vessels becomes markedly reduced due to proliferative endarteritis with mucbid and fibrotic changes. Malignant hypertension is known to be associated with intravascular coagulation 19 and factors that stimulate cellular proliferation have been isolated from platelets. 10 The processes of evolution and healing of vascular lesions in malignant hypertension are not clear.…”

Section: Discussionmentioning

confidence: 99%

Metaischemic (post-Goldblatt) hypertensive vascular disease in rats.

Queiroz¹,

Rojo-Ortega²,

Genest³

1980

Hypertension

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SUMMARY Malignant hypertension was induced in rats by aortic ligation above the left renal artery. After 7-and 28-day periods of hypertension, the characteristics of the vascular disease were studied and the kidney below the aortic ligation was removed. The blood pressure and the vascular disease were reexamined at the end of the first and fourth weeks after nephrectomy. The evolution of the vascular disease was assessed in the contralateral kidney, in the heart, and in the superior mesentery. The results obtained allowed the following conclusions: 1) when the predominant lesions are of fibrinoid necrosis and moderate intimal hyperplasia without fibromucoid changes (initial phase), the hypertension and the hypertensive vascular disease are completely reversible after the nephrectomy; 2) when the predominant lesions are proliferative endarteritis with fibromucoid changes (chronic phase), neither the hypertension nor the vascular disease are reversible after the left nephrectomy and during the period of follow-up. Therefore, the type of vascular lesion seems to be one important determinant of the reversibility of the hypertensive process after nephrectomy.

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“…On a pas encore élucidé le mécanisme qui cause la fragmentation des érythrocytes dans les cas de pression artérielle excessivement élevée, mais ce phénomène est souvent observé dans l'hypertension maligne [23]. Une partie des patients présente en plus une discrète thrombopénie.…”

Section: Hypertension Maligneunclassified

Diagnostic étiologique des anémies, 2e partie

Peghini¹,

Fehr²

2002

Forum Med Suisse

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Microangiopathic Hæmolytic Anæmia and the Pathogenesis of Malignant Hypertension

Cited by 98 publications

References 44 publications

Infection by verocytotoxin-producing Escherichia coli

Infection by verocytotoxin-producing Escherichia coli

Metaischemic (post-Goldblatt) hypertensive vascular disease in rats.

Diagnostic étiologique des anémies, 2e partie

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