Henry VIII, McLeod syndrome and Jacquetta’s curse

Stride, Peter; Floro, Kylie Lopes

doi:10.4997/jrcpe.2013.417

Cited by 5 publications

(5 citation statements)

References 22 publications

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“…Une cardiomyopathie a également été rapportée à plusieurs reprises dans la litté-rature, généralement après la cinquantaine [5,6,8]. McLeod mais ceci n'a jamais pu être formellement démontré [9]. Quant aux acanthocytes, ils donnent de magnifiques images en microscopie électronique.…”

Section: Discussionunclassified

Une cause inhabituelle d’hyperCKémie

et al. 2016

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Les élévations du taux de créatine-phospho-kinase (CPK), ou hyperCKémies, constituent le lot quotidien de nombreux myologues. Leur grande diversité étiologique rend les choses difficiles en pratique clinique, plus encore lorsque l’hyperCKémie est isolée. Mis à part les élévations transitoires liées à certaines circonstances facilement identifiables (naissance, traumatisme, exercice musculaire extrême, exposition aux statines) ou certains facteurs ethniques, de nombreuses maladies neuromusculaires peuvent en être à l’origine. Il s’agit en premier lieu des dystrophies musculaires progressives et des myopathies métaboliques (glycogénoses surtout). Les progrès obtenus dans l’identification des causes des hyperCKémies ont sensiblement progressé ces dernières années grâce, notamment, à l’utilisation plus large du NGS. Dans l’observation ci-dessous, l’accent est mis sur une cause rare d’hyperCKémie pour laquelle un marqueur érythrocytaire simple permet d’évoquer le diagnostic.

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Section: Discussionunclassified

Une cause inhabituelle d’hyperCKémie

et al. 2016

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“…It has been postulated that Henry VIII of England suffered from McLeod syndrome, as an explanation for the apparent change in his personality in adulthood, in addition to his inability to father a son [ 103 ]. However, as refuted elsewhere [ 104 ], McLeod syndrome does not affect fertility, and is not transmitted to male children, thus would not cause death in utero nor of male infants.…”

Section: Mcleod Syndromementioning

confidence: 92%

Untangling the Thorns: Advances in the Neuroacanthocytosis Syndromes

Walker

2015

JMD

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There have been significant advances in neuroacanthocytosis (NA) syndromes in the past 20 years, however, confusion still exists regarding the precise nature of these disorders and the correct nomenclature. This article seeks to clarify these issues and to summarise the recent literature in the field. The four key NA syndromes are described here–chorea-acanthocytosis, McLeod syndrome, Huntington’s disease-like 2, and pantothenate kinase- associated neurodegeneration. In the first two, acanthocytosis is a frequent, although not invariable, finding; in the second two, it occurs in approximately 10% of patients. Degeneration affecting the basal ganglia is the key neuropathologic finding, thus the clinical presentations can be remarkably similar. The characteristic phenotype comprises a variety of movement disorders, including chorea, dystonia, and parkinsonism, and also psychiatric and cognitive symptoms attributable to basal ganglia dysfunction. The age of onset, inheritance patterns, and ethnic background differ in each condition, providing diagnostic clues. Other investigations, including routine blood testing and neuroimaging can be informative. Genetic diagnosis, if available, provides a definitive diagnosis, and is important for genetic counseling, and hopefully molecular therapies in the future. In this article I provide a historical perspective on each NA syndrome. The first 3 disorders, chorea-acanthocytosis, McLeod syndrome, Huntington’s disease-like 2, are discussed in detail, with a comprehensive review of the literature to date for each, while pantothenate kinase-associated neurodegeneration is presented in summary, as this disorder has recently been reviewed in this journal. Therapy for all of these diseases is, at present, purely symptomatic.

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“…Physical conditions, including brain damage from the 1524 head injury, pain of the ulcerated wound and disgust at the smell, other leg ulcers, other health problems and their consequences. Genetic predisposition, including McLeod's syndrome 38 and Cushing's syndrome. 39 Henry had leg ulcers for many years, and was treated by the same team of doctors.…”

Section: The Questionmentioning

confidence: 99%

A hypothesis: King Henry VIII’s (1491–1547) personality change: A case of lead poisoning?

Charlton

2017

J Med Biogr

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Henry VIII (1491-1547) became King of England in 1509. He started out as a good monarch, sensible, reasonable and pleasant, but later his behaviour changed drastically. He became irascible, intolerant, violent and tyrannical. In January 1536, Henry had a serious jousting accident and was unconscious for 2 h. It is generally believed that this accident played a major role in his personality change. Letters of that time, however, indicate that the change began insidiously in 1534 and became most drastic in 1535, a year before the accident. Henry had suffered from leg ulcers before and after the accident and had been constantly treated for them for many years. Sloane MS1047, now in the British Library in London, contains the prescriptions for the medications used to treat these ulcers. Many of the medications contain a high proportion of lead in various forms. Lead can be absorbed through skin, especially damaged skin. Absorbed lead can affect the brain, causing psychiatric problems, especially those associated with violence. The author presents a hypothesis that absorbed lead from his medications might have been a major factor in King Henry's personality change.

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Henry VIII, McLeod syndrome and Jacquetta’s curse

Cited by 5 publications

References 22 publications

Une cause inhabituelle d’hyperCKémie

Une cause inhabituelle d’hyperCKémie

Untangling the Thorns: Advances in the Neuroacanthocytosis Syndromes

A hypothesis: King Henry VIII’s (1491–1547) personality change: A case of lead poisoning?

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