Pathophysiology of acute falciparum malaria

Malloy, John P.; Brooks, Marion H.; Barry, Kevin G.

doi:10.1016/0002-9343(67)90116-7

Cited by 46 publications

(12 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This is considered unlikely since values for the concentration of serum 'I-T, decreased rather than increased as one would have predicted with hemoconcentration, and no change was noted in estimates of To distribution space. In this regard, studies of fluid compartmentalization during acute falciparum malaria have revealed that vasodilation occurs, with increases in plasma volume secondary to a compensatory shift of fluid into the vascular space (27). This might lead to a shortened To half-life during acute infection, which makes the observation of a decreased To turnover even more remarkable.…”

Section: Methodsmentioning

confidence: 99%

Alterations in thyroid iodine release and the peripheral metabolism of thyroxine during acute falciparum malaria in man

Wartofsky¹,

Martı́n²,

Earll³

1972

J. Clin. Invest.

View full text Add to dashboard Cite

A B S T R A C T Previous studies of thyroid function during various infections have yielded conflicting results, but most have suggested an acceleration of peripheral thyroxine (Ti) turnover during the acute infectious illness. In the present studies, thyroid function was examined by a method allowing simultaneous analysis of both endogenous thyroidal release and peripheral To disposal in normal volunteers after induction of acute falciparum malaria. Subjects received iodide-'I, followed in 5-7 days by 'I-T4 intravenously. 4 days later, infection was induced by the injection of parasitized red blood cells. Bidaily measurements of serum protein-bound 'I and protein-bound 'I, and urinary 125I and 'I, together with frequent estimates of serum "'I-T4 (Murphy-Pattee) and free T4 (FT4), were made during a control period, during acute illness, and during convalescence. Alterations in the peripheral metabolism of '"'I-T4 during infection included significant decreases in the fractional disappearance rate for To [(k)], and in the clearance and daily disposal of T4, all of which returned to control values during convalescence. Total serum 'I-T4 increased late in the infected period to become greater during convalescence than either before or during infection, while FT4 did not increase significantly until convalescence. An analysis of serum 'I-T4/I-Ti and 'I-T4/ PB'I ratios confirmed these observations. The slope with time of ratios for urinary 'I/I, a reflection of thyroidal iodine release, was decreased during infection, but rebounded to control values during the convalescent period. The observed increments in serum 'I-T, concentration in the convalescent phase mnay reflect in part A preliminary report on this work appeared in abstract form in 1971. Clin. Res. 19: 384.

show abstract

Section: Methodsmentioning

confidence: 99%

Alterations in thyroid iodine release and the peripheral metabolism of thyroxine during acute falciparum malaria in man

Wartofsky¹,

Martı́n²,

Earll³

1972

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…Hypotension is rare [59] and measurements of cardiac output [59], circulating volume [81,82] and total body water [83][84][85] are all normal or slightly elevated. Renal failure observed in severe adult malaria is not related to hypovolaemia [59,81,82].…”

Section: Circulatory Failurementioning

confidence: 99%

Severe Malaria: Metabolic Complications

Planche¹,

Krishna²

2006

CMM

View full text Add to dashboard Cite

Metabolic complications of severe malaria are some of the most important and potentially treatable manifestations of this deadly disease. The commonest metabolic complications (lactic acidosis and hypoglycaemia) arise from increased host anaerobic metabolism probably due to a mismatch between tissue oxygen supply and requirement. Optimising treatments for these complications should be guided by detailed understanding of their underlying pathophysiology, and may help to reduce the intolerably high case fatality rate of severe malaria.

show abstract

“…The pathophysiology of malaria has been most carefully studied in infections of nonimmune individuals with P. falciparum [57,58]. At present, the following sequence of events during severe infection with P. falciparum is plausible.…”

Section: Host Responses To Malarial Infectionmentioning

confidence: 99%

“…Secretion of antidiuretic hormone and aldosterone increases [58] and causes a decrease in free-water clearance. When the degree of renal water resorption exceeds sodium conservation, hyponatremia results.…”

Section: Host Responses To Malarial Infectionmentioning

confidence: 99%

Malaria: Host-Pathogen Biology

Wyler

1982

Clinical Infectious Diseases

View full text Add to dashboard Cite

Pathophysiology of acute falciparum malaria

Cited by 46 publications

References 20 publications

Alterations in thyroid iodine release and the peripheral metabolism of thyroxine during acute falciparum malaria in man

Alterations in thyroid iodine release and the peripheral metabolism of thyroxine during acute falciparum malaria in man

Severe Malaria: Metabolic Complications

Malaria: Host-Pathogen Biology

Contact Info

Product

Resources

About