Hibernation, Puberty and Chronic Kidney Disease in Troglodytes from Spain Half a Million Years Ago
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Metabolic Bone Disease 5
g Metabolic Bone Disease 5 Introduction, 272 History and examination, 275 Osteoporosis, 283 STRUCTURE AND FUNCTION, 272 Investigation, 276 Paget’s disease of bone, 288 Structure of bone, 272 Management, 279 Hyperparathyroidism, 290 Function of bone, 272 DISEASES AND THEIR MANAGEMENT, 280 Hypercalcaemia of malignancy, 293 APPROACH TO THE PATIENT, 275 Rickets and osteomalacia, 280 Hypocalcaemia, 295 Introduction Calcium- and phosphate-containing crystals: set in a structure• similar to hydroxyapatite and deposited in holes Metabolic bone diseases are a heterogeneous group of between adjacent collagen fibrils, which provide rigidity. disorders characterized by abnormalities in calcium At least 11 non-collagenous matrix proteins (e.g. osteo- metabolism and/or bone cell physiology. They lead to an calcin,• osteonectin): these form the ground substance altered serum calcium concentration and/or skeletal fail- and include glycoproteins and proteoglycans. Their exact ure. The most common type of metabolic bone disease in function is not yet defined, but they are thought to be developed countries is osteoporosis. Because osteoporosis involved in calcification. is essentially a disease of the elderly, the prevalence of this condition is increasing as the average age of people Cellular constituents in developed countries rises. Osteoporotic fractures may lead to loss of independence in the elderly and is imposing Mesenchymal-derived osteoblast lineage: consist of an ever-increasing social and economic burden on society. osteoblasts,• osteocytes and bone-lining cells. Osteoblasts Other pathological processes that affect the skeleton, some synthesize organic matrix in the production of new bone. of which are also relatively common, are summarized in Osteoclasts: derived from haemopoietic precursors, Table 3.20 (see Chapter 4). -
A Case of Osteitis Fibrosa Cystica (Osteomalacia?) with Evidence of Hyperactivity of the Para-Thyroid Bodies
A CASE OF OSTEITIS FIBROSA CYSTICA (OSTEOMALACIA?) WITH EVIDENCE OF HYPERACTIVITY OF THE PARA-THYROID BODIES. METABOLIC STUDY II Walter Bauer, … , Fuller Albright, Joseph C. Aub J Clin Invest. 1930;8(2):229-248. https://doi.org/10.1172/JCI100262. Research Article Find the latest version: https://jci.me/100262/pdf A CASE OF OSTEITIS FIBROSA CYSTICA (OSTEOMALACIA?) WITH EVIDENCE OF HYPERACTIVITY OF THE PARA- THYROID BODIES. METABOLIC STUDY IIF By WALTER BAUER,2 FULLER ALBRIGHT3 AND JOSEPH C. AUB (From the Medical Clinic of the Massachutsetts General Hospital, Boston) (Received for publication February 5, 1929) INTRODUCTION In a previous paper (1) we have pointed out certain characteristic responses in the calcium and phosphorus metabolisms resulting from parathormone4 administration to essentially normal individuals. In the present paper, similar studies will be reported on a patient who presented a condition suggestive of idiopathic hyperparathyroidism. CASE HISTORY The patient, Mr. C. M., sea captain, aged 30, was transferred from the Bellevue Hospital Service to the Special Study Ward of the Massachusetts General Hospital through the courtesy of Dr. Eugene F. DuBois, for further investigation of his calcium metabolism and for consideration of parathyroidectomy. His complete case history has been reported by Hannon, Shorr, McClellan and DuBois (2). It describes a man invalided for over three years with symptoms resulting from a generalized skeletal decalcification. (See x-rays, figs. 1 to 4.) 1 This is No. VII of the series entitled "Studies of Calcium and Phosphorus Metabolism" from the Medical Clinic of the Massachusetts General Hospital. 2 Resident Physician, Massachusetts General Hospital. ' Research Fellow, Massachusetts General Hospital and Harvard Medical School. -
CKD: Bone Mineral Metabolism Peter Birks, Nephrology Fellow
CKD: Bone Mineral Metabolism Peter Birks, Nephrology Fellow CKD - KDIGO Definition and Classification of CKD ◦ CKD: abnormalities of kidney structure/function for > 3 months with health implications ≥1 marker of kidney damage: ACR ≥30 mg/g Urine sediment abnormalities Electrolyte and other abnormalities due to tubular disorders Abnormalities detected by histology Structural abnormalities (imaging) History of kidney transplant OR GFR < 60 Parathyroid glands 4 glands behind thyroid in front of neck Parathyroid physiology Parathyroid hormone Normal circumstances PTH: ◦ Increases calcium ◦ Lowers PO4 (the renal excretion outweighs the bone release and gut absorption) ◦ Increases Vitamin D Controlled by feedback ◦ Low Ca and high PO4 increase PTH ◦ High Ca and low PO4 decrease PTH In renal disease: Gets all messed up! Decreased phosphate clearance: High Po4 Low 1,25 OH vitamin D = Low Ca Phosphate binds calcium = Low Ca Low calcium, high phosphate, and low VitD all feedback to cause more PTH release This is referred to as secondary hyperparathyroidism Usually not seen until GFR < 45 Who cares Chronically high PTH ◦ High bone turnover = renal osteodystrophy Osteoporosis/fractures Osteomalacia Osteitis fibrosa cystica High phosphate ◦ Associated with faster progression CKD ◦ Associated with higher mortality Calcium-phosphate precipitation ◦ Soft tissue, blood vessels (eg: coronary arteries) Low 1,25 OH-VitD ◦ Immune status, cardiac health? KDIGO KDIGO: Kidney Disease Improving Global Outcomes Most recent update regarding -
Pathological Fracture of the Tibia As a First Sign Of
ANTICANCER RESEARCH 41 : 3083-3089 (2021) doi:10.21873/anticanres.15092 Pathological Fracture of the Tibia as a First Sign of Hyperparathyroidism – A Case Report and Systematic Review of the Current Literature ALEXANDER KEILER 1, DIETMAR DAMMERER 1, MICHAEL LIEBENSTEINER 1, KATJA SCHMITZ 2, PETER KAISER 1 and ALEXANDER WURM 1 1Department of Orthopaedics and Traumatology, Medical University of Innsbruck, Innsbruck, Austria; 2Institute for Pathology, INNPATH GmbH, Innsbruck, Austria Abstract. Background/Aim: Pathological fractures are rare, of the distal clavicles, a “salt and pepper” appearance of the suspicious and in some cases mentioned as the first sign of a skull, bone cysts, and brown tumors of the bones (3). malignant tumor. We present an uncommon case with a Primary hyperparathyroidism (PHPT), also known as “brown pathological fracture of the tibia diaphysis as the first sign of tumor”, also involves unifocal or multifocal bone lesions, which severe hyperparathyroidism. Case Report: We report the case represent a terminal stage of hyperparathyroidism-dependent of a female patient who was referred to the emergency bone pathology (4). This focal lesion is not a real neoplasm. In department with a history of progressively worsening pain in localized regions where bone loss is particularly rapid, the lower left leg and an inability to fully bear weight. No hemorrhage, reparative granulation tissue, and active, vascular, history of trauma or any other injury was reported. An x-ray proliferating fibrous tissue may replace the healthy marrow revealed an extensive osteolytic lesion in the tibial shaft with contents, resulting in a brown tumor. cortical bone destruction. Conclusion: Our case, together with Histologically, the tumor shows bland spindle cell very few cases described in the current literature, emphasizes proliferation with multinucleated osteoclastic giant cells and that in the presence of hypercalcemia and lytic lesions primary signs of bone resorption. -
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extrait du symposium REIN ET CALCIUM les trois epis (haut-rhin) 14-17decembre 1972 A SANDOZ EDITIONS HYPERPARATHYROIDISM AFTER KIDNEY HOMOTRANSPLANTATION I. RELATION TO HOMOGRAFT FUNCTION M.M. POPOVTZER, W.P. GElS, T. E. STARZL Departments of Medicine and Surgery. Division of Renal Diseases. University of Colorado Medical Center and Veterans Administration Hospital. Denver. Colorado. U.S.A. INTRODUCTION Secondary hyperparathyroidism is present in most patients with chronic renal failure (11. 20. 21). The effect of renal transplan tation on parathyroid function has been generally studied over a relatively short period of time after surgery (1. 6). Thus the information which could be obtained was insufficient to provide evidence regarding the long-term variations in the parathyroid activity in renal homograft recipients. Acute .hypercalcemia immediately after kidney transplantation has been reported in detail by several investigators (12. 11. 19). Parathyroidectomy which was the treatment of choice resulted in a prompt reduction of the high serum calcium concentrations and a relief. of the attendant clinical manifestations in the reported cases (12. 11. 19). The pathogenesis of acute post-transplant hypercalcemia has not 145 been fully defined, yet several contributing factors could be implicated: (1) the presence of high levels of parathyroid hormone with restored to normal bone responsiveness to the hormone, (2) fall in serum concentration of phosphorus with a reciprocal rise in serum calcium, and (3) correction of the abnormal meta bolism of Vitamin 0 with an enhanced conversion of the vitamin to its active metabolites. Several workers postulated that resolution of secondary hyper parathyroidism after kidney transplantation occurs almost uni versally whereas hypercalcemia is unfrequent and if present it is usually associated with phosphate depletion and can be easily controlled with phosphate supplementation (1, 6, 7). -
Abstracts of the Panhellenic Conference of the Hellenic
Journal of Research and Practice on the Musculoskeletal System JOURNAL OF RESEARCH AND PRACTICE ON THE MUSCULOSKELETAL SYSTEM Proceedings Abstracts of the Panhellenic Conference of the Hellenic Osteoporosis Foundation 13th-15th September 2019, Volos, Greece Organizer: George Kapetanos Emeritus Professor of Orthopaedics, Faculty of Medicine, Aristotle University of Thessaloniki, Greece President of Hellenic Osteoporosis Foundation SARCOPENIA-FALLS AND HIP FRACTURES issue. Reduction in physical function can lead to loss of Styliani Papakosta independence, need for hospital and long-term nursing “ΕΥ PRATTEIN- KENTAVROS” & ΕΛ.Ε.Π.Α.Π. Volou Rehabilitation home care and premature death. Prevention of sarcopenia Center, Greece and falls includes exercises, cognitive and physical training, dietary and psychological support. Additional Sarcopenia is the degenerative loss of skeletal muscle research, preferably by means of controlled randomized mass, quality, strength and functionality associated with trials, is needed to confirm these findings. aging. It is a component of the frailty syndrome. Severity of sarcopenia is associated with postural balance and falls especially among community older people. Falls of A COMPREHENSIVE MANAGEMENT OF SARCOPENIA elderly people cause severe injuries such as femoral neck AND BONE LOSS - OSTEOSARCOPENIA SCHOOL fracture and can lead the patient to become bed-ridden. Frailty, sarcopenia and falls are strongly correlated and Yannis Dionyssiotis st both are predictors of negative health outcomes such 1 Physical Medicine & Rehabilitation Department, National as falls, disability, hospitalization and death. Multiple Rehabilitation Center EKA-KAT, Athens, Greece factors contribute collectively to frailty, sarcopenia and In older persons, the combination of osteopenia/ falls, which include cellular and tissue changes, as well osteoporosis and sarcopenia - known as osteosarcopenia as environmental and behavioral factors. -
A Patient with a History of Breast Cancer and Multiple Bone Lesions
Schnyder et al. Journal of Medical Case Reports (2017) 11:127 DOI 10.1186/s13256-017-1296-1 CASE REPORT Open Access A patient with a history of breast cancer and multiple bone lesions: a case report Marie-Angela Schnyder1*, Paul Stolzmann2, Gerhard Frank Huber3 and Christoph Schmid1 Abstract Background: Long-term severe hyperparathyroidism leads to thinning of cortical bone and cystic bone defects referred to as osteitis fibrosa cystica. Cysts filled with hemosiderin deposits may appear colored as “brown tumors.” Osteitis fibrosa cystica and brown tumors are occasionally visualized as multiple, potentially corticalis-disrupting bone lesions mimicking metastases by bone scintigraphy or 18F-fluorodeoxyglucose positron emission tomography. Case presentation: We report a case of a 72-year-old white woman who presented with malaise, weight loss, and hypercalcemia. She had a history of breast cancer 7 years before. The practitioner, suspecting bone metastases, initiated bone scintigraphy, which showed multiple bone lesions, and referred her to our hospital for further investigations. Laboratory investigations confirmed hypercalcemia but revealed a constellation of primary hyperparathyroidism and not hypercalcemia of malignancy; in the latter condition, a suppressed rather than an increased value of parathyroid hormone would have been expected. A parathyroid adenoma was found and surgically removed. The patient’s postoperative course showed a hungry bone syndrome, and brown tumors were suspected. With the background of a previous breast cancer and lytic, partly corticalis-disrupting bone lesions, there was a great concern not to miss a concomitant malignant disease. Biopsies were not diagnostic for either malignancy or brown tumor. Six months after the patient’s neck surgery, imaging showed healing of the bone lesions, and bone metastases could be excluded. -
Primary Hyperparathyroidism and Osteoporosis• a Case Report
292 SA MEDICAL JOURNAL VOLUME 63 19 FEBRUARY 1983 Primary hyperparathyroidism and osteoporOsIs• A case report M. SANDLER U). A skeletal survey was negative except for diffuse osteopenia Summary in the skull, clavicles, lumbar spine and pelvis - butno evidence of bone fracture. Subsequent investigation of the hypercalcae A case of osteoporosis secondary to primary hyper mia confirmed the diagnosis of primary hyperparathyroidism. parathyroidism is reported. A 55-year-old woman She underwent surgical exploration of the neck and a parathy presented with a history of persistent lumbar back roid adenoma was removed. Calcium levels then returned to ache for 3 years; numerous radiographs taken normal and have remained so over the 3 postoperative months. during this period had shown 'osteoporosis in keep There has also been some subjective improvement of the back ing with age'. Referral to the Endocrine Clinic to ache. evaluate the osteoporosis resulted in baseline inves tigations which revealed a raised serum calcium level, further investigation of which led to the diag Discussion nosis of primary hyperparathyroidism. Recent stu dies have shown that, over the past two decades, There has been a recent trend for patients with primary hyper diffuse undermineralization of the bones (osteo parathyroidism to present with radiological evidence of diffuse penial is the most common radiological feature in osteopenia as opposed to the more classic changes of subperios primary hyperparattiyroidism. teal bone resorption or osteitis fibrosa cystica. In a study of 138 cases of primary hyperparathyroidism from 1930 to 1960, it was S AIr Med J 1983: 63: 292. found that between 1930 and 1939, 53% of patients had sympto matic and radiographic evidence of osteitis fibrosa cystica, whereas 21 %showed the same features between 1949 and 1960. -
Human Osteology Method Statement N
Human osteology method statement N. Powers (ed) Published online March 2008 Revised February 2012 2 LIST OF CONTRIBUTORS Museum of London Archaeology Centre for Human Bioarchaeology Service (MoLAS) (CHB) Brian Connell HND MSc Jelena Bekvalac BA MSc Amy Gray Jones BSc MSc Lynne Cowal BSc MSc Natasha Powers BSc MSc MIFA RFP Tania Kausmally BSc MSc Rebecca Redfern BA MSc PhD Richard Mikulski BA MSc Don Walker BA MSc AIFA Bill White Dip Arch FRSC FSA 3 CONTENTS Introduction ........................................................................................................................ 8 1 Preservation and archaeological data................................................................... 9 2 Catalogue of completeness ................................................................................... 10 2.1 Cranial elements ..................................................................................................... 10 2.2 Post-cranial elements.............................................................................................. 10 2.3 Cartilage.................................................................................................................. 11 2.4 Dentition ................................................................................................................. 11 3 Age at death estimation........................................................................................ 12 3.1 Subadult age at death............................................................................................. -
A Rare Manifestation of Primary Hyperparathyroidism Vikram Singh Shekhawat, Anil Bhansali
Images in… BMJ Case Reports: first published as 10.1136/bcr-2017-220676 on 1 August 2017. Downloaded from Vanishing metatarsal: a rare manifestation of primary hyperparathyroidism Vikram Singh Shekhawat, Anil Bhansali Department of Endocrinology, DESCRIPTION Post Graduate Institute A 31-year-old woman presented with a history of Medical Education and of bone pains, difficulty in walking and painless Research, Chandigarh, India swelling of the left foot for the last 1 year (figure 1). X-ray of the left foot showed multiple lytic lesions Correspondence to Dr Anil Bhansali, in metatarsal bones and the absence of proximal anilbhansa lien docr ine@ gma il. half of shaft of second metatarsal. Biochemistry com, ashuendo@ gmail. com results revealed corrected serum calcium 11.2 mg/ dL, phosphate 2.0 mg/dL, alkaline phosphatase Accepted 25 July 2017 1049 IU/mL, intact parathyroid hormone (iPTH) 2543 pg/mL, 25-hydroxyvitamin D 16.2 ng/mL, and serum creatinine 0.6 mg/dL. She had no history of pancreatitis or evidence of renal/gall stone disease. The skeletal survey showed multiple osteitis fibrosa cystica (OFC) lesions, pathological Figure 2 (A) X–ray of both foot showing generalised fracture of shaft of the left femur and salt and demineralization of foot bones, multiple lytic lesions pepper appearance of the skull (figure 2a, b, c). (brown tumours) and apparent disappearance of proximal Sestamibi scan revealed right inferior parathyroid half of second metatarsal of the left foot. (B) X–ray of adenoma measuring 3.0×2.9×2.2 cm. Based on pelvis showing ill-defined lucencies in bilateral iliac, pubic the above findings, a diagnosis of primary hyper- and ischial bones, and pathological fracture of left femur. -
Clinical and Laboratory Considerations in Metabolic Bone Disease
ANNALS OF CLINICAL AND LABORATORY SCIENCE, Vol. 5, No. 4 Copyright ® 1975, Institute for Clinical Science Clinical and Laboratory Considerations in Metabolic Bone Disease LYNWOOD H. SMITH, M.D. AND B. LAWRENCE RIGGS, M.D. Mayo Clinic and Mfiyo Foundation Rochester, MN 55901 ABSTRACT An overview of the common types of metabolic bone disease is described. When the disease is present in pure form, diagnosis is not difficult. When mixed disease is present, as may be the case, the pathophysiology involved must be clearly under stood for accurate diagnosis and treatment. Introduction opausal or senile osteoporosis, a disorder of unknown etiology, is the commonest form of There are many metabolic disorders that bone disease in the Western hemisphere. affect human bones; but, fortunately, the This disorder may simply represent an exag ways in which bones can respond are limited geration of the normal loss of bone that oc so that certain generalizations are valid for a curs with aging. It is estimated that the total group of diseases causing a characteristic bone loss between youth and old age is metabolic abnormality in the bone. The about 35 percent in women and somewhat common pathologic responses to metabolic less in men. The loss of bone that has oc bone disease include osteoporosis, os curred in some patients with osteoporosis is teomalacia, Paget’s disease, osteitis fibrosa not significantly different from that in age- cystica and renal osteodystrophy. These are matched normals without osteoporosis. not mutually exclusive, and it is not uncom In osteoporosis there is a greater propor mon to find more than one abnormality in tional loss of trabecular than of cortical the same patient. -
Orthopedic Consideration of Hyperparathyroidism
University of Nebraska Medical Center DigitalCommons@UNMC MD Theses Special Collections 5-1-1935 Orthopedic consideration of hyperparathyroidism J. E. Jacobs University of Nebraska Medical Center This manuscript is historical in nature and may not reflect current medical research and practice. Search PubMed for current research. Follow this and additional works at: https://digitalcommons.unmc.edu/mdtheses Part of the Medical Education Commons Recommended Citation Jacobs, J. E., "Orthopedic consideration of hyperparathyroidism" (1935). MD Theses. 633. https://digitalcommons.unmc.edu/mdtheses/633 This Thesis is brought to you for free and open access by the Special Collections at DigitalCommons@UNMC. It has been accepted for inclusion in MD Theses by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. The ORTHOPEDIC CONSIDERATION of' HYPERPARATHYROIDISM by J. E. Jacobs, B. A. A Thesis Submitted to the Faculty of the University of Nebraska College of Medicine in Partial Fulfillment of the Requirements for the Degree of Doctor of' Medicine. 1935. TABLE OF CONTENTS Pages I. INTRODUCTION -------------------- 1-2 II. HISTORY -------------------- 3-7 III. ETIOLOGY -------------------- 8-13 IV. PATHOLOGICAL PHYSIOLOGY 14-24 ~---------------............ v. CLINICAL SYMPTOMATOLOGY -------------------- 25-31 VI. DIAGNOSIS -------------------- 32-36 VII. DIFFERENTlAL DIAGNOSIS -------------------- 37-51 A. Skeletal System 1. Osteoporosis 2. Osteitis Deformans 3. Osteomalacia 4. Focal Osteitis Fibrosa 5. Polycystic Osteitis Fibrosa 6. Multiple Bone Cysts 7. Giant Cell Tumors 8. Osteitis Tuberoulosa Multiplez Cystica 9. Osteogenesis Imperfeota 10. Xanthomatosis Generalisata Ossium 11. Multiple Myeloma 12. Metastatic Malignancy 13 •. Ankylosing Polya.rthritis 14. Miscellaneous Group B. Muscular System c. Renal System VIII. PROGNOSIS -------------------- 52 IX. TREATMENT -------------------- 52-55 x.