This case report describes a patient with severe uremic leontiasis ossea (ULO), or "lion face syndrome", due to longstanding uncontrolled secondary and tertiary hyperparathyroidism from end-stage renal disease. Over many years, the patient's hyperparathyroidism progressed due to non-compliance with treatment, resulting in extensive bone deformities, fractures, and disfigurement of the facial bones. Imaging showed thickening and enlargement of the maxilla and mandible bones, giving her face a lion-like appearance. The report discusses the pathophysiology of hyperparathyroidism in kidney disease and reviews the management challenges posed by this rare but preventable complication.
This document summarizes various metabolic bone diseases and their imaging manifestations. It discusses osteoporosis, rickets, osteomalacia, hypophosphatasia, hyperparathyroidism, renal osteodystrophy, hypoparathyroidism, hypothyroidism, hyperthyroidism, acromegaly, and scurvy. For each condition, it describes the pathophysiology, typical skeletal findings on imaging, and examples of radiographic manifestations. Common findings include generalized osteopenia, vertebral fractures, Looser zones, subperiosteal bone resorption, brown tumors, and osteosclerosis in varying patterns depending on the specific disease process.
This document describes cherubism, a rare genetic condition characterized by bilateral swelling of the jaws causing a cherubic facial appearance. It results from mutations in the SH3BP2 gene in most cases, causing excess bone growth in the jaws during childhood that typically resolves by adulthood. Symptoms range from mild jaw enlargement to severe issues with vision, breathing, speech or swallowing depending on the severity.
This document discusses chronic kidney disease-mineral and bone disorder (CKD-MBD). It notes that abnormalities in mineral metabolism are common even in early stages of CKD and accelerate with worsening kidney function. The factors involved in secondary hyperparathyroidism pathogenesis are described. Different types of renal osteodystrophy are defined based on laboratory abnormalities and presence of bone disease and soft tissue calcification. The document also outlines clinical manifestations of renal osteodystrophy including bone pain, fractures, and tendon ruptures.
Hyperparathyroidism and diabetes can influence periodontal health in several ways:
1. They can alter immune responses, such as impairing neutrophil function, which helps bacteria evade the immune system and worsen periodontal disease.
2. Chronic hyperglycemia and hyperparathyroidism can impair collagen structure and function, damaging the integrity of the periodontium.
3. They may qualitatively change the subgingival microbiome, promoting pathogens like Porphyromonas and Prevotella that are linked to periodontitis.
The document discusses several bone diseases including osteogenesis imperfecta, osteopetrosis, cleidocranial dysplasia, focal osteoporotic marrow defect, Paget's disease of bone, central giant cell granuloma, cherubism, and fibro-osseous lesions of the jaws. It describes the clinical features, radiographic findings, histopathology, treatment, and prognosis of each condition. The conditions vary in severity from mild to severe and are characterized by abnormalities in bone formation, resorption, and remodeling leading to fragile or dense bones.
The document discusses several bone diseases including osteogenesis imperfecta, osteopetrosis, cleidocranial dysplasia, focal osteoporotic marrow defect, Paget's disease of bone, central giant cell granuloma, cherubism, and fibro-osseous lesions of the jaws. It provides details on the clinical features, radiographic findings, histopathology, treatment, and prognosis of each condition. The diseases involve abnormalities in bone formation, resorption, and remodeling leading to fragile or dense bones, deformities, and other complications.
Heterotopic Ossification (HO) is defined as pathological bone formation at locations where bone normally does not exist. The
presence of HO has been found to be a rare complication after stroke in several studies, whereas there are only sporadic references relating HO to Cerebral Palsy (CP) and few for CP and stroke. No effective treatment for HO has yet been found, whereas the cellular and molecular mechanisms have not been completely understood. Therefore, increased awareness among physicians is required, as a challenge for early diagnosis and treatment. A case of a male patient with CP, who developed HO on the paretichip joint following an ischemic stroke is presented.
This document discusses a case of uremic leontiasis ossea in a 62-year-old male with chronic kidney disease and secondary hyperparathyroidism. He presented with severe bone deformities and high parathyroid hormone levels. Tests found hyperplasia of the parathyroid glands. He underwent parathyroidectomy with removal of five glands, one being supernumerary. Post-operatively, his calcium, phosphorus, and parathyroid hormone levels improved significantly. The case demonstrates how prolonged secondary hyperparathyroidism can lead to severe bone deformities but can be treated with surgery.
This document summarizes various metabolic bone diseases and their imaging manifestations. It discusses osteoporosis, rickets, osteomalacia, hypophosphatasia, hyperparathyroidism, renal osteodystrophy, hypoparathyroidism, hypothyroidism, hyperthyroidism, acromegaly, and scurvy. For each condition, it describes the pathophysiology, typical skeletal findings on imaging, and examples of radiographic manifestations. Common findings include generalized osteopenia, vertebral fractures, Looser zones, subperiosteal bone resorption, brown tumors, and osteosclerosis in varying patterns depending on the specific disease process.
This document describes cherubism, a rare genetic condition characterized by bilateral swelling of the jaws causing a cherubic facial appearance. It results from mutations in the SH3BP2 gene in most cases, causing excess bone growth in the jaws during childhood that typically resolves by adulthood. Symptoms range from mild jaw enlargement to severe issues with vision, breathing, speech or swallowing depending on the severity.
This document discusses chronic kidney disease-mineral and bone disorder (CKD-MBD). It notes that abnormalities in mineral metabolism are common even in early stages of CKD and accelerate with worsening kidney function. The factors involved in secondary hyperparathyroidism pathogenesis are described. Different types of renal osteodystrophy are defined based on laboratory abnormalities and presence of bone disease and soft tissue calcification. The document also outlines clinical manifestations of renal osteodystrophy including bone pain, fractures, and tendon ruptures.
Hyperparathyroidism and diabetes can influence periodontal health in several ways:
1. They can alter immune responses, such as impairing neutrophil function, which helps bacteria evade the immune system and worsen periodontal disease.
2. Chronic hyperglycemia and hyperparathyroidism can impair collagen structure and function, damaging the integrity of the periodontium.
3. They may qualitatively change the subgingival microbiome, promoting pathogens like Porphyromonas and Prevotella that are linked to periodontitis.
The document discusses several bone diseases including osteogenesis imperfecta, osteopetrosis, cleidocranial dysplasia, focal osteoporotic marrow defect, Paget's disease of bone, central giant cell granuloma, cherubism, and fibro-osseous lesions of the jaws. It describes the clinical features, radiographic findings, histopathology, treatment, and prognosis of each condition. The conditions vary in severity from mild to severe and are characterized by abnormalities in bone formation, resorption, and remodeling leading to fragile or dense bones.
The document discusses several bone diseases including osteogenesis imperfecta, osteopetrosis, cleidocranial dysplasia, focal osteoporotic marrow defect, Paget's disease of bone, central giant cell granuloma, cherubism, and fibro-osseous lesions of the jaws. It provides details on the clinical features, radiographic findings, histopathology, treatment, and prognosis of each condition. The diseases involve abnormalities in bone formation, resorption, and remodeling leading to fragile or dense bones, deformities, and other complications.
Heterotopic Ossification (HO) is defined as pathological bone formation at locations where bone normally does not exist. The
presence of HO has been found to be a rare complication after stroke in several studies, whereas there are only sporadic references relating HO to Cerebral Palsy (CP) and few for CP and stroke. No effective treatment for HO has yet been found, whereas the cellular and molecular mechanisms have not been completely understood. Therefore, increased awareness among physicians is required, as a challenge for early diagnosis and treatment. A case of a male patient with CP, who developed HO on the paretichip joint following an ischemic stroke is presented.
This document discusses a case of uremic leontiasis ossea in a 62-year-old male with chronic kidney disease and secondary hyperparathyroidism. He presented with severe bone deformities and high parathyroid hormone levels. Tests found hyperplasia of the parathyroid glands. He underwent parathyroidectomy with removal of five glands, one being supernumerary. Post-operatively, his calcium, phosphorus, and parathyroid hormone levels improved significantly. The case demonstrates how prolonged secondary hyperparathyroidism can lead to severe bone deformities but can be treated with surgery.
7.oral manifest of systemic diseases part iLama K Banna
Oral examination can reveal findings indicative of underlying systemic conditions. Careful oral evaluation includes inspection of the mucosa, periodontal tissues, and teeth. Oral manifestations of anemia may include pallor, glossitis, and candidiasis. Many systemic diseases are reflected in oral changes such as ulceration, bleeding, infections, bone disease, and dental issues. Local factors may also contribute to oral lesions in patients with systemic conditions. Diseases of the endocrine, hematologic, immune, and gastrointestinal systems can all impact the oral cavity. Medications prescribed for systemic illnesses can additionally cause oral side effects.
This document provides information on bone disease in chronic kidney disease (CKD). It discusses the pathogenesis of bone disease in CKD, which is caused by disrupted calcium and phosphate homeostasis as kidney function declines. This leads to secondary hyperparathyroidism as phosphate levels rise and calcitriol production decreases. The document describes different classifications of bone disease in CKD including high turnover disease and adynamic bone disease. Diagnosis involves monitoring levels of PTH, calcium, and phosphate from blood tests. Treatment aims to control these mineral levels as well as vitamin D to prevent complications of CKD-mineral and bone disorder like cardiovascular disease.
This document provides information on chronic kidney disease-mineral and bone disorder (CKD-MBD). It discusses the pathogenesis of CKD-MBD, classifications of bone disease seen in CKD patients, diagnostic evaluations, and treatment approaches. Key points include that CKD disrupts calcium and phosphate homeostasis, leading to secondary hyperparathyroidism and bone disease. Bone abnormalities range from high turnover disease to adynamic bone disease. Treatment focuses on controlling calcium, phosphate, PTH, and vitamin D levels to prevent complications of CKD-MBD such as cardiovascular disease.
This document discusses bone disease in chronic kidney disease. It begins with an introduction and overview of pathogenesis. It then discusses normal bone remodeling and hyperparathyroidism. It classifies bone diseases in CKD and discusses their diagnosis. Finally, it addresses treatment of bone disease in CKD, focusing on controlling calcium, phosphorus, PTH and vitamin D levels to prevent complications. The goal is to prevent mineral and bone disorder and cardiovascular disease to lower mortality rates in patients with CKD.
Chronic renal failure is caused by various etiologies and leads to progressive loss of kidney function. Major symptoms include fluid and electrolyte disorders, bone disease, cardiovascular abnormalities, anemia, and neurological issues. Treatment focuses on slowing disease progression through protein restriction and blood pressure control, and managing complications like mineral metabolism disorders, hypertension, and anemia.
Chronic renal failure is caused by various etiologies and leads to progressive loss of kidney function. It is characterized by fluid and electrolyte abnormalities, bone disease, cardiovascular complications, anemia, and other systemic effects. Treatment focuses on slowing progression through blood pressure control and protein restriction, and managing complications through treatment of mineral metabolism disorders, anemia, and other issues.
This document discusses chronic kidney disease-mineral and bone disorder (CKD-MBD). It provides stages of CKD based on glomerular filtration rate. It also discusses abnormalities in mineral metabolism that occur in later CKD stages including elevated PTH, phosphorus, and decreased calcium and vitamin D. The document outlines classifications of bone disease in CKD including osteitis fibrosa, adynamic bone disease, and amyloidosis. It discusses treatments for abnormal mineral metabolism including phosphate binders and vitamin D analogs to control calcium, phosphorus, and PTH levels.
Chronic kidney disease associated mineral bone disordersArshad Ali Awan
This document discusses chronic kidney disease-mineral and bone disorder (CKD-MBD), which represents a systemic disorder of mineral and bone metabolism that occurs as a complication of chronic kidney disease. As kidney function declines in CKD, there are progressive changes in the serum concentrations of calcium, phosphorus, vitamins D and PTH that lead to abnormalities in bone turnover, mineralization, and structure as well as soft tissue calcification. The document outlines the pathogenesis of CKD-MBD and its skeletal complications including renal osteodystrophy, and discusses treatment goals and management strategies to address abnormal mineral metabolism and bone disease in CKD.
Arthropathy in haematological disorders in childrendattasrisaila
This document discusses various hematological disorders that can present with rheumatological symptoms in children. It describes benign disorders like sickle cell disease, thalassemias, and hemophilia that can cause joint pain, swelling, and damage. It also covers malignant disorders like leukemic arthritis and how certain cancers like leukemia can initially manifest as musculoskeletal complaints. For each condition, it provides details on presentations, treatments, and long term complications involving the bones and joints.
Dr. Ahmed Mohamed Albeyaly is a nephrology specialist and moderator in Dakahlia Health directorate. He specializes in treating bone disease in patients with chronic kidney disease. Bone disease in CKD is caused by abnormalities in calcium, phosphorus, PTH, and vitamin D metabolism which disrupt bone remodeling. It is classified based on bone turnover and the presence of soft tissue calcification. Diagnosis involves monitoring laboratory values of calcium, phosphorus and PTH over time alongside imaging studies. Treatment focuses on controlling these mineral and hormone levels through diet, phosphate binders, vitamin D analogues and parathyroidectomy to prevent further bone disease and cardiovascular complications.
Dr. Ahmed Mohamed Albeyaly is a nephrology specialist and moderator in Dakahlia Health directorate. The document discusses chronic kidney disease-mineral and bone disorder (CKD-MBD), which is a systemic disorder affecting bone disease, soft tissue calcification, and abnormalities in mineral metabolism that result from kidney disease and kidney failure. The document covers pathogenesis of CKD-MBD, classifications of bone disease seen in CKD patients, diagnosis through laboratory tests and imaging, and treatment approaches including controlling calcium, phosphorus, PTH, and vitamin D levels.
Orthopedic Clinical Manifestations of Ectodermal Dysplasia. Case Presentationkomalicarol
Ectodermal dysplasias represent a heterogeneous group of alterations, characterized by the abnormal development of embryological derivatives of the ectoderm.We present a patient who, upon
examination of the osteomyoarticular system, presents intense
rotation of the lower limbs with the toes backwards, which the
patient performed without difficulty, in an unforced, voluntary and
painless way. Orthopedic clinical manifestations are infrequent in
skeletal dysplasias, lower limb disorders even rarer, which is why
we present these striking alterations, a fundamental objective of
the study
Osteoarthritis is a chronic degenerative joint disease characterized by the breakdown of articular cartilage. It commonly affects weight-bearing joints like the hips and knees, causing pain and stiffness. While the exact causes are unknown, risk factors include aging, obesity, joint injury, and genetic factors. The pathogenesis involves structural and biochemical changes to cartilage and surrounding bone and tissues that disrupt the normal balance between degradation and regeneration of cartilage. Treatments aim to reduce pain and inflammation, maintain joint function, and may include medications, weight loss, exercise, bracing, and joint replacement surgery in severe cases.
Biochemical tests are used to diagnose bone diseases. Serum tests measure calcium, phosphate, alkaline phosphatase, parathyroid hormone, and vitamin D levels. Urine tests measure calcium, phosphate, and bone turnover markers. Common bone diseases include arthritis, osteoporosis, rickets/osteomalacia, and Paget's disease. Arthritis causes joint symptoms. Osteoporosis weakens bones and increases fracture risk. Rickets/osteomalacia cause soft bones from vitamin D deficiency. Paget's disease involves abnormal bone remodeling.
The document discusses renal osteodystrophy, which refers to bone diseases that occur in patients with impaired kidney function. It outlines several types of renal osteodystrophy, including osteitis fibrosa, adynamic bone disease, and osteomalacia. It describes the pathogenesis of secondary hyperparathyroidism in kidney disease and the effects of parathyroid hormone and vitamin D on bone and mineral metabolism. Treatment goals are to control parathyroid hormone levels, calcium, phosphorus, and vitamin D to prevent bone complications in renal patients.
This document discusses several diseases that can affect bone density and structure, including hyperparathyroidism, osteoporosis, osteomalacia, leukemia, Langerhans cell disease, Paget's disease, and multiple myeloma. It provides details on the clinical features, radiographic manifestations, differential diagnosis, and management of each condition. The document contains radiographic images showing examples of bone changes associated with some of the diseases.
This document discusses osteoporosis and related bone diseases. It defines osteoporosis as a metabolic bone disease characterized by low bone density and increased bone fragility. Common fracture sites are the forearm, vertebrae, humerus and hip. Hip fractures are the most serious with a 12% immediate mortality rate. The document outlines risk factors, pathophysiology, clinical features, investigations and management strategies for osteoporosis as well as related diseases including vitamin D deficiency, osteomalacia, rickets, and hereditary disorders.
Crouzon syndrome is a rare genetic disorder characterized by abnormal fusion of skull bones resulting in an abnormally shaped head and face. It occurs in approximately 1 in 25,000 births. The clinical features may include premature closure of skull sutures, bulging eyes, retruded midface, dental crowding, hearing loss, and respiratory issues. Treatment involves surgical release of fused skull sutures in early childhood along with multidisciplinary care from specialists. Future nonsurgical treatments using drugs that inhibit abnormal bone fusion may help reduce severity.
This case report describes a 9-year-old female patient with fibrous dysplasia of the maxilla and a port wine stain on her face. Clinical examination and radiographic imaging showed abnormal bone growth replacing the maxilla. A biopsy confirmed the diagnosis of fibrous dysplasia. The patient underwent surgical recontouring of the maxilla and was happy with the results at her 2-week follow up appointment. Fibrous dysplasia is a benign condition where abnormal bone growth replaces normal bone, usually becoming inactive in adulthood, though some cases like this one may continue progressing during childhood growth.
1) Disasters can increase the risk of cardiovascular diseases like hypertension, myocardial infarction, and stroke in the aftermath. Rates of these conditions increased by 1.5 to 1.9 times after some earthquakes.
2) The prevalence of hypertension in humanitarian crises ranges widely from 3% to 83% with higher rates overall in high-income countries compared to low and middle-income countries. Blood pressure and stress levels also tend to rise acutely after disasters.
3) Long term effects on hypertension control can also occur if access to healthcare is disrupted by disasters, as demonstrated by worse control rates persisting up to 2 years after Hurricane Sandy interrupted services for some patients.
HTN Among ESRD Patients Cardiology meeting .pptxJAFAR ALSAID
The document discusses blood pressure among hemodialysis patients. It covers the epidemiology of blood pressure in this population and measurement of blood pressure, including intradialytic and interdialytic blood pressure. It also discusses management of blood pressure in hemodialysis patients. Graphs and tables are presented showing patterns of blood pressure variation during multiple dialysis sessions and the relationship between dialysis unit blood pressure and cardiovascular events. Target blood pressures associated with best outcomes are highlighted.
7.oral manifest of systemic diseases part iLama K Banna
Oral examination can reveal findings indicative of underlying systemic conditions. Careful oral evaluation includes inspection of the mucosa, periodontal tissues, and teeth. Oral manifestations of anemia may include pallor, glossitis, and candidiasis. Many systemic diseases are reflected in oral changes such as ulceration, bleeding, infections, bone disease, and dental issues. Local factors may also contribute to oral lesions in patients with systemic conditions. Diseases of the endocrine, hematologic, immune, and gastrointestinal systems can all impact the oral cavity. Medications prescribed for systemic illnesses can additionally cause oral side effects.
This document provides information on bone disease in chronic kidney disease (CKD). It discusses the pathogenesis of bone disease in CKD, which is caused by disrupted calcium and phosphate homeostasis as kidney function declines. This leads to secondary hyperparathyroidism as phosphate levels rise and calcitriol production decreases. The document describes different classifications of bone disease in CKD including high turnover disease and adynamic bone disease. Diagnosis involves monitoring levels of PTH, calcium, and phosphate from blood tests. Treatment aims to control these mineral levels as well as vitamin D to prevent complications of CKD-mineral and bone disorder like cardiovascular disease.
This document provides information on chronic kidney disease-mineral and bone disorder (CKD-MBD). It discusses the pathogenesis of CKD-MBD, classifications of bone disease seen in CKD patients, diagnostic evaluations, and treatment approaches. Key points include that CKD disrupts calcium and phosphate homeostasis, leading to secondary hyperparathyroidism and bone disease. Bone abnormalities range from high turnover disease to adynamic bone disease. Treatment focuses on controlling calcium, phosphate, PTH, and vitamin D levels to prevent complications of CKD-MBD such as cardiovascular disease.
This document discusses bone disease in chronic kidney disease. It begins with an introduction and overview of pathogenesis. It then discusses normal bone remodeling and hyperparathyroidism. It classifies bone diseases in CKD and discusses their diagnosis. Finally, it addresses treatment of bone disease in CKD, focusing on controlling calcium, phosphorus, PTH and vitamin D levels to prevent complications. The goal is to prevent mineral and bone disorder and cardiovascular disease to lower mortality rates in patients with CKD.
Chronic renal failure is caused by various etiologies and leads to progressive loss of kidney function. Major symptoms include fluid and electrolyte disorders, bone disease, cardiovascular abnormalities, anemia, and neurological issues. Treatment focuses on slowing disease progression through protein restriction and blood pressure control, and managing complications like mineral metabolism disorders, hypertension, and anemia.
Chronic renal failure is caused by various etiologies and leads to progressive loss of kidney function. It is characterized by fluid and electrolyte abnormalities, bone disease, cardiovascular complications, anemia, and other systemic effects. Treatment focuses on slowing progression through blood pressure control and protein restriction, and managing complications through treatment of mineral metabolism disorders, anemia, and other issues.
This document discusses chronic kidney disease-mineral and bone disorder (CKD-MBD). It provides stages of CKD based on glomerular filtration rate. It also discusses abnormalities in mineral metabolism that occur in later CKD stages including elevated PTH, phosphorus, and decreased calcium and vitamin D. The document outlines classifications of bone disease in CKD including osteitis fibrosa, adynamic bone disease, and amyloidosis. It discusses treatments for abnormal mineral metabolism including phosphate binders and vitamin D analogs to control calcium, phosphorus, and PTH levels.
Chronic kidney disease associated mineral bone disordersArshad Ali Awan
This document discusses chronic kidney disease-mineral and bone disorder (CKD-MBD), which represents a systemic disorder of mineral and bone metabolism that occurs as a complication of chronic kidney disease. As kidney function declines in CKD, there are progressive changes in the serum concentrations of calcium, phosphorus, vitamins D and PTH that lead to abnormalities in bone turnover, mineralization, and structure as well as soft tissue calcification. The document outlines the pathogenesis of CKD-MBD and its skeletal complications including renal osteodystrophy, and discusses treatment goals and management strategies to address abnormal mineral metabolism and bone disease in CKD.
Arthropathy in haematological disorders in childrendattasrisaila
This document discusses various hematological disorders that can present with rheumatological symptoms in children. It describes benign disorders like sickle cell disease, thalassemias, and hemophilia that can cause joint pain, swelling, and damage. It also covers malignant disorders like leukemic arthritis and how certain cancers like leukemia can initially manifest as musculoskeletal complaints. For each condition, it provides details on presentations, treatments, and long term complications involving the bones and joints.
Dr. Ahmed Mohamed Albeyaly is a nephrology specialist and moderator in Dakahlia Health directorate. He specializes in treating bone disease in patients with chronic kidney disease. Bone disease in CKD is caused by abnormalities in calcium, phosphorus, PTH, and vitamin D metabolism which disrupt bone remodeling. It is classified based on bone turnover and the presence of soft tissue calcification. Diagnosis involves monitoring laboratory values of calcium, phosphorus and PTH over time alongside imaging studies. Treatment focuses on controlling these mineral and hormone levels through diet, phosphate binders, vitamin D analogues and parathyroidectomy to prevent further bone disease and cardiovascular complications.
Dr. Ahmed Mohamed Albeyaly is a nephrology specialist and moderator in Dakahlia Health directorate. The document discusses chronic kidney disease-mineral and bone disorder (CKD-MBD), which is a systemic disorder affecting bone disease, soft tissue calcification, and abnormalities in mineral metabolism that result from kidney disease and kidney failure. The document covers pathogenesis of CKD-MBD, classifications of bone disease seen in CKD patients, diagnosis through laboratory tests and imaging, and treatment approaches including controlling calcium, phosphorus, PTH, and vitamin D levels.
Orthopedic Clinical Manifestations of Ectodermal Dysplasia. Case Presentationkomalicarol
Ectodermal dysplasias represent a heterogeneous group of alterations, characterized by the abnormal development of embryological derivatives of the ectoderm.We present a patient who, upon
examination of the osteomyoarticular system, presents intense
rotation of the lower limbs with the toes backwards, which the
patient performed without difficulty, in an unforced, voluntary and
painless way. Orthopedic clinical manifestations are infrequent in
skeletal dysplasias, lower limb disorders even rarer, which is why
we present these striking alterations, a fundamental objective of
the study
Osteoarthritis is a chronic degenerative joint disease characterized by the breakdown of articular cartilage. It commonly affects weight-bearing joints like the hips and knees, causing pain and stiffness. While the exact causes are unknown, risk factors include aging, obesity, joint injury, and genetic factors. The pathogenesis involves structural and biochemical changes to cartilage and surrounding bone and tissues that disrupt the normal balance between degradation and regeneration of cartilage. Treatments aim to reduce pain and inflammation, maintain joint function, and may include medications, weight loss, exercise, bracing, and joint replacement surgery in severe cases.
Biochemical tests are used to diagnose bone diseases. Serum tests measure calcium, phosphate, alkaline phosphatase, parathyroid hormone, and vitamin D levels. Urine tests measure calcium, phosphate, and bone turnover markers. Common bone diseases include arthritis, osteoporosis, rickets/osteomalacia, and Paget's disease. Arthritis causes joint symptoms. Osteoporosis weakens bones and increases fracture risk. Rickets/osteomalacia cause soft bones from vitamin D deficiency. Paget's disease involves abnormal bone remodeling.
The document discusses renal osteodystrophy, which refers to bone diseases that occur in patients with impaired kidney function. It outlines several types of renal osteodystrophy, including osteitis fibrosa, adynamic bone disease, and osteomalacia. It describes the pathogenesis of secondary hyperparathyroidism in kidney disease and the effects of parathyroid hormone and vitamin D on bone and mineral metabolism. Treatment goals are to control parathyroid hormone levels, calcium, phosphorus, and vitamin D to prevent bone complications in renal patients.
This document discusses several diseases that can affect bone density and structure, including hyperparathyroidism, osteoporosis, osteomalacia, leukemia, Langerhans cell disease, Paget's disease, and multiple myeloma. It provides details on the clinical features, radiographic manifestations, differential diagnosis, and management of each condition. The document contains radiographic images showing examples of bone changes associated with some of the diseases.
This document discusses osteoporosis and related bone diseases. It defines osteoporosis as a metabolic bone disease characterized by low bone density and increased bone fragility. Common fracture sites are the forearm, vertebrae, humerus and hip. Hip fractures are the most serious with a 12% immediate mortality rate. The document outlines risk factors, pathophysiology, clinical features, investigations and management strategies for osteoporosis as well as related diseases including vitamin D deficiency, osteomalacia, rickets, and hereditary disorders.
Crouzon syndrome is a rare genetic disorder characterized by abnormal fusion of skull bones resulting in an abnormally shaped head and face. It occurs in approximately 1 in 25,000 births. The clinical features may include premature closure of skull sutures, bulging eyes, retruded midface, dental crowding, hearing loss, and respiratory issues. Treatment involves surgical release of fused skull sutures in early childhood along with multidisciplinary care from specialists. Future nonsurgical treatments using drugs that inhibit abnormal bone fusion may help reduce severity.
This case report describes a 9-year-old female patient with fibrous dysplasia of the maxilla and a port wine stain on her face. Clinical examination and radiographic imaging showed abnormal bone growth replacing the maxilla. A biopsy confirmed the diagnosis of fibrous dysplasia. The patient underwent surgical recontouring of the maxilla and was happy with the results at her 2-week follow up appointment. Fibrous dysplasia is a benign condition where abnormal bone growth replaces normal bone, usually becoming inactive in adulthood, though some cases like this one may continue progressing during childhood growth.
1) Disasters can increase the risk of cardiovascular diseases like hypertension, myocardial infarction, and stroke in the aftermath. Rates of these conditions increased by 1.5 to 1.9 times after some earthquakes.
2) The prevalence of hypertension in humanitarian crises ranges widely from 3% to 83% with higher rates overall in high-income countries compared to low and middle-income countries. Blood pressure and stress levels also tend to rise acutely after disasters.
3) Long term effects on hypertension control can also occur if access to healthcare is disrupted by disasters, as demonstrated by worse control rates persisting up to 2 years after Hurricane Sandy interrupted services for some patients.
HTN Among ESRD Patients Cardiology meeting .pptxJAFAR ALSAID
The document discusses blood pressure among hemodialysis patients. It covers the epidemiology of blood pressure in this population and measurement of blood pressure, including intradialytic and interdialytic blood pressure. It also discusses management of blood pressure in hemodialysis patients. Graphs and tables are presented showing patterns of blood pressure variation during multiple dialysis sessions and the relationship between dialysis unit blood pressure and cardiovascular events. Target blood pressures associated with best outcomes are highlighted.
Final Ultrasound measured renal parenchyhmal thickness and sinus fat and thei...JAFAR ALSAID
This study examined the relationship between ultrasound measurements of renal sinus fat, parenchymal thickness, interstitial fibrosis and renal function in 52 patients. Renal sinus fat length and parenchymal thickness were significantly correlated with serum creatinine and eGFR, but not with demographic factors. Interstitial fibrosis levels correlated significantly with age, gender, BMI, hypertension, diabetes, serum creatinine and eGFR, but not sinus fat or parenchymal thickness. The results suggest ultrasound measurements of sinus fat and parenchymal thickness relate to renal function, while interstitial fibrosis associates more with demographic and clinical factors.
Renal interstitial fibrosis and its associated independent clinical factors.docxJAFAR ALSAID
This study analyzed kidney biopsies from 60 patients over two years to determine the correlation between clinical factors and the degree of interstitial fibrosis. The study found that older age, male gender, hypertension, diabetes mellitus, higher serum creatinine, and lower estimated GFR were significantly associated with greater interstitial fibrosis. Patients with hypertension or diabetes had higher levels of interstitial fibrosis and were older than patients without these conditions. Diabetic patients also had higher BMI and worse renal function compared to non-diabetic patients. The study concludes that several clinical factors can help predict the extent of interstitial fibrosis seen on kidney biopsy.
Hypertension in Middle East and North Africa regionJAFAR ALSAID
Hypertension is a growing problem in the Middle East and North Africa region. According to studies reviewed, hypertension prevalence has increased from 1990 to 2020 in the region. However, awareness, treatment and control rates have improved only modestly. Looking forward, population growth and aging will further increase hypertension rates in MENA unless steps are taken to improve prevention, screening, treatment and control of hypertension.
Ultrasound basics for Nephrologists.pptxJAFAR ALSAID
This document provides an overview of ultrasound basics for nephrologists. It discusses ultrasound physics, how to perform and interpret a renal ultrasound exam, and recognizes some abnormalities. The document aims to establish ultrasound as a useful examination tool for nephrologists and provides several case examples of using ultrasound to determine the cause of renal disease or kidney abnormalities.
The differenece betweeen central and peripheral Blood pressure and its clinic...JAFAR ALSAID
Central blood pressure provides a more accurate assessment of the pressure load on target organs like the heart, brain and kidneys compared to brachial blood pressure. Three key points:
1. Central systolic pressure is usually higher than brachial pressure due to amplification of the pressure wave in the arteries. Central pressure correlates better with organ damage and predicts cardiovascular outcomes more strongly.
2. Increased arterial stiffness, measured by a higher pulse wave velocity, is a strong predictor of cardiovascular events and mortality. Pulse wave velocity increases with age and cardiovascular risk factors.
3. Augmentation index, a measure of wave reflections and arterial stiffness, is associated with increased risk of mortality and cardiovascular disease when elevated. It predicts
Hemodialysis catheter related infection JAFAR ALSAID
The document discusses hemodialysis catheter-related infections. It notes that catheter infections are a major cause of morbidity and mortality for hemodialysis patients. It provides statistics on catheter use and infection rates. It then describes different types of catheter infections including exit site infections, tunnel infections, and bloodstream infections. Signs and symptoms of infections are outlined. The document proposes a strict infection control protocol for nurses to follow during catheter care and dialysis to help reduce infection rates. This includes recommendations for site cleaning, dressing changes, tubing changes, and staff education.
Hemodialysis catheter related infection 5JAFAR ALSAID
This document discusses hemodialysis catheter-related infections. It provides statistics on catheter use and infection rates. It describes different types of catheter infections including exit site infections, tunnel infections, and bloodstream infections. Signs and symptoms of infection and methods for diagnosis are outlined. The document proposes a strict infection control protocol for catheters and discusses efforts at one facility to reduce infection rates through improved catheter care and adherence to infection guidelines.
International Society of Hypertension 2020 guidlinesJAFAR ALSAID
The document outlines key points from a presentation on hypertension given by Dr. Jafar Alsaid at the Iraqi Hypertension Conference in November 2021. It discusses the global burden of hypertension, challenges in low-income countries, definitions and classifications of hypertension, measuring blood pressure, common risk factors, target organ damage, lifestyle modifications, pharmacological treatments, and the importance of patient education.
Uric acid and htn saudi htn conference final 3JAFAR ALSAID
Uric acid plays a role in cardiovascular disease and hypertension. High levels of uric acid are associated with hypertension and lowering uric acid, such as through allopurinol, can reduce blood pressure. Treating hyperuricemia may help slow the progression of chronic kidney disease and loss of kidney function. Studies in adolescents with newly diagnosed hypertension found that allopurinol reduced both office and 24-hour blood pressure readings. Elevated uric acid may contribute to hypertension through various mechanisms like reducing nitric oxide, activating the renin-angiotensin-aldosterone system, causing renal vasoconstriction, and inducing microvascular renal disease.
This document discusses factors to consider when prescribing hemodialysis, including machine settings, filter selection, and patient characteristics. It covers dialysis targets, complications to prevent, and how blood and dialysate flow rates impact filtration coefficient. The goal is to individualize treatment and achieve a balanced dialysis prescription that addresses clearance needs while preventing harm.
This three-part document discusses hemodialysis prescription and targets. It begins with an introduction and overview of hemodialysis history and statistics on end-stage renal disease from the USRDS 2020 report. Part I covers breaking the news to patients about needing dialysis and variables in deciding on dialysis. Parts II and III will discuss choosing filters and dialysate composition, hemodynamics, ultrafiltration, and research aspects of optimizing hemodialysis prescription. The goal is targeting a dialysis treatment that is friendly to patients.
The document discusses kidney involvement in COVID-19 patients. It notes that acute kidney injury (AKI) occurs in 3-9% of early COVID-19 patients, rising to 19-50% of ICU patients. AKI is associated with higher mortality, between 35-90% among those with COVID-19. Pathological findings include collapsing glomerulopathy and acute tubular injury. Viral particles have been found in podocytes and tubular cells on postmortem and kidney biopsy studies.
The document summarizes the link between hypertension (HTN) and COVID-19. It finds that approximately 22.5% of COVID-19 patients have HTN, making it the most common comorbidity. Patients with HTN who contract COVID-19 have a higher risk of severe outcomes like intensive care unit admission and death. The document also discusses how the renin-angiotensin-aldosterone system, which HTN medications target, may impact the interaction of the COVID-19 virus with the body. Specifically, angiotensin-converting enzyme 2 is utilized by the COVID-19 virus to enter cells and HTN medications like ACE inhibitors may alter ACE2 expression levels.
Outcome of 16 years of hemodialysis infection controlJAFAR ALSAID
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Learning objectives:
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4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
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1. 1
Title Page
Uremic Leontiasis Ossea
A Case Report
Sara W. Fakhredine(1) , Jafar Alsaid(2) , Teerath Kumar(1) , Rayees Yousif Sheikh(1).
1 Division of Nephrology and Hypertension, Department of Internal Medicine,
Bahrain Specialist Hospital, Bahrain.
2 Ochsner Health Center, New Orleans Louisiana. USA. Queensland University Australia.
Corresponding author:
Jafar Alsaid, M.B.ChB, MD. FASN. FACP.
Assistant Professor University of Queensland- Ochsner Clinical School.
Nephrology and Interventional Consultant Ochsner Medical Center.
New Orleans, Louisiana, USA
Clinic building, fifth floor. Nephrology Department.
1514 Jefferson Hwy, LA 70121
Conflict of Interest: The authors declared no conflicts of interest.
Funding: The authors received no financial support.
2. 2
Introduction:
Lion face syndrome or leontiasis ossea is a rare complication of severe hyperparathyroidism in
end-stage renal disease patients (1). It is a severe form of bone remodeling characterized by
abnormal bone mineralization with diffuse enlargement of the facial bones, particularly the
maxilla and mandible. Bone expansion results in facial disfigurement that appears in some cases
like a lion's face (2). Given the widespread use of dialysis, calcimimetics, and phosphate binders,
Uremic Leontiasis Ossea (ULO) is rare these days (3). We are presenting a clinical case of this rare
complication in an ESRD patient. The clinic presentation, pathophysiology, and management will
be discussed according to the latest published data.
Clinical history and progress:
A 37-year-old female patient was seen in the renal clinic in September 2008. She had a past
medical history of recurrent UTIs during childhood, hypertension since the age of 14,
hyperuricemia, morbid obesity, hypothyroidism, depression, and CKD. A kidney biopsy showed
FSGS with focal collapsing features with moderate arteriosclerosis and severe interstitial fibrosis
with approximately 90% tubular atrophy. In October 2010, she progressed to ESRD and was
started on Hemodialysis.
A few years after the initiation of dialysis, the patient secondary hyperparathyroidism was noticed
to be uncontrolled. She was not compliant with dialysis sessions or medications and
unfortunately, her condition progressed to tertiary hyperparathyroidism in 2015. The patient's
case was refractory to medical treatment because of poor compliance. She refused surgery
despite multiple attempts to convince her to get a parathyroidectomy. She continued having
progressive facial changes with deformity in the maxillary and mandibular bone as well as severe
osteoporosis. She had multiple fractures including left femoral, cervical, lumbar, and Tibia
fractures. With time she developed calciphylaxis. Her main complaints were headache, diplopia
on lateral gaze with nasal and gums bleeding in addition to bone pain secondary to the fractures.
Her mobility was declining, and she was most of the time bound to a wheelchair.
On physical exam, the patient had severe maxillary and mandibular bony prominence and
enlarged gums with widening of the interdental spaces (Image 1). Her Ca, PO4, and PTH over the
years are shown in figures(1 and 2). PTH levels were elevated and reached as high as 1600-5800
pg/mL. Maxillofacial CT showed a pepper pot appearance of the skull with markedly expansile
facial and jaw bones (Images 2a, 2b & 3). Ultrasound of the neck showed bilateral hypoechoic
nodules posterior-inferior to both thyroid lobes, the largest measuring 29 x 26 mm (Image 4).
3. 3
Pathophysiology:
During human growth, bone modeling will shape the skeleton. After maturity, bone remodeling
takes place, and the old bone gets replaced by new bone through resorption and bone formation.
In normal adults, bone resorption and formation are balanced, and any abnormality can result in
an alteration of the bone mass. The major balance in this process is kept by the calcium-regulating
hormones; parathyroid hormone (PTH) and calcitriol.
With intact kidney, phosphate, and calcium concentrations are regulated through interaction
between PTH, 1,25(OH)2D (calcitriol), Fibroblast growth factor-23 (FGF-23), and their principal
targets: bone, kidney, the GI tract, and parathyroid glands (figure 2) (1).
CKD-MBD is defined by KDIGO as a systemic disorder of mineral and bone metabolism due to
CKD, manifested by a combination of factors including (i) changes in calcium, phosphorus, PTH,
and vitamin D metabolism. (ii) variation in bone turnover, mineralization, volume, linear growth,
or strength. (iii) vascular or other soft tissue calcification. (11) CKD-MBD is invariably present
beyond CKD stage III. The treatment represents a significant clinical challenge. (1) Renal
osteodystrophy is an alteration of bone morphology in patients with CKD leading ultimately to
diminished bone strength. (11)
When CKD develops, the loss of renal function will result in phosphate accumulation, and FGF-23
will increase causing decreased 1,25(OH) Vitamin D which will decrease serum calcium. This will
increase PTH synthesis and release, resulting in secondary hyperparathyroidism. Prolonged
stimulation of parathyroid tissue will cause clonal proliferation of Parathyroid cells with areas of
nodular hyperplasia. Failure of the hyperplasic, overactive glands to be suppressed adequately in
response to optimal medical therapy will result in tertiary/autonomous Hyperparathyroidism.
The persistently elevated PTH will cause skeletal as well as non-skeletal complications such as
LVH, cardiac fibrosis, extraskeletal calcifications, and peripheral neuropathy (1).
Discussion:
Secondary HPT is a frequent endocrinal disease in the CKD population. If untreated properly, this
condition can evolve into severe skeletal disorders (renal osteodystrophy), in addition to high
cardiovascular morbidity and mortality due to vascular calcifications (4). This was clear in our
case, because of the poor compliance which led to the disease progression.
Renal osteodystrophy can lead to numerous craniofacial changes, including demineralization or
osteomalacia that can predispose to fractures, mixed osteolysis, and sclerosis that produce a salt-
and-pepper appearance, brown tumors, and Uremic Leontiasis Ossea (ULO) (5). All these features
are clearly illustrated in our patient's x-rays, skull CT scan, and DEXA scan.
4. 4
The patient showed a pathognomonic facial deformity due to long-standing renal failure along
with poorly controlled and progressive hyperparathyroidism. All the facial deformities and bony
changes known as Uremic Leontiasis Ossea (ULO) are reported to be preventable if the
Parathyroid disease is properly treated.
The disease was first described in 1940 when the term ULO (lion head) was first used by Kienböck
(3). It is a very rare manifestation of renal osteodystrophy and only a few cases have been
published (5,6). It is characterized by the massive craniofacial bones thickening (5). Patients
present typically with progressive painless jaw enlargement, widening of the nares, flattening of
the nasal bridge, and increased interdental spacing. In addition, to the cosmetic impact, patients
often suffer functional impairment, including dysphagia, speech impairment, respiratory distress,
and cranial nerve paralysis that can lead to blindness. (7,3).
ULO affects mainly young people, often with a long dialysis history. The major reported risk factors
are attributed to insufficient access to healthcare with poor management of CKD-MBD control(8).
ESRD patients who are non-adherent to hemodialysis regimens and medications are susceptible
more to the disease (9). Both factors led to the form of severe Mineral bone deformity. The poor
compliance and refusal to undergo Parathyroidectomy early in the disease course led to the
continuous progression and development of multiple fractures. We do not have evidence of the
bone healing process in such cases. We noticed that the pain was the main problem in our case
and because she was immobile most of the time the functional impairment in her daily lifestyle
was not appreciated.
The physiopathology of ULO is unclear, however, there is a significant bone remodeling mainly in
the facial bones compared to the rest of the skeleton. (8) Why this happens mainly in the face is
not known.
The diagnosis can be ascertained based on the combination of clinical picture, laboratory, and
diagnostic imaging (7). The treatment for ULO usually includes (1) reduction of phosphate levels,
(2) treatment for hyperparathyroidism, and (3) surgical contouring of the enlarged facial bones if
needed (3). The standard management of secondary and tertiary hyperparathyroidism with
consideration of parathyroidectomy (7). Percutaneous fine needle ethanol injection of the
parathyroid gland and percutaneous injection using Calcitriol and vitamin D Analogue were other
reported treatment options for non-surgical candidates. (10).
5. 5
When untreated bone remodeling may cause progressive disfigurement, visual impairment,
deafness, dysphagia, airway obstruction, and even compressive myelopathy (8). However, there
are conflicting reports of partial improvement, stabilization, or worsening of facial deformity after
parathyroidectomy. Alternatively, some patients may benefit from corrective reconstructive
surgery (7).
Keywords: Uremic leontiasis ossea, secondary hyperparathyroidism, lion face, ULO, CKD.
References:
1)Simon Steddon, Neil Ashman, Alistair Chesser, John Cunningham. CKD-MBD Chapter 3 Chronic
Kidney Diseases. Oxford handbook of nephrology and hypertension second edition. Oxford,
Oxford University Press, 2014.
2) Heard B, Raj K, Yu FF, Agarwal A. Uremic Leontiasis Ossea. J Clin Imaging Sci. 2021 Apr 29;11:27.
doi: 10.25259/JCIS_18_2021. PMID: 33948342; PMCID: PMC8088473.
3) Wang J, Zhao X, Shi H, Zhu L, Tao X. Radiological diagnostic features of uremic leontiasis ossea:
a case report. Dentomaxillofac Radiol 2019; 48: 20190253.
4) Luchi, W.M., Vianna, J.G.P., Roberto, L.E.V. et al. Uremic leontiasis ossea. Endocrine 65, 707–
709 (2019). https://doi.org/10.1007/s12020-019-01976-z
5) Donoso-Hofer F, Gunther-Wood M, Romero-Romano P, Pezoa-Opazo N, Fernández-Toro MA,
Ortega-Pinto AV. Uremic leontiasis ossea, is a rare presentation of severe renal osteodystrophy
secondary to hyperparathyroidism. J Stomatol Oral Maxillofac Surg. 2018 Feb;119(1):56-60. doi:
10.1016/j.jormas.2017.10.006. Epub 2017 Oct 14. PMID: 29037869.
6) Gameiro J, Duarte I, Outerelo C, Lopes JA. Uremic lion face syndrome. J Bras Nefrol.
2019;41(2):304-305. doi:10.1590/2175-8239-JBN-2018-0198
7) Haroyan H, Bos A, Ginat DT. Uremic leontiasis ossea. Am J Otolaryngol. 2015 Jan-Feb;36(1):74-
6. doi: 10.1016/j.amjoto.2014.08.007. Epub 2014 Aug 20. PMID: 25224511.
6. 6
8) Tassin C, Moscatelli L, Di Ascia L, Vacher-Coponat H, Gosset C. Reversible bone deformities in a
severe case of uremic Leontiasis Ossea. J Nephrol. 2021 Jan 28. doi: 10.1007/s40620-021-00968-
5. Epub ahead of print. PMID: 33507522.
9) Nasra K, Dervishi M, Li S, et al. (October 20, 2020) Uremic Leontiasis Ossea in a Patient With
End-Stage Renal Disease in Hemodialysis. Cureus 12(10): e11060. doi:10.7759/cureus.11060
10) Chandran M, Wong J. Secondary and Tertiary Hyperparathyroidism in Chronic Kidney Disease:
An Endocrine and Renal Perspective. Indian J Endocrinol Metab. 2019;23(4):391-399.
doi:10.4103/ijem.IJEM_292_19
11) KDIGO, Kidney Disease: Improving Global Outcomes. KDIGO clinical practice guidelines for the
diagnosis, evaluation, prevention, and treatment of chronic kidney disease-mineral and bone
disorder (CKD-MBD) (2009). Kidney Int, 76 (Suppl 113), 1–132.