DOCSLIB.ORG

A Case of Osteitis Fibrosa Cystica (Osteomalacia?) with Evidence of Hyperactivity of the Para-Thyroid Bodies

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
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. 4 Parathormone is Eli Lilly and Co.'s trade name for Collip's parathyroid extract. 229 230 OSTEITIS FIBROSA CYSTICA. II I' A)A r:.. *: .u.. Por .J. .4 ...... Ad, FIG. 1. X-RAY OF RIGHT HAND SHOWING MODERATE GENERALIZED DECAL- CIF1CATION AND COARSE TRABECULATIONS W. BAUER, F. ALBRIGHT AND J. C. AUB 231 u z .. I.;;:. A FIG. 2. X-RAY OF RIGHT SHOULDER SHOWING OLD FRACTURE AT THE LOWER END OF THE HUinERUS. ABSENCE OF MOST OF THE BoNE TRABECULAE IN THE MIDDLE HALF, WITH THINNING OF THE CORTEX AND SLIGHT BULGING OF THE SHAFT. AiLSO INDEFINITELY DEFINED CYSTIC AREAS IN THE LOWER THIRD. 232 OSTEITIS FIBROSA CYSTICA. II q FIG. 3. X-RAY OF RIGHT FEMUR SHOWING A CYSTic AREA ABOUT 1 INCH IN DIAMETER IN THE UPPER THIRD just above and lateral to this area are two smaller areas of similar appearance W. BAUER, F. ALBRIGHT AND J. C. AUB 233 _.s".t .. ..:: wtj _.. ;s . v vY.^F .: .. x JF :8. ..... t _... ..._EN .,. :s s.N .. sr ' e l_ i ; ...... ... FB. <22R*^ .. s :.: s , .. s . w _. w :_. .F t; / *i ^-.i d... :s - :s S - :: e. #X^ e ._: r ,' a __i. g. .":: f _B } f: .t ._s FIG. 4. X-RAY OF THE LEFT HUMERUS SHOW\IN\G WAELL-DEFINED ATROPHY WITH THINNING OF THE CORTEX AND IRREGULARITY IN THE HEAD OF THE H1U- MERUS IN THE REGION OF THE TUBEROSITY. 234 OSTEITIS FIBROSA CYSTICA. II FIcG. 5. FITAMS OF THE SKULL SHOW THE POSTERIOR PORTION OF THE CALVARIUM TO 13E THINNER THAN USUAL The bone in the frontal region appears to be thickened and has a rather mottled appearance. EXPERIMENTAL DATA The investigation, in accordance with the principles set forth in previous papers (3), consisted of complete calcium, phosphorus and nitrogen metabolism studies as well as frequent determinations of the serum calcium and serum phosphorus. Whereas our previous studies have been confined almost entirely to low calcium intakes, in this study some periods on a high calcium diet were also included for three reasons. In the first place, we wished to confirm the findings of the Cornell group, who had studied this patient while on a relatively high calcium diet. Secondly, it seemed essential from a therapeutic standpoint to determine whether a positive calcium balance could be maintained on a high calcium diet. Lastly, because of the patient's marked skeletal decalcification, it was not considered wise to study him for more than a very short period on a low calcium diet. During the patient's stay in the Hospital, two normal parathyroid glands were removed by Dr. Edward P. Richardson. Our studies include periods of high and low calcium diet before and after the operations. W. BAUER, F. ALBRIGHT AND J. C. AUB 235 The methods employed in the collection of the excreta and in the analyses of the material have been given in previous papers (3 and 4). The details of the operations and the pathological reports of the tissues removed are given in the appendix (q. v.). The essential point is that two normal appearing parathyroid glands were removed at operation. RESULTS In table 1 and charts 1A, 1B, and IC are found the data for the calcium, phosphorus and nitrogen excretion. Each study period is three days unless otherwise indicated. In table 1 are also included the serum calcium and serum phosphorus values. A. Serum calcium and serum phosphorus On examination of these blood findings one notes that the serum calcium is markedly elevated above normal and that the serum phos- phorus is considerably reduced below normal; indeed relatively more than the serum calcium is elevated. Such a fall of the blood phos- phorus we have found to be the case on administration of parathor- mone, provided that the serum calcium does not rise sufficiently high to produce a secondary phenomenon which is associated with a marked increase of the serum phosphorus. The serum calcium in this patient was not sufficiently high to produce this phenomenon and the low serum phosphorus is in accordance with the findings in patients receiv- ing parathormone. The removal of the two parathyroid glands was apparently without effect on the blood findings. B. Metabolism findings The discussion of the metabolic findings (table 1 and charts 1A, lB and 1C) will be divided into four parts. a. A comparison of the findings before operation, while the patient was on a low calcium diet, with those of normal individuals on a similar diet. b. A comparison of the findings in respect to both calcium and phosphorus metabolism before operation while the patient was on a low calcium diet with those of an individual receiving 100 units of parathormone per day. 0 0 0 ..0 'e ;.W - a 0 E >, 01 c$ u: nO0 .! -~ .T- E snloqdsoq,j t4 0') 00.-. 01 o0 '.0 0 - ') C.) en~~') 0 )14 "r) e1),0 0 0 Q 0000 00 .0 m 00 0000- 0 ---- o -- - r, 00 0 0~ 0 0, 00000 00)0 00 C C 000 000 o -0..-<D ) \0 00in).-. I t0CD1. \- o'-V I0i+II+TI ++++++ + + 00U n00 00 00 0o-o'e)0C,m00C- 000 00 00 0 10 - O m01 0) CD0 C'~) In0In 00) r CD10 D010 C)1CD C)10 0 0C 0 C~010-0t0c i; C,00oo 10) 0,I 00010 0,0 07q c * 0 \-100t"00>- 00I r --0n1 \0 t- .C0-100,0o- 00 o 00 00 01 > 0 ) - 0=- 01~~~~~~~~~~~~~~~~"' 0--t ,00 011rq,- \0 C\01 C oC ,00) C> 0110 00 C 1C)0N00o00o )en 00~ C400\- Il c 0 C1 ON100110o .. 00 0-00000-00 ) 1 0100 c ;00 t-', 14~ 101iiwi 00C c010)t00 0C-4 c) oo,o') 1o 00 0 0 e 0 0 \010 01 01 C,10 n W010-0 00o 0 I 0 001000000100-t t 0) 0 00r 1~0)ell C) C- 00\00 00 0C 000 )0000000 0 0 0 0 )C)--00-- C0- c 00,0 0 0-0 n 00 \01 01 0 110)0t--C1 0 0100 0) 0n 01v 000-o-.10o'en000C, m'0o 00 "It \0 \0\0 \00- \0 )0100 00 ' C)~ 100 1 0 0001!"0010) 00 0q-!I0 - 000-1\000)- 1nll 000 00 ox 0S 00 00C.!'-00001O0 o 0 0) C)0 00)-o-0C C )C 0C)0)0) 0 C)- 00 C) C, C:00) cD 00 01- 000C\0-01,,, o 0- C,--00 00001 0101400000 \00')~ -17 0 0 .~~~~~~ ~ ~~~~ 0-~~~ -0 t 000-" 0)0000001rt 1- 00)- C) In C,, t- 10 NO N00 -00) 0-0.W. oz ddooooo\oo-0e l 0 0000000oI-~ ~ *@.- D . " c 010\0C \00 0\ 10 C0 00 0t-'0 It000m- 010 -0' '0 O0 ; 0) r')1C)01C00000000100)00U'O"A." 00) 0D 10 -o000000-)-C0a,0- 00 0-0 \0,t- C C 0 0-4 U- ) - c-0-0 '0 \ 1LI)A 0 10 10 00 01 1- 00) 00)00)00\. 00) 0000tnr 00 0100 0) r 01° 000Q0000000000 00 C 000000 0 0 0 0 0 0 C 00t U -00t0-10In0 'IO0 C1t-00cl 236 W. BAUER, F. ALBRIGHT AND J. C. AUB 237 c. A comparison of the findings while the patient was on a high calcium diet with the findings of the Cornell group (2). d. A comparison of the findings, during both high and low calcium periods before operation, with similar periods after operation. In a previous paper (3) giving the calcium excretion of normal individuals on a low calcium diet, it was pointed out that before GM OsTeomalocia + + (7.51) 6.0 - Charles M. df IG.i 275890 5.5 E8 a X +++ 5.0 _ C 45 -- o3. so35F1-C-+M%-~>_ i 4E t6 E10 + 4, i 25 1Ia01,62 8aJn 4i4uy1 92 U69~ et81Ot quniaiecmaioscudb mad wlithCear tote 4acu meaols-ewe iniiul,fctrtaoobitoue hc took into account the sex, age, weight, activity, acid-base balance of diet, proportion of other bases in diet, and phosphorus metabolism.
Load more

Recommended publications
  • Hypophosphatasia: Current Literature for Pathophysiology, Clinical Manifestations, Diagnosis, and Treatment
    Open Access Review Article DOI: 10.7759/cureus.8594 Hypophosphatasia: Current Literature for Pathophysiology, Clinical Manifestations, Diagnosis, and Treatment Abdulai Bangura 1 , Lisa Wright 2 , Thomas Shuler 2 1. Department of Research, Trinity School of Medicine, Ratho Mill, VCT 2. Department of Orthopaedics, Carilion Clinic, Roanoke, USA Corresponding author: Abdulai Bangura, [email protected] Abstract Hypophosphatasia (HPP) is a rare inherited bone disorder identified by impaired bone mineralization. There are seven subtypes of HPP mainly characterized by their age of onset. These subtypes consist of perinatal (prenatal) benign, perinatal lethal, infantile, childhood, adult, odontohypophosphatasia, and pseudohypophosphatasia. Due to limited awareness of the condition, either misdiagnosis or delayed diagnosis is common. Furthermore, the condition is frequently treated with contraindicated drugs. This literature illustrates the most recent findings on the etiology, pathophysiology, clinical manifestations, diagnosing, and treatment for HPP and its subtypes. The etiology of the disease consists of loss-of-function mutations of the ALPL gene on chromosome one, which encodes for tissue nonspecific isoenzyme of alkaline phosphatase (TNAP). A decrease of TNAP reduces inorganic phosphate (Pi) for bone mineralization and allows for an increase in inorganic pyrophosphate (PPi) and phosphorylated osteopontin (p-OPN), which further reduces bone mineralization. The combination of these processes softens bone and mediates a clinical presentation similar to rickets/osteomalacia. HPP has an additional wide range of clinical features depending on its subtype. Although a concrete diagnostic guideline has not yet been established, many studies have supported a similar method of identifying HPP. Clinical features, radiological findings, and/or biomarker levels of the disorder should raise suspicion and encourage the inclusion of HPP as a differential diagnosis.
    [Show full text]
  • Osteomalacia and Osteoporosis D
    Postgrad. med.J. (August 1968) 44, 621-625. Postgrad Med J: first published as 10.1136/pgmj.44.514.621 on 1 August 1968. Downloaded from Osteomalacia and osteoporosis D. B. MORGAN Department of Clinical Investigation, University ofLeeds OSTEOMALACIA and osteoporosis are still some- in osteomalacia is an increase in the alkaline times confused because both diseases lead to a phosphatase activity in the blood (SAP); there deficiency of calcium which can be detected on may also be a low serum phosphorus or a low radiographs of the skeleton. serum calcium. This lack of calcium is the only feature Our experience with the biopsy of bone is that common to the two diseases which are in all a large excess of uncalcified bone tissue (osteoid), other ways easily distinguishable. which is the classic histological feature of osteo- malacia, is only found in patients with the other Osteomalacia typical features of the disease, in particular the Osteomalacia will be discussed first, because it clinical ones (Morgan et al., 1967a). Whether or is a clearly defined disease which can be cured. not more subtle histological techniques will detect Osteomalacia is the result of an imbalance be- earlier stages of the disease remains to be seen. tween the supply of and the demand for vitamin Bone pains, muscle weakness, Looser's zones, D. The the following description of disease is raised SAP and low serum phosphate are the Protected by copyright. based on our experience of twenty-two patients most reliable aids to the diagnosis of osteomalacia, with osteomalacia after gastrectomy; there is no and approximately in that order.
    [Show full text]
  • 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).
    [Show full text]
  • 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
    [Show full text]
  • 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.
    [Show full text]
  • Adult Osteomalacia a Treatable Cause of “Fear of Falling” Gait
    VIDEO NEUROIMAGES Adult osteomalacia A treatable cause of “fear of falling” gait Figure Severe osteopenia The left hand x-ray suggested the diagnosis of osteomalacia because of the diffuse demineralization. A 65-year-old man was hospitalized with a gait disorder, obliging him to shuffle laterally1 (video on the Neurology® Web site at www.neurology.org) because of pain and proximal limb weakness. He had a gastrectomy for cancer 7 years previously, with severe vitamin D deficiency; parathormone and alkaline phosphatase were increased, with reduced serum and urine calcium and phosphate. There was reduced bone density (figure). He was mildly hypothyroid and pancytopenic. B12 and folate levels were normal. Investigation for an endocrine neoplasm (CT scan, Octreoscan) was negative. EMG of proximal muscles was typical for chronic myopathy; nerve conduction studies had normal results. After 80 days’ supplementation with calcium, vitamin D, and levothyroxine, the patient walked properly without assistance (video); pancytopenia and alkaline phosphatase improved. Supplemental data at This unusual but reversible gait disorder may have resulted from bone pain and muscular weakness related to www.neurology.org osteomalacia2 and secondary hyperparathyroidism, with a psychogenic overlay. Paolo Ripellino, MD, Emanuela Terazzi, MD, Enrica Bersano, MD, Roberto Cantello, MD, PhD From the Department of Neurology, University of Turin (P.R.), and Department of Neurology, University of Eastern Piedmont (E.T., E.B., R.C.), AOU Maggiore della Carità, Novara, Italy. Author contributions: Dr. Ripellino: acquisition of data, video included; analysis and interpretation of data; writing and editing of the manuscript and of the video. Dr. Terazzi: analysis and interpretation of data.
    [Show full text]
  • Download (2MB)
    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).
    [Show full text]
  • Michael P. Whyte, M.D
    Melorheostosis Michael P. Whyte, M.D. Center for Metabolic Bone Disease and Molecular Research, Shriners Hospital for Children; and Division of Bone and Mineral Diseases, Washington University School of Medicine at Barnes-Jewish Hospital; St. Louis, Missouri, U.S.A. 1 History • 1922 – Léri and Joanny (define the disorder) • “Léri’s disease” • 5000 BC (Chilean burial site 2-year-old girl) • 1500-year-old skeleton in Alaska 2 Definitions (Greek) melo=“limb” rhein=“to flow” osteon=“bone” • Melorheostosis means "limb and I(me)-Flow“ • Flowing Periosteal Hyperostosis • Candle guttering (dripping wax) on x-ray in adults • OMIM (Online Mendelian Inheritance of Man) % 155950 DISORDERS THAT CAUSE OSTEOSCLEROSIS Dysplasias Craniodiaphyseal dysplasia Osteoectasia with hyperphosphatasia Craniometaphyseal dysplasia Mixed sclerosing bone dystrophy Dysosteosclerosis Oculodento-osseous dysplasia Endosteal hyperostosis Osteodysplasia of Melnick and Needles Van Buchem Disease Osteoectasia with hyperphosphatasia Sclerosteosis (hyperostosis corticalis) Frontometaphyseal dysplasia Osteopathia striata Infantile cortical hyperostosis Osteopetrosis (Caffey disease) Osteopoikilosis Melorheostosis Progressive diaphyseal dysplasia Metaphyseal dysplasia (Pyle disease) (Engelmann disease) Pyknodysostosis Metabolic Carbonic anhydrase II deficiency Hyper-, hypo- and pseudohypoparathyroidism Fluorosis Hypophosphatemic osteomalacia Heavy metal poisoning Milk-alkali syndrome Hypervitaminosis A,D Renal osteodystrophy Other Axial osteomalacia Multiple myeloma Paget’s disease
    [Show full text]
  • 21362 Arthritis Australia a to Z List
    ARTHRITISINFORMATION SHEET Here is the A to Z of arthritis! A D Goodpasture’s syndrome Achilles tendonitis Degenerative joint disease Gout Achondroplasia Dermatomyositis Granulomatous arteritis Acromegalic arthropathy Diabetic finger sclerosis Adhesive capsulitis Diffuse idiopathic skeletal H Adult onset Still’s disease hyperostosis (DISH) Hemarthrosis Ankylosing spondylitis Discitis Hemochromatosis Anserine bursitis Discoid lupus erythematosus Henoch-Schonlein purpura Avascular necrosis Drug-induced lupus Hepatitis B surface antigen disease Duchenne’s muscular dystrophy Hip dysplasia B Dupuytren’s contracture Hurler syndrome Behcet’s syndrome Hypermobility syndrome Bicipital tendonitis E Hypersensitivity vasculitis Blount’s disease Ehlers-Danlos syndrome Hypertrophic osteoarthropathy Brucellar spondylitis Enteropathic arthritis Bursitis Epicondylitis I Erosive inflammatory osteoarthritis Immune complex disease C Exercise-induced compartment Impingement syndrome Calcaneal bursitis syndrome Calcium pyrophosphate dehydrate J (CPPD) F Jaccoud’s arthropathy Crystal deposition disease Fabry’s disease Juvenile ankylosing spondylitis Caplan’s syndrome Familial Mediterranean fever Juvenile dermatomyositis Carpal tunnel syndrome Farber’s lipogranulomatosis Juvenile rheumatoid arthritis Chondrocalcinosis Felty’s syndrome Chondromalacia patellae Fibromyalgia K Chronic synovitis Fifth’s disease Kawasaki disease Chronic recurrent multifocal Flat feet Kienbock’s disease osteomyelitis Foreign body synovitis Churg-Strauss syndrome Freiberg’s disease
    [Show full text]
  • 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.
    [Show full text]
  • Bone Scan in Tumor-Induced Osteomalacia
    Bone Scan in Tumor-Induced Osteomalacia Hee K. Lee, Wei Wen Sung, Paul Solodnik and Mona Shimshi Section of Nuclear Medicine, Department of Medicine and Department of Radiology, Mount Sinai School of Medicine and Elmhurst Hospital Center, Elmhurst, New York revealed markedly improved focal lesions while diffusely in A 66-yr-old female was admitted with a 3-yr history of general creased activity, especially in the skull remained (Fig. 2). ized bone pain and nasal obstruction. CT and MRI of the head revealed a large nasal mass. A whole-body bone scan revealed multifocal lesions of increased activity. Surgical removal of the DISCUSSION nasal tumor revealed hemangiopericytoma. The patient im Tumor-induced osteomalacia or oncogenic osteomalacia proved clinically and a repeat bone scan 10 mo after surgery is a rare phenomenon with less than 100 reported cases in revealed markedly improved findings. the literature. Most of the tumors are benign, mesenchymal Key Words: oncogenous;osteomalacia;bone scan in origin and highly vascular (1,2). Benign tumors associ ated with osteomalacia include giant-cell granuloma, J NucíMed 1995; 36:247-249 cavernous hemangioma, nonossifying fibroma, benign ossifying mesenchymal tumors, fibrous xanthoma, heman giopericytoma, angiosarcoma, osteoblastoma and fibroan- 'ncogenous osteomalacia is a rarely described clinical gioma. Malignant tumors associated with oncogenic osteo o, malacia are extremely rare with less than 10reported cases entity that may mimic metastatic bone lesions in bone (3). There is one reported case each of prostate cancer (4) scanning. It is most commonly associated with benign tu and oat-cell lung cancer (5). More common are the malig mors of mesenchymal origin and can be cured after surgical nant soft-tissue sarcomas and malignant neurinoma.
    [Show full text]
  • 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.
    [Show full text]