Methemoglobinemia historical perspective

Methemoglobinemia Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Methemoglobinemia from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
Diagnostic Study of Choice
History and Symptoms
Physical Examination
Laboratory Findings
Chest X Ray
CT
MRI
Ultrasound
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Methemoglobinemia historical perspective On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Methemoglobinemia historical perspective All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Methemoglobinemia historical perspective
on Methemoglobinemia historical perspective
Methemoglobinemia historical perspective in the news
Blogs on Methemoglobinemia historical perspective
Directions to Hospitals Treating Methemoglobinemia
Risk calculators and risk factors for Methemoglobinemia historical perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Historical Perspective

• It has been reported (Heard & Ashworth 1968 apud Basrani et al. 2007) that, when placed in an aqueous solution, Chlorhexidine Gluconate (antiseptic) slowly hydrolyzes and forms para-chloroaniline (4-Chloroaniline, p-Chloroaniline or PCA) (24). Para-chloroaniline (PCA) has been shown to be toxic (28, 29). As an aromatic amine, the primary toxic effect is methemogloblin formation (28). Toxicological studies in rats and mice have shown that the hemopoietc system is the major target for PCA (28). In 1990, Chhabra et al (28) conducted a 90-day study (with p-chloroaniline) and found that methaemoglobin formation and accompanying haemolytic anaemia, extra-medullary haematopoiesis, and splenomegaly were indicative of erythrocyte toxicity and regenerative anemia.
• The Fugates, a family that lived in the hills of Kentucky, are the most famous example of this hereditary chromosomal error. Known as the Blue Fugates, Martin Fugate, settled near Hazard, Kentucky, circa 1800. His wife was a carrier of the recessivemethemoglobinemia (met-H) gene, as was a nearby clan with whom the Fugates intermarried. As a result, many descendants of the Fugates were born with met-H.

• The 'blue men of Lurgan' were a pair of Lurgan men suffering from what was described as 'familial idiopathic methaemoglobinaemia' who were treated by Dr. James Deeny in 1942. Deeny, who would later become the Chief Medical Officer of the Republic of Ireland, prescribed a course of ascorbic acid and sodium bicarbonate. In case one, by the eighth day of treatment there was a marked change in appearance and by the twelfth day of treatment the patient's complexion was normal. In case two, the patient's complexion reached normality over a month-long duration of treatment. Reference to these cases is found in the British Medical Journal, June 12, Vol. 1 ,pg. 721, written by J. Deeny, E.T. Murdock and J.J. Rogan and appears also in the book of essays, The End of an Epidemic, by James Deeny ISBN I 899047 06 9.

References

Reference to these cases is found in the British Medical Journal, June 12, Vol. 1 ,pg. 721, written by J. Deeny, E.T. Murdock and J.J. Rogan and appears also in the book of essays, The End of an Epidemic, by James Deeny ISBN I 899047 06 9. Template:WH Template:WS