[A medical biography of Ludwig van Beethoven]. / Ludwig van Beethoven, el genio de Bonn atormentado por sus enfermedades: su historia médica.

Much emphasis has been given to the deafness of Ludwig van Beethoven and its potential causes. However, when analyzing several symptoms reported by himself throughout his life in many letters and his final illness, a common etiology emerges. This article reports the medical history of this artist, based on authoritative scientific sources.

Ludwig van Beethoven, el genio de Bonn atormentado por sus enfermedades: su historia médica / A medical biography of Ludwig van Beethoven

Much emphasis has been given to the deafness of Ludwig van Beethoven and its potential causes. However, when analyzing several symptoms reported by himself throughout his life in many letters and his final illness, a common etiology emerges. This article reports the medical history of this artist, based on authoritative scientific sources.

[Beethoven's ringlets--from a medical point of view]. / Beethovens Locken--medizinisch betrachtet.

Ludwig van Beethoven suffered from various constitutional disorders, most publicly known his deafness. He died in 1827 from a decompensated liver cirrhosis. On his deathbed, admirers cut some ringlets from his head that can nowadays be used for scientific analyses. Hair analyses demonstrated that Beethoven was increasedly exposed to lead in his last 110 living days that may have contributed to the hepatic decompensation. The reason for the lead exposition was probably consumption of wines mixed with lead sugar, but also iatrogenic by lead-containing preparations administered for pneumonia in winter 1826/1827 as well as wound closure after puncturing for ascites four times.

Changes in the social class gradient of cirrhosis mortality in England and Wales across the 20th century.

AIM: To explore the nature of the social class gradient of cirrhosis mortality in England and Wales across the 20th century. METHODS: Data on male cirrhosis mortality by social class were obtained from the Registrar General's Decennial Supplements for the years 1921-1991. Data for 1941 were not collected because of the second World War. RESULTS: In 1921, cirrhosis mortality was substantially higher among the professional and managerial classes (I and II) than among the other social classes (III-V). This marked social class difference persisted until 1961 when the differences between the social classes were inconsistent. By 1991, the gradient had reversed and the lower social classes (IV and V) had the higher mortality. The excess mortality was greatest for social class V. The change in the mortality gradient is stark: in 1921social classes I and II had a cirrhosis mortality at least twice that of social classes IV and V, but by 1991 this ratio had reversed. CONCLUSIONS: The reversal in the social class gradient of cirrhosis mortality indicates a major change in risk factor distribution across social classes. Differential changes in alcohol consumption are a possible explanation for this change, although the 1991 social class gradient in cirrhosis is inconsistent with alcohol consumption data from national surveys. Further research is required to clarify the explanation for the observed gradient, so that appropriate preventive measures can be put into place.

Syphilis and cirrhosis: a lethal combination in a XIX century individual identified from the medical schools collection at the university of Coimbra (Portugal).

Syphilis is a chronic infection that is categorized by a three-stage progression. The tertiary stage may affect bones and produce distinctive skull lesions called caries sicca. This paper aims to present an unusual case of syphilis associated with a diagnosis of cirrhosis, which was recorded as the cause of death in a 28-year-old female in 1899. The appearance and distribution of the lesions were compatible with acquired syphilis, as observed in the skull from the Medical Schools Collection of the University of Coimbra. However, the cause of death was recorded as "hypertrophic cirrhosis of the liver", this is a condition that is compatible with several liver disorders, including a primary liver disorder, such as cirrhosis provoked by alcoholism, infection of the liver by syphilis pathogens or by damage to the liver from the use of mercury compounds, which was the common treatment for syphilis at the time. This paper represents a contribution to the understanding of the natural evolution of syphilis.

The liver and the waistline: Fifty years of growth.

Fifty years of the Gastroenterological Society of Australia have witnessed the changing appearance of Australians. Asian immigration has transformed the dominant urban culture from European to Eurasian, with some unique Australian attributes. Meanwhile, global conditions have altered body shape, and our sports-proud country is now fat! Thus, as in North America, Europe, China, and affluent Asia-Pacific countries, prosperity and lifestyle, cheap processed foods coupled with reduced physical activity have created an epidemic of over-nutrition resulting in overweight/obesity. Additional genetic factors are at the core of the apple shape (central obesity) that typifies over-nourished persons with metabolic syndrome. Indigenous Australians, once the leanest and fittest humans, now have exceedingly high rates of obesity and type 2 diabetes, contributing to shorter life expectancy; Asian Australians are also at higher risk. Like non-steroidal anti-inflammatory drugs (NSAIDs) and cigarette smoking, obesity now contributes much to gastrointestinal morbidity and mortality (gastroesophageal reflux disease, cancers, gallstones, endoscopy complications). This review focuses on Australian research about fatty liver, particularly roles of central obesity/insulin resistance in non-alcoholic fatty liver disease/steatohepatitis (NAFLD/NASH). The outputs include many highly cited original articles and reviews and the first book on NAFLD. Studies have identified community prevalence, clinical outcomes, association with insulin resistance, metabolic syndrome and hypoadiponectinemia, developed and explored animal models for mechanisms of inflammation and fibrosis, conceptualized etiopathogenesis, and demonstrated that NASH can be reversed by lowering body weight and increasing physical activity. The findings have led to development of regional guidelines on NAFLD, the first internationally, and should now inform daily practice of gastroenterologists.

Changing the pathogenetic roadmap of liver fibrosis? Where did it start; where will it go?

The pathophysiology of liver injury has attracted the interest of experimentalists and clinicians over many centuries. With the discovery of liver-specific pericytes - formerly called fat-storing cells, Ito-cells, lipocytes, and currently designated as hepatic stellate cells (HSC) - the insight into the cellular and molecular pathobiology of liver fibrosis has evolved and the pivotal role of HSC as a precursor cell-type for extracellular matrix-producing myofibroblasts has been established. Although activation and transdifferentiation of HSC to myofibroblasts is still regarded as the pathogenetic key mechanism of fibrogenesis, recent studies point to a prominent heterogeneity of the origin of myofibroblasts. Currently, the generation of matrix-synthesizing fibroblasts by epithelial-mesenchymal transition, by influx of bone marrow-derived fibrocytes into damaged liver tissue, and by differentiation of circulating monocytes to fibroblasts after homing in the injured liver are discussed as important complementary mechanisms to enlarge the pool of (myo-)fibroblasts in the fibrosing liver. Among the molecular mediators, transforming growth factor-beta (TGF-beta) plays a central role, which is controlled by the bone-morphogenetic protein (BMP)-7, an important antagonist of TGF-beta action. The newly discovered pathways supplement the linear concept of HSC activation to myofibroblasts, point to fibrosis as a systemic response involving extrahepatic organs and reactions, add further evidence to a more or less uniform concept of organ fibrosis in general (e.g. liver, lung, kidney), and offer innovative approaches for the development of non-invasive biomarkers and antifibrotic trials.

Miguel de Cervantes: saberes médicos, enfermedades y muerte / Miguel de Cervantes: medical knowledges, ailments and death

Existe un reconocimiento generalizado de los amplios conocimientos médicos que Cervantes poseía para su época, hasta el punto de haberse afirmado que pudo ser médico. Parte de tales saberes pudieron serle trasmitidos por su padre que era cirujano-barbero y que le legó varios libros sobre materias médicas. Sin embargo, existe un desconocimiento casi total respecto a su patobiografía y las causas que originaron su muerte. Además de una posible malaria, tomando como base su propio testimonioy aceptando como síntomas cardinales la hidropesía y la sed incoercible, se le ha diagnosticado de cirrosis hepática con desarrollo final de una diabetes mellitus. No obstante, son también posibles otras alternativas como una insuficiencia cardiaca y existen ciertos argumentos a favor de que su dolencia final pudo ser una insuficiencia renal terminal

There is no doubt about the extensive medical knowledge of Cervantes at his time and some biographers affirm that he was a physician. Probably, part of these knowledges were the legacy of his father, a barber and surgeon, that bequeathed to him several medical books. However, there is an almost absolute ignorance related to his ailments and the cause of his death. Apart from a possible malaria, some authors have diagnosed him liver cirrhosis and diabetes mellitus, taking in account the Cervantes’s own testimony, with hydropsy and uncontrollable thirst as importants findings. However, some others explanations like heart failure are possible and certain data suggest terminal renal failure as his last illness