Calcified uterine leiomyoma from an 18th-century nunnery in North Italy.

OBJECTIVE: To develop a differential diagnosis of a mass retrieved alongside skeletal remains in the crypt of the church of Santissima Annunziata of Valenza (Province of Alessandria, Northern Italy). MATERIAL: A calcified mass measuring 40 × 39 mm and 17.62 × 16.3817.62 × 16.38 mm. METHOD: The analysis utilized macroscopic assessment and histologic examination (including histochemical and immunohistochemical analyses). RESULTS: Morphological traits include an irregular and spongy external surface. Holes of different sizes lead toward the inner part of the object. A section of the mass shows an "intertwined bundle" pattern, confirmed by microscopic examination. CONCLUSIONS: Differential diagnosis determined the mass to be consistent with calcified leiomyoma. SIGNIFICANCE: Identifying uterine leiomyoma adds to the paucity of paleopathological literature on the condition and to calcified tumors more broadly. It also allows for an important discussion of women's gynecological health in the past and potentially among nulliparous women. LIMITATIONS: Neither histochemical staining nor immunohistochemical analysis demonstrated the certain muscular nature of the specimens due to the rehydration and decalcification processes, for which there are no gold standards. SUGGESTIONS FOR FURTHER RESEARCH: Calcified masses are common in the clinical literature but remain rare in paleopathological literature. Careful excavation and improved recognition of apparently calcified masses are necessary to improve recognition, diagnosis, and interpretation.

Síndrome de Fahr por hipoparatiroidismo secundario / Fahr syndrome due to secondary hypoparatiroidism

Objetivo: Describir la obtención del diagnóstico etiológico del síndrome de Fahr en una paciente sin antecedentes familiares de calcificaciones cerebrales.Caso clínico: Se presenta una paciente que ingresó con trastornos psiquiátricos,convulsiones y movimientos involuntarios. Se le realizó una tomografía computarizada de cráneo donde fue evidente gruesas y simétricas calcificaciones en ganglios basales,cerebelo y en sustancia blanca. Se diagnosticó un síndrome de Fahr por hipoparatiroidismo secundario debido a las lesiones observadas, los resultados de las pruebas hormonales y losantecedentes de tiroidectomía de varios años atrás. Fue tratada con gluconato de calcio y fenitoína. Falleció posteriormente por shock cardiogénico.Conclusión: El análisis de las características clínicas, los hallazgos de neuroimagen, las pruebas de laboratorio, los resultados anatomopatológicos y antecedentes quirúrgicos, permitieron el diagnóstico etiológico del síndrome de Fahr en esta paciente(AU)

Objective: To describe the etiological diagnosis process of Fahr syndrome in a patient with no family history of brain calcifications.Clinical case report: We report a female patient who was admitted because of psychiatric disorders, seizures and involuntary movements. A computed tomography scan of the skull was performed, which showed thick and symmetrical calcifications in the basal ganglia, cerebellum, and white matter. Fahr syndrome was diagnosed from secondary hypoparathyroidism because of the injuries observed, the results of hormonal tests, and a history of thyroidectomy from several years. She was treated with calcium gluconate andphenytoin, and subsequently died of cardiogenic shock.Conclusions: The analysis of the clinical characteristics, the neuroimaging findings, the laboratory tests, the pathological results and the surgical history, allowed the etiologicaldiagnosis of Fahr syndrome in this patient(AU)

Differential diagnosis of calcified nodules from a medieval Székely woman in Transylvania.

OBJECTIVE: To differentially diagnose two calcified objects found with the well-preserved and nearly complete skeletal remains excavated in June 2012 by the Haáz Rezso Múzeum in Odorheiu Secuiesc, Romania. MATERIAL: Two objects measuring 25.55 × 18.23 mm and 17.62 × 16.38 mm found with the skeletal remains of a probable female approximately 25-35 years old at the time of death. METHODS: Analysis utilized X-ray, SEM, EDS, CT scanning, and gross morphology to assess pathological conditions with calcification as a common sign. RESULTS: Multiple analyses of the objects revealed two roughened ovoid nodes with internal hollows and openings. Elemental analysis indicated an organic origin, likely representing calcified soft tissue. CONCLUSIONS: Differential diagnosis determined the calcified nodules to be consistent with calcified tumors, and most consistent with a calcified leiomyoma with cystic degeneration, potentially uterine. SIGNIFICANCE: The identification of the calcified nodules as most consistent with calcified uterine leiomyomas adds to the paucity of paleopathological literature on calcified leiomyomas and calcified tumors more broadly. It also allows for an important discussion of the health of women in medieval Transylvania. LIMITATIONS: Interpretation would be aided if a more precise origination within the body was known. Careful excavation and improved recognition of organic objects is necessary for a more definite diagnosis. SUGGESTIONS FOR FURTHER RESEARCH: Soft tissue calcifications are a common process in a wide variety of diseases and can arise in all areas of the body. Pathological calcifications are relatively common in modern contexts, but remain rare in paleopathological literature.

The Pellegrini-Stieda Lesion Dissected Historically.

The Pellegrini-Stieda lesion is a common finding on conventional X-rays. Whether it originates in the medial collateral ligament (MCL) of the knee or the medial head of the gastrocnemius muscle or another structure remains under debate. We discuss the difference in the articles by Pellegrini and Stieda and follow the vision on the origin of the lesion through time. A systematic research in PubMed/MEDLINE was conducted, identifying all articles on the Pellegrini-Stieda lesion and analyzing them for proposed origin of the lesion. The articles with their conclusion based on either finding during surgery or magnetic resonance imaging (MRI)/computed tomography were analyzed in more detail. Our PubMed/Medline search identified 4,997 articles. After exclusion of articles that were not on the Pellegrini-Stieda lesion and of doubles, 27 articles remained. By checking the references manually, 10 more articles were identified. Proposed origins were MCL, medial gastrocnemius, adductor magnus, vastus medialis, deep MCL, and superficial MCL. Although the MCL was most often coined as origin of the lesion (54% overall, 25% on MRI, and 57% during surgery), many cases remained undecided (50% on MRI) or no specific structure was found to be the origin (29% during surgery). There are diverse proposed origins of a calcification on the medial side of the knee. The eponymous term Pellegrini-Stieda lesion seems fitting, as it comprises two different thoughts on the origin of the lesion. MRI seems to be a noninvasive and quite accurate method for future research.

Probable hepatic capillariosis and hydatidosis in an adolescent from the late Roman period buried in Amiens (France).

Two calcified objects recovered from a 3rd to 4th-century grave of an adolescent in Amiens (Northern France) were identified as probable hydatid cysts. By using thin-section petrographic techniques, probable Calodium hepaticum (syn. Capillaria hepatica) eggs were identified in the wall of the cysts. Human hepatic capillariosis has not been reported from archaeological material so far, but could be expected given the poor level of environmental hygiene prevalent in this period. Identification of tissue-dwelling parasites such as C. hepaticum in archaeological remains is particularly dependent on preservation conditions and taphonomic changes and should be interpreted with caution due to morphological similarities with Trichuris sp. eggs.

Vessels of Stone: Lenin's "circulatory disturbance of the brain".

Many have wondered what might have become of the totalitarian state Lenin founded on merciless terror, had he not died so young. He was 52 and at the height of his power when he had his first stroke. Six months later he had another and then a third stroke three months after that. He died 3 months shy of his 54th birthday with cerebral arteries so calcified that when tapped with tweezers at the time of his autopsy, they sounded like stone. The reason for his premature atherosclerosis has yet to be explained. He had a family history of cardiovascular disease and, therefore, is suspected of having had an inherited lipid disorder. Stress too might have had a role in the progression of his atherosclerosis. However, neither would explain the extent of the calcification of his cerebral arteries identified at post mortem examination. A recently described variant of the NT5E mutation might explain such calcification, as well as Lenin's family history of cardiovascular disease, and his premature cerebrovascular attacks.

Atherosclerosis in ancient Egyptian mummies: the Horus study.

OBJECTIVES: The purpose of this study was to determine whether ancient Egyptians had atherosclerosis. BACKGROUND: The worldwide burden of atherosclerotic disease continues to rise and parallels the spread of diet, lifestyles, and environmental risk factors associated with the developed world. It is tempting to conclude that atherosclerotic cardiovascular disease is exclusively a disease of modern society and did not affect our ancient ancestors. METHODS: We performed whole body, multislice computed tomography scanning on 52 ancient Egyptian mummies from the Middle Kingdom to the Greco-Roman period to identify cardiovascular structures and arterial calcifications. We interpreted images by consensus reading of 7 imaging physicians, and collected demographic data from historical and museum records. We estimated age at the time of death from the computed tomography skeletal evaluation. RESULTS: Forty-four of 52 mummies had identifiable cardiovascular (CV) structures, and 20 of these had either definite atherosclerosis (defined as calcification within the wall of an identifiable artery, n = 12) or probable atherosclerosis (defined as calcifications along the expected course of an artery, n = 8). Calcifications were found in the aorta as well as the coronary, carotid, iliac, femoral, and peripheral leg arteries. The 20 mummies with definite or probable atherosclerosis were older at time of death (mean age 45.1 ± 9.2 years) than the mummies with CV tissue but no atherosclerosis (mean age 34.5 ± 11.8 years, p < 0.002). Two mummies had evidence of severe arterial atherosclerosis with calcifications in virtually every arterial bed. Definite coronary atherosclerosis was present in 2 mummies, including a princess who lived between 1550 and 1580 BCE. This finding represents the earliest documentation of coronary atherosclerosis in a human. Definite or probable atherosclerosis was present in mummies who lived during virtually every era of ancient Egypt represented in this study, a time span of >2,000 years. CONCLUSIONS: Atherosclerosis is commonplace in mummified ancient Egyptians.

[A dermatologist and a rheumatologist define a syndrome. George Thibierge (1856-1926), Raymond J. Weissenbach (1885-1963)]. / Ein Dermatologe und ein Rheumatologe definieren ein Syndrom: Georges Thibierge (1856-1926), Raymond J. Weissenbach (1885-1963).

For decades, G. Thibierge and R.J. Weissenbach worked at the Hôpital St. Louis in Paris, one of the first and largest dermatological centers.In 1911 they described the occurrence of subcutaneous calcification in scleroderma patients, emphasizing that this was not a coincidental finding, but rather a causal link. Since then this syndrome has been given their names worldwide.Thibierge gave his attention solely to dermatology and venereology. Weissenbach initially concentrated on the overlapping areas between dermatology and rheumatology, such as gonococcal arthritis, joint disease in Lues and psoriatic arthritis. He later dealt with all areas of rheumatology, set up a large rheuma clinic at the hospital, wrote a series of authoritative books and a considerable number of individual papers. Thus he became a rheumatologist even before the specialty rheumatology existed.

[A pregnancy of 10-years duration]. / Et "tiaarigt Svangerskab"

In January 1813 the peasant woman Randi Jonsdatter from Kvikne in Hedmark had been pregnant for 10 years. One day she slipped in her cattle-shed, and soon after "gave birth" to the remains of a decomposed stone child (lithopaedion) through an incision above her navel. The woman, who was about 50 years old, lived for many years after the "birth". This is the earliest known Norwegian case of a lithopaedion, a dead calcified fetus from an extra uterine pregnancy. The case is documented in a letter written only three months after the event. This letter is now archived in The Norwegian National Library's Manuscript Collection. The case was also published by the physician Christian Stengel at the Røros mines, in the medical periodical EYR: in 1827. Stone children occur very rarely. Only two other cases, from 1858 and 1885, are known in Norway.

Cardiovascular calcification in patients with end-stage renal disease: a century-old phenomenon.

The mortality risk from cardiovascular disease is increased in patients with end-stage renal disease (ESRD). This is due to both traditional and dialysis-specific factors. Recently, a number of the dialysis-specific risk factors have been implicated in the pathogenesis of cardiovascular calcification. These include: hyperphosphatemia, high calcium-phosphate (Ca x P) product, elevated parathyroid hormone levels, duration of dialysis, and treatment with calcium-containing phosphate binders and vitamin D analogs. The recent availability of electron beam computed tomography (EBCT) has triggered increased awareness of the occurrence of cardiovascular calcification in ESRD patients. Given the development of transient hypercalcemia with calcium-containing binders, a link between calcium load from use of calcium-containing phosphate binders and development coronary calcification has been proposed. However, a causal relationship between use of these agents and cardiovascular calcification has not been established. Moreover, this phenomenon had been recognized over a century ago, long before these phosphate binders became available. Although its pathogenesis is likely to be multifactorial, available data strongly implicate elevated serum phosphorus as the primary culprit. Furthermore, the risk of calcification may be aggravated by vitamin D therapy, particularly in patients with severe secondary hyperparathyroidism. Therefore, achieving vigorous control of serum phosphorus, Ca x P product and parathyroid hormone level might decrease cardiovascular calcification and improve survival of patients on maintenance hemodialysis. Since calcium acetate is the most cost-effective phosphate binder available, we recommend that it should remain the first line treatment of hyperphosphatemia in patients with ESRD.

As you like it, Part 3: A critique and historical review of calcification as seen with the electron microscope.

As You Like It, Part 3, is a continuation of the lectures given by the author (Ultra Path VIII and Ultra Path IX). It is a critical historical review of topics of interest to electron microscopists, attempting to show what went wrong and perhaps also why. The topics chosen this time demonstrate the prominent role electron microscopy has played in elucidating the diverse ways in which calcification can occur. The classic concept of dystropic and metastatic calcification is now inadequate to explain all observed phenomena. The electron microscope shows that calcification occurs in many different intracellular and extracellular sites and that each has its own morphology and etiology. Thus, a new classification based on ultrastructural morphology is born, but few seem to be aware of it. The author examines the ubiquitous but not too well-known phenomenon of cell remodeling, which often, but not always, leads to calcification. Topics are presented under the following headings: (1) matrical lipidic debris, (2) spherical microparticles, (3) matrix vesicles, (4) intramitochondrial calcification, (5) intralysosomal calcification, (6) calcification of collagen, (7) calcification of elastic fibers, and (8) calcification of secretory products.