CREST Syndrome
Dermatomyositis
Hyperphosphatemia
N-Acetylgalactosaminyltransferases
Skin Diseases
Scleroderma, Systemic
Calciphylaxis
Joint Diseases
Telangiectasis
Hyperostosis, Cortical, Congenital
Skin Ulcer
Calcium Gluconate
Nadroparin
Eyelid Diseases
Calcium Pyrophosphate
Nephrocalcinosis
Durapatite
alpha-2-HS-Glycoprotein
Basal Ganglia Diseases
Raynaud Disease
Fibroblast Growth Factors
Cardiomyopathies
Antibodies, Antinuclear
Glucuronidase
Phosphorus
Centromere
Osteopontin
Autoantibodies
Skin
Biopsy
Calcium
Kidney Failure, Chronic
Broncholithiasis: rare but still present. (1/3283)
Broncholithiasis is a rare but distinct and potentially dangerous pulmonary problem that still needs to be considered in the differential diagnosis of some patients with bronchial obstruction. Broncholiths originate from calcified material in peribronchial lymph nodes eroding into the tracheobronchial tree. The clinical and chest X-ray signs are usually non-specific, but the diagnosis can nowadays be made based on clinical suspicion, CT-scan and fibre-optic bronchoscopy findings, so that a malignant cause of airway obstruction can be ruled out. The removal of broncholiths during fibre-optic bronchoscopy is seldom possible and rather dangerous. They can be removed safely by rigid bronchoscopy with the aid of Nd-YAG laser photocoagulation. Thoracotomy is indicated in complicated cases with fistula formation or severe bleeding. (+info)Role of glutaraldehyde in calcification of porcine aortic valve fibroblasts. (2/3283)
Glutaraldehyde-treated porcine aortic valve xenografts frequently fail due to calcification. Calcification in the prostheses begins intracellularly. In a previous study, various types of cell injury to canine valvular fibroblasts, including glutaraldehyde treatment, led to calcification. An influx of extracellular Ca2+ into the phosphate-rich cytosol was theorized to be the mechanism of calcification. To test the Ca2+ influx theory, cytosolic Ca2+ and Pi concentrations were assessed in glutaraldehyde-treated porcine aortic valve fibroblasts, and their relationship to a subsequent calcification was studied. Glutaraldehyde caused an immediate and sustained massive cytosolic Ca2+ increase that was dose dependent and a several-fold increase in Pi. Calcification of cells followed within a week. The earliest calcification was observed in blebs formed on glutaraldehyde-treated cells. Live control cells or cells fixed with glutaraldehyde in Ca2+-free solution did not calcify under the same conditions. Concomitant increases in Ca2+ and Pi in glutaraldehyde-treated cells appear to underlie the mechanism of calcification, and the presence of extracellular Ca2+ during glutaraldehyde fixation promotes calcification. (+info)Histology and tissue chemistry of tidemark separation in hamsters. (3/3283)
Adult articular cartilage is divided by the tidemark into a deep calcified layer and a more superficial uncalcified layer. Histologic examination of articular cartilage from the knee joint of golden Syrian hamsters 123 days of age or older revealed defects at the tidemark in the tibia. Defects ranged from small separations of the calcified and uncalcified layers along the tidemark to progressively larger defects apparently formed by dissolution. These larger defects appeared as cavities in the noncalcified cartilage, had smooth rather than rough edges, frequently contained coalesced debris, and often resulted in a bulge in the articular surface. Occasionally, these large defects broke through the articular surface. Defects were not observed in tibial cartilage of younger (<90 days old) hamsters or in femoral cartilage from hamsters of any age. Exercise neither protected against nor increased the severity of the defects. Collagen cross-linking by pyridinoline was examined as a function of age and increased from 1,090 to 3,062 micromoles of pyridinoline/mole of hydroxyproline over the period of 1-9 months of age but was not correlated with defect formation. With increasing age, these focal tidemark defects could lead to osteoarthrosis-like cartilage lesions. (+info)Incidence and clinical relevance of coronary calcification detected by electron beam computed tomography in heart transplant recipients. (4/3283)
BACKGROUND: Patients treated by cardiac transplantation who survive beyond one year are at significant risk from fatal coronary artery disease. The development of coronary artery calcification in these patients is discussed and methods available to detect it are reviewed. OBJECTIVES: To assess the clinical importance of coronary artery calcium in heart transplant recipients. METHODS: In a cohort of 102 cardiac transplant recipients, electron beam computed tomography was used to measure calcium in the coronary arterial wall 63 days to 9.1 years (median 4.6 years) after transplantation. The results were compared with angiographic findings and with conventional coronary disease risk factors. The patients were followed for a mean of 2.12 years (1.2-4.02 years) to assess the relationship between these findings and future cardiac events. RESULTS: Forty-one (40.2%) had a stenosis of > 24% in one or more major coronary artery at angiography. Forty-six (45%) had a coronary calcium score > 0. The absence of calcium had a negative predictive value with respect to angiographic disease in any vessels of 87.5%. Logistic regression revealed that dyslipidaemia, systemic hypertension and organ ischaemic time were significant predictors of calcification. At follow-up, both an abnormal coronary angiogram and coronary calcium were found to be the only significant predictors of late events. Multivariate analysis suggested that the detection of coronary calcium did not offer any additional predictive information over that provided by the angiogram itself. CONCLUSION: Electron beam computed tomography is well suited to the assessment of calcium in the coronary arteries of heart transplant recipients, although the mechanisms of this calcification remain poorly understood. Calcium is detected more frequently than would be suggested by studies using intravascular ultrasound. It is associated with the presence of angiographic disease, and with some conventional risk factors for coronary disease. At follow-up the presence of coronary calcium was associated with an adverse clinical outcome, as it is in conventional ischaemic heart disease. (+info)Renal biopsy in the milk-alkali syndrome. (5/3283)
In milk-alkali syndrome the degree of renal impairment varies greatly. Few reports have been published describing structural changes on renal biopsy. In three illustrative cases, impairment of renal function was related to morphological changes shown on percutaneous biopsy. Milk-alkali syndrome should be considered as a cause of renal dysfunction in patients with a long history of dyspensia. (+info)Degenerative changes in aortic root allografts placed in the right ventricular outflow tract of growing puppies. (6/3283)
Differently prepared aortic root allografts were implanted in the right ventricular outflow tract of growing puppies to determine the site of origin and progress of degenerative changes in these conduits. The three preparations assessed were as follows: group A, fresh and sterile grafts; group B, antibiotic sterilized grafts in nutrient medium; and group C, beta-propiolactone sterilized grafts. Although calcification of the aortic wall occurred in all groups, the aortic leaflets were minimally affected. A correlation between viability and lack of calcification and between viability and long-term function is emphasized. (+info)Calcific myonecrosis. (7/3283)
Calcific myonecrosis is a rare and late sequela of compartment syndrome, which becomes symptomatic years after the initial trauma. We diagnosed this condition in a 64-year old man, 42 years after he sustained a shot-gun wound to the right lower leg. Total excision of a peripherally calcified, cystic mass, continuous with the anterior tibial muscle belly resulted in complete resolution of symptoms. Consideration of the diagnosis is warranted in patients with a history of major injury who develop a soft tissue mass in the traumatized compartment. The treatment of choice is marginal excision. (+info)Angiographic correlation of CT calcification in the carotid siphon. (8/3283)
BACKGROUND AND PURPOSE: Calcification in the coronary arteries has been correlated with significant vessel stenosis. The predictive value of calcification within the carotid siphon has not been characterized; however, stenosis in the carotid siphon is potentially important in determining management of patients with ipsilateral carotid bifurcation stenosis. The purpose of this study was to determine optimal parameters for assessing carotid siphon calcification on head CT scans and to compare the CT findings with angiographic results. METHODS: We performed a retrospective review of patients referred for diagnostic carotid arteriography. Those patients who also had undergone a head CT study at our institution were selected. The CT scans and angiograms of 64 patients (128 vessels) were reviewed. Carotid siphon calcification on CT scans was characterized on brain and bone windows as mild, moderate, or severe. Comparison was then made with angiographic findings. RESULTS: The sensitivity and specificity of CT for depicting greater than 50% angiographic stenosis in the carotid siphon were 86% and 98%, respectively, for bone windows and 100% and 0%, respectively, for brain windows. The positive predictive value (PPV) for a stenosis of greater than 50% as evidenced by severe calcification was 86% on bone windows and 11% on brain windows. The PPV for mild and moderate calcification on bone windows was 2.5% and 0%, respectively. CONCLUSION: Severe CT calcification in the carotid siphon as characterized on bone windows correlates with a carotid siphon stenosis of greater than 50% as determined angiographically. Therefore, the identification of severe calcification offers a potential noninvasive method for identifying stenosis of the carotid siphon. This information may be essential in determining management and prognosis for patients with carotid bifurcation stenosis. (+info)Calcinosis is a medical condition characterized by the abnormal deposit of calcium salts in various tissues of the body, commonly under the skin or in the muscles and tendons. These calcium deposits can form hard lumps or nodules that can cause pain, inflammation, and restricted mobility. Calcinosis can occur as a complication of other medical conditions, such as autoimmune disorders, kidney disease, and hypercalcemia (high levels of calcium in the blood). In some cases, the cause of calcinosis may be unknown. Treatment for calcinosis depends on the underlying cause and may include medications to manage calcium levels, physical therapy, and surgical removal of large deposits.
CREST syndrome is a subtype of a autoimmune connective tissue disorder called scleroderma (systemic sclerosis). The name "CREST" is an acronym that stands for the following five features:
* Calcinosis: The formation of calcium deposits in the skin and underlying tissues, which can cause painful ulcers.
* Raynaud's phenomenon: A condition in which the blood vessels in the fingers and toes constrict in response to cold or stress, causing the digits to turn white or blue and become numb or painful.
* Esophageal dysmotility: Difficulty swallowing due to weakened muscles in the esophagus.
* Sclerodactyly: Thickening and tightening of the skin on the fingers.
* Telangiectasias: Dilated blood vessels near the surface of the skin, causing red spots or lines.
It's important to note that not everyone with CREST syndrome will have all five of these features, and some people may have additional symptoms not included in the acronym. Additionally, CREST syndrome is a chronic condition that can cause a range of complications, including lung fibrosis, kidney problems, and digital ulcers. Treatment typically focuses on managing specific symptoms and slowing the progression of the disease.
Metabolic skin diseases are a group of cutaneous disorders that result from abnormalities in the metabolism of cells or systemic substances affecting the skin. These conditions can be caused by genetic defects, hormonal imbalances, nutritional deficiencies, or other underlying medical issues. Examples of metabolic skin diseases include:
1. Diabetic dermopathy: A condition characterized by the appearance of brown, scaly patches on the shins due to changes in small blood vessels caused by diabetes.
2. Porphyria cutanea tarda: A genetic disorder affecting heme biosynthesis, leading to blistering and scarring of sun-exposed skin.
3. Xanthomas: Deposits of fatty material (lipids) under the skin or in other tissues, often associated with high cholesterol levels or other lipid metabolism disorders.
4. Calciphylaxis: A rare condition characterized by calcification of small blood vessels and subsequent tissue death, typically affecting patients with chronic kidney disease.
5. Erythropoietic protoporphyria: A genetic disorder affecting heme biosynthesis, leading to photosensitivity, burning, itching, and scarring after sun exposure.
6. Gout: A form of arthritis caused by the buildup of uric acid crystals in joints, which can also lead to the formation of tophi (nodules) on the skin.
7. Amyloidosis: A group of diseases characterized by the abnormal accumulation of amyloid proteins in various organs and tissues, including the skin.
Treatment for metabolic skin diseases often involves addressing the underlying metabolic issue or disorder, as well as managing symptoms and preventing complications.
Dermatomyositis is a medical condition characterized by inflammation and weakness in the muscles and skin. It is a type of inflammatory myopathy, which means that it causes muscle inflammation and damage. Dermatomyositis is often associated with a distinctive rash that affects the skin around the eyes, nose, mouth, fingers, and toes.
The symptoms of dermatomyositis can include:
* Progressive muscle weakness, particularly in the hips, thighs, shoulders, and neck
* Fatigue
* Difficulty swallowing or speaking
* Skin rash, which may be pink or purple and is often accompanied by itching
* Muscle pain and tenderness
* Joint pain and swelling
* Raynaud's phenomenon, a condition that affects blood flow to the fingers and toes
The exact cause of dermatomyositis is not known, but it is believed to be related to an autoimmune response in which the body's immune system mistakenly attacks healthy tissue. Treatment for dermatomyositis typically involves medications to reduce inflammation and suppress the immune system, as well as physical therapy to help maintain muscle strength and function.
Hyperphosphatemia is a medical condition characterized by an excessively high level of phosphate (a form of the chemical element phosphorus) in the blood. Phosphate is an important component of various biological molecules, such as DNA, RNA, and ATP, and it plays a crucial role in many cellular processes, including energy metabolism and signal transduction.
In healthy individuals, the concentration of phosphate in the blood is tightly regulated within a narrow range to maintain normal physiological functions. However, when the phosphate level rises above this range (typically defined as a serum phosphate level greater than 4.5 mg/dL or 1.46 mmol/L), it can lead to hyperphosphatemia.
Hyperphosphatemia can result from various underlying medical conditions, including:
* Kidney dysfunction: The kidneys are responsible for filtering excess phosphate out of the blood and excreting it in the urine. When the kidneys fail to function properly, they may be unable to remove enough phosphate, leading to its accumulation in the blood.
* Hypoparathyroidism: The parathyroid glands produce a hormone called parathyroid hormone (PTH), which helps regulate calcium and phosphate levels in the body. In hypoparathyroidism, the production of PTH is insufficient, leading to an increase in phosphate levels.
* Hyperparathyroidism: In contrast, excessive production of PTH can also lead to hyperphosphatemia by increasing the release of phosphate from bones and decreasing its reabsorption in the kidneys.
* Excessive intake of phosphate-rich foods or supplements: Consuming large amounts of phosphate-rich foods, such as dairy products, nuts, and legumes, or taking phosphate supplements can raise blood phosphate levels.
* Tumor lysis syndrome: This is a complication that can occur after the treatment of certain types of cancer, particularly hematological malignancies. The rapid destruction of cancer cells releases large amounts of intracellular contents, including phosphate, into the bloodstream, leading to hyperphosphatemia.
* Rhabdomyolysis: This is a condition in which muscle tissue breaks down, releasing its contents, including phosphate, into the bloodstream. It can be caused by various factors, such as trauma, infection, or drug toxicity.
Hyperphosphatemia can have several adverse effects on the body, including calcification of soft tissues, kidney damage, and metabolic disturbances. Therefore, it is essential to diagnose and manage hyperphosphatemia promptly to prevent complications. Treatment options may include dietary modifications, medications that bind phosphate in the gastrointestinal tract, and dialysis in severe cases.
N-Acetylgalactosaminyltransferases (GalNAc-Ts) are a family of enzymes that play a crucial role in the process of protein glycosylation. Protein glycosylation is the attachment of carbohydrate groups, also known as glycans, to proteins. This modification significantly influences various biological processes such as protein folding, stability, trafficking, and recognition.
GalNAc-Ts specifically catalyze the transfer of N-acetylgalactosamine (GalNAc) from a donor molecule, UDP-GalNAc, to serine or threonine residues on acceptor proteins. This initial step of adding GalNAc to proteins is called mucin-type O-glycosylation and sets the stage for further glycan additions by other enzymes.
There are at least 20 different isoforms of GalNAc-Ts identified in humans, each with distinct substrate specificities, tissue distributions, and subcellular localizations. Aberrant expression or dysfunction of these enzymes has been implicated in various diseases, including cancer, where altered glycosylation patterns contribute to tumor progression and metastasis.
Skin diseases, also known as dermatological conditions, refer to any medical condition that affects the skin, which is the largest organ of the human body. These diseases can affect the skin's function, appearance, or overall health. They can be caused by various factors, including genetics, infections, allergies, environmental factors, and aging.
Skin diseases can present in many different forms, such as rashes, blisters, sores, discolorations, growths, or changes in texture. Some common examples of skin diseases include acne, eczema, psoriasis, dermatitis, fungal infections, viral infections, bacterial infections, and skin cancer.
The symptoms and severity of skin diseases can vary widely depending on the specific condition and individual factors. Some skin diseases are mild and can be treated with over-the-counter medications or topical creams, while others may require more intensive treatments such as prescription medications, light therapy, or even surgery.
It is important to seek medical attention if you experience any unusual or persistent changes in your skin, as some skin diseases can be serious or indicative of other underlying health conditions. A dermatologist is a medical doctor who specializes in the diagnosis and treatment of skin diseases.
Systemic Scleroderma, also known as Systemic Sclerosis (SSc), is a rare, chronic autoimmune disease that involves the abnormal growth and accumulation of collagen in various connective tissues, blood vessels, and organs throughout the body. This excessive collagen production leads to fibrosis or scarring, which can cause thickening, hardening, and tightening of the skin and damage to internal organs such as the heart, lungs, kidneys, and gastrointestinal tract.
Systemic Scleroderma is characterized by two main features: small blood vessel abnormalities (Raynaud's phenomenon) and fibrosis. The disease can be further classified into two subsets based on the extent of skin involvement: limited cutaneous systemic sclerosis (lcSSc) and diffuse cutaneous systemic sclerosis (dcSSc).
Limited cutaneous systemic sclerosis affects the skin distally, typically involving fingers, hands, forearms, feet, lower legs, and face. It is often associated with Raynaud's phenomenon, calcinosis, telangiectasias, and pulmonary arterial hypertension.
Diffuse cutaneous systemic sclerosis involves more extensive skin thickening and fibrosis that spreads proximally to affect the trunk, upper arms, thighs, and face. It is commonly associated with internal organ involvement, such as interstitial lung disease, heart disease, and kidney problems.
The exact cause of Systemic Scleroderma remains unknown; however, it is believed that genetic, environmental, and immunological factors contribute to its development. There is currently no cure for Systemic Scleroderma, but various treatments can help manage symptoms, slow disease progression, and improve quality of life.
Calciphylaxis is a rare but serious medical condition characterized by the formation of calcium deposits in small blood vessels and surrounding tissues, particularly in the skin and fatty tissue beneath the skin. This can lead to tissue death (necrosis) and ulceration, often resulting in severe pain, infection, and other complications.
Calciphylaxis is most commonly seen in patients with chronic kidney disease or end-stage renal failure, although it has also been reported in patients with normal kidney function. Other risk factors include obesity, female gender, diabetes, and use of warfarin or corticosteroids.
The exact cause of calciphylaxis is not fully understood, but it is believed to involve a combination of factors such as abnormal mineral metabolism, inflammation, and vascular injury. Treatment typically involves addressing any underlying medical conditions, wound care, and sometimes surgical debridement or skin grafting. In some cases, medications such as sodium thiosulfate or bisphosphonates may be used to help dissolve the calcium deposits and improve symptoms.
Foot diseases refer to various medical conditions that affect the foot, including its structures such as the bones, joints, muscles, tendons, ligaments, blood vessels, and nerves. These conditions can cause symptoms like pain, swelling, numbness, difficulty walking, and skin changes. Examples of foot diseases include:
1. Plantar fasciitis: inflammation of the band of tissue that connects the heel bone to the toes.
2. Bunions: a bony bump that forms on the joint at the base of the big toe.
3. Hammertoe: a deformity in which the toe is bent at the middle joint, resembling a hammer.
4. Diabetic foot: a group of conditions that can occur in people with diabetes, including nerve damage, poor circulation, and increased risk of infection.
5. Athlete's foot: a fungal infection that affects the skin between the toes and on the soles of the feet.
6. Ingrown toenails: a condition where the corner or side of a toenail grows into the flesh of the toe.
7. Gout: a type of arthritis that causes sudden, severe attacks of pain, swelling, redness, and tenderness in the joints, often starting with the big toe.
8. Foot ulcers: open sores or wounds that can occur on the feet, especially in people with diabetes or poor circulation.
9. Morton's neuroma: a thickening of the tissue around a nerve between the toes, causing pain and numbness.
10. Osteoarthritis: wear and tear of the joints, leading to pain, stiffness, and reduced mobility.
Foot diseases can affect people of all ages and backgrounds, and some may be prevented or managed with proper foot care, hygiene, and appropriate medical treatment.
Joint diseases is a broad term that refers to various conditions affecting the joints, including but not limited to:
1. Osteoarthritis (OA): A degenerative joint disease characterized by the breakdown of cartilage and underlying bone, leading to pain, stiffness, and potential loss of function.
2. Rheumatoid Arthritis (RA): An autoimmune disorder causing inflammation in the synovial membrane lining the joints, resulting in swelling, pain, and joint damage if left untreated.
3. Infectious Arthritis: Joint inflammation caused by bacterial, viral, or fungal infections that spread through the bloodstream or directly enter the joint space.
4. Gout: A type of arthritis resulting from the buildup of uric acid crystals in the joints, typically affecting the big toe and characterized by sudden attacks of severe pain, redness, and swelling.
5. Psoriatic Arthritis (PsA): An inflammatory joint disease associated with psoriasis, causing symptoms such as pain, stiffness, and swelling in the joints and surrounding tissues.
6. Juvenile Idiopathic Arthritis (JIA): A group of chronic arthritis conditions affecting children, characterized by joint inflammation, pain, and stiffness.
7. Ankylosing Spondylitis: A form of arthritis primarily affecting the spine, causing inflammation, pain, and potential fusion of spinal vertebrae.
8. Bursitis: Inflammation of the fluid-filled sacs (bursae) that cushion joints, leading to pain and swelling.
9. Tendinitis: Inflammation or degeneration of tendons, which connect muscles to bones, often resulting in pain and stiffness near joints.
These conditions can impact the function and mobility of affected joints, causing discomfort and limiting daily activities. Proper diagnosis and treatment are essential for managing joint diseases and preserving joint health.
Telangiectasia is a medical term that refers to the dilation and widening of small blood vessels called capillaries, leading to their visibility under the skin or mucous membranes. These dilated vessels often appear as tiny red lines or patterns, measuring less than 1 millimeter in diameter.
Telangiectasias can occur in various parts of the body, such as the face, nose, cheeks, legs, and fingers. They are typically harmless but may cause cosmetic concerns for some individuals. In certain cases, telangiectasias can be a sign of an underlying medical condition, like rosacea, hereditary hemorrhagic telangiectasia (HHT), or liver disease.
It is essential to consult with a healthcare professional if you notice any unusual changes in your skin or mucous membranes, as they can provide appropriate evaluation and treatment recommendations based on the underlying cause of the telangiectasias.
Congenital cortical hyperostosis is a rare, inherited bone disorder that is characterized by abnormal thickening of the outer layer of bones (cortical hyperostosis). This condition primarily affects the skull and long bones of the arms and legs. The exact cause of congenital cortical hyperostosis is not fully understood, but it is believed to be related to mutations in certain genes that regulate bone growth and development.
The symptoms of congenital cortical hyperostosis can vary widely from person to person, depending on the severity and location of the bone abnormalities. Some common features of this condition include:
* A thickened skull, which may cause a prominent forehead or a misshapen head
* Abnormally thick and dense long bones in the arms and legs, which can make them heavy and difficult to move
* Delayed growth and development
* Increased risk of fractures
* Pain and stiffness in the affected bones
Congenital cortical hyperostosis is typically diagnosed based on a combination of clinical symptoms, imaging studies (such as X-rays or CT scans), and genetic testing. There is no cure for this condition, but treatment may involve pain management, physical therapy, and surgery to correct any bone deformities. In some cases, the symptoms of congenital cortical hyperostosis may improve over time, but in others, they may persist throughout life.
A skin ulcer is a defined as a loss of continuity or disruption of the skin surface, often accompanied by inflammation and/or infection. These lesions can result from various causes including pressure, venous or arterial insufficiency, diabetes, and chronic dermatological conditions. Skin ulcers are typically characterized by their appearance, depth, location, and underlying cause. Common types of skin ulcers include pressure ulcers (also known as bedsores), venous leg ulcers, arterial ulcers, and diabetic foot ulcers. Proper evaluation, wound care, management of underlying conditions, and prevention strategies are crucial in the treatment of skin ulcers to promote healing and prevent complications.
Calcium gluconate is a medical compound that is used primarily as a medication to treat conditions related to low calcium levels in the body (hypocalcemia) or to prevent calcium deficiency. It is also used as an antidote for treating poisoning from certain chemicals, such as beta-blockers and fluoride.
Calcium gluconate is a form of calcium salt, which is combined with gluconic acid, a natural organic acid found in various fruits and honey. This compound has a high concentration of calcium, making it an effective supplement for increasing calcium levels in the body.
In medical settings, calcium gluconate can be administered orally as a tablet or liquid solution, or it can be given intravenously (directly into a vein) by a healthcare professional. The intravenous route is typically used in emergency situations to quickly raise calcium levels and treat symptoms of hypocalcemia, such as muscle cramps, spasms, or seizures.
It's important to note that while calcium gluconate can be beneficial for treating low calcium levels, it should only be used under the guidance of a healthcare provider, as improper use or overdose can lead to serious side effects, including kidney damage and heart problems.
Nadroparin is defined as a low molecular weight heparin (LMWH) drug, which is used as an anticoagulant. It is derived from unfractionated heparin and works by inhibiting the activity of coagulation factor Xa and to a lesser extent, thrombin. Nadroparin is commonly used for the prevention and treatment of deep vein thrombosis (DVT) and pulmonary embolism (PE), as well as for the management of unstable angina and non-Q wave myocardial infarction.
The drug is administered subcutaneously, and its anticoagulant effect is monitored by measuring the activated partial thromboplastin time (APTT) or anti-Xa activity. The half-life of nadroparin is approximately 4 hours, and it has a lower risk of heparin-induced thrombocytopenia (HIT) compared to unfractionated heparin.
It's important to note that the use of nadroparin or any other anticoagulant medication should be under the supervision of a healthcare professional, and patients should be closely monitored for bleeding risks and other potential adverse effects.
Eyelid diseases refer to a variety of medical conditions that affect the function and/or appearance of the eyelids. These can include structural abnormalities, such as entropion (inward turning of the eyelid) or ectropion (outward turning of the eyelid), as well as functional issues like ptosis (drooping of the upper eyelid). Other common eyelid diseases include blepharitis (inflammation of the eyelid margin), chalazion (a blocked oil gland in the eyelid), and cancerous or benign growths on the eyelid. Symptoms of eyelid diseases can vary widely, but often include redness, swelling, pain, itching, tearing, and sensitivity to light. Treatment for these conditions depends on the specific diagnosis and may range from self-care measures and medications to surgical intervention.
Calcium pyrophosphate is a mineral compound made up of calcium and pyrophosphate ions. In the body, it can form crystals that deposit in joints, causing a type of arthritis known as calcium pyrophosphate deposition (CPPD) disease or pseudogout. CPPD disease is characterized by sudden attacks of joint pain and swelling, often in the knee or wrist. The condition is more common in older adults and can also occur in people with underlying medical conditions such as hyperparathyroidism, hemochromatosis, and hypophosphatasia. Calcium pyrophosphate crystals may also be found in the fluid around the heart (pericardial fluid) or in other tissues, but they do not always cause symptoms.
Nephrocalcinosis is a medical condition characterized by the deposition of calcium salts in the renal parenchyma, specifically within the tubular epithelial cells and interstitium of the kidneys. This process can lead to chronic inflammation, tissue damage, and ultimately impaired renal function if left untreated.
The condition is often associated with metabolic disorders such as hyperparathyroidism, distal renal tubular acidosis, or hyperoxaluria; medications like loop diuretics, corticosteroids, or calcineurin inhibitors; and chronic kidney diseases. The diagnosis of nephrocalcinosis is typically made through imaging studies such as ultrasound, CT scan, or X-ray. Treatment usually involves addressing the underlying cause, modifying dietary habits, and administering medications to control calcium levels in the body.
Dura Mater: The tough, outer membrane that covers the brain and spinal cord.
Hydroxyapatite: A naturally occurring mineral form of calcium apatite, also known as dahllite, with the formula Ca5(PO4)3(OH), is the primary mineral component of biological apatites found in bones and teeth.
Therefore, "Durapatite" isn't a recognized medical term, but it seems like it might be a combination of "dura mater" and "hydroxyapatite." If you meant to ask about a material used in medical or dental applications that combines properties of both dura mater and hydroxyapatite, please provide more context.
Alpha-2-HS-Glycoprotein (AHSG), also known as fetuin-A, is a plasma protein synthesized primarily in the liver. It belongs to the group of proteins called acute phase reactants, which means its levels can increase or decrease in response to inflammation or injury. AHSG plays a role in several physiological processes, including inhibition of tissue calcification, regulation of insulin sensitivity, and modulation of immune responses. Structurally, it is a glycoprotein with two homologous domains, each containing three disulfide bridges. The function and regulation of AHSG are subjects of ongoing research due to its potential implications in various diseases, such as diabetes, cardiovascular disease, and chronic kidney disease.
Basal ganglia diseases are a group of neurological disorders that affect the function of the basal ganglia, which are clusters of nerve cells located deep within the brain. The basal ganglia play a crucial role in controlling movement and coordination. When they are damaged or degenerate, it can result in various motor symptoms such as tremors, rigidity, bradykinesia (slowness of movement), and difficulty with balance and walking.
Some examples of basal ganglia diseases include:
1. Parkinson's disease - a progressive disorder that affects movement due to the death of dopamine-producing cells in the basal ganglia.
2. Huntington's disease - an inherited neurodegenerative disorder that causes uncontrolled movements, emotional problems, and cognitive decline.
3. Dystonia - a movement disorder characterized by sustained or intermittent muscle contractions that cause twisting and repetitive movements or abnormal postures.
4. Wilson's disease - a rare genetic disorder that causes excessive copper accumulation in the liver and brain, leading to neurological and psychiatric symptoms.
5. Progressive supranuclear palsy (PSP) - a rare brain disorder that affects movement, gait, and balance, as well as speech and swallowing.
6. Corticobasal degeneration (CBD) - a rare neurological disorder characterized by progressive loss of nerve cells in the cerebral cortex and basal ganglia, leading to stiffness, rigidity, and difficulty with movement and coordination.
Treatment for basal ganglia diseases varies depending on the specific diagnosis and symptoms but may include medication, surgery, physical therapy, or a combination of these approaches.
Phosphates, in a medical context, refer to the salts or esters of phosphoric acid. Phosphates play crucial roles in various biological processes within the human body. They are essential components of bones and teeth, where they combine with calcium to form hydroxyapatite crystals. Phosphates also participate in energy transfer reactions as phosphate groups attached to adenosine diphosphate (ADP) and adenosine triphosphate (ATP). Additionally, they contribute to buffer systems that help maintain normal pH levels in the body.
Abnormal levels of phosphates in the blood can indicate certain medical conditions. High phosphate levels (hyperphosphatemia) may be associated with kidney dysfunction, hyperparathyroidism, or excessive intake of phosphate-containing products. Low phosphate levels (hypophosphatemia) might result from malnutrition, vitamin D deficiency, or certain diseases affecting the small intestine or kidneys. Both hypophosphatemia and hyperphosphatemia can have significant impacts on various organ systems and may require medical intervention.
Dermatologic agents are medications, chemicals, or other substances that are applied to the skin (dermis) for therapeutic or cosmetic purposes. They can be used to treat various skin conditions such as acne, eczema, psoriasis, fungal infections, and wounds. Dermatologic agents include topical corticosteroids, antibiotics, antifungals, retinoids, benzoyl peroxide, salicylic acid, and many others. They can come in various forms such as creams, ointments, gels, lotions, solutions, and patches. It is important to follow the instructions for use carefully to ensure safety and effectiveness.
Raynaud's disease, also known as Raynaud's phenomenon or syndrome, is a condition that affects the blood vessels, particularly in the fingers and toes. It is characterized by episodes of vasospasm (constriction) of the small digital arteries and arterioles, which can be triggered by cold temperatures or emotional stress. This results in reduced blood flow to the affected areas, causing them to become pale or white and then cyanotic (blue) due to the accumulation of deoxygenated blood. As the episode resolves, the affected areas may turn red as blood flow returns, sometimes accompanied by pain, numbness, or tingling sensations.
Raynaud's disease can be primary, meaning it occurs without an underlying medical condition, or secondary, which is associated with connective tissue disorders, autoimmune diseases, or other health issues such as carpal tunnel syndrome, vibration tool usage, or smoking. Primary Raynaud's is more common and tends to be less severe than secondary Raynaud's.
Treatment for Raynaud's disease typically involves avoiding triggers, keeping the body warm, and using medications to help dilate blood vessels and improve circulation. In some cases, lifestyle modifications and smoking cessation may also be recommended to manage symptoms and prevent progression of the condition.
Fibroblast Growth Factors (FGFs) are a family of growth factors that play crucial roles in various biological processes, including cell survival, proliferation, migration, and differentiation. They bind to specific tyrosine kinase receptors (FGFRs) on the cell surface, leading to intracellular signaling cascades that regulate gene expression and downstream cellular responses. FGFs are involved in embryonic development, tissue repair, and angiogenesis (the formation of new blood vessels). There are at least 22 distinct FGFs identified in humans, each with unique functions and patterns of expression. Some FGFs, like FGF1 and FGF2, have mitogenic effects on fibroblasts and other cell types, while others, such as FGF7 and FGF10, are essential for epithelial-mesenchymal interactions during organ development. Dysregulation of FGF signaling has been implicated in various pathological conditions, including cancer, fibrosis, and developmental disorders.
Cardiomyopathies are a group of diseases that affect the heart muscle, leading to mechanical and/or electrical dysfunction. The American Heart Association (AHA) defines cardiomyopathies as "a heterogeneous group of diseases of the myocardium associated with mechanical and/or electrical dysfunction that usually (but not always) exhibit inappropriate ventricular hypertrophy or dilatation and frequently lead to heart failure."
There are several types of cardiomyopathies, including:
1. Dilated cardiomyopathy (DCM): This is the most common type of cardiomyopathy, characterized by an enlarged left ventricle and impaired systolic function, leading to heart failure.
2. Hypertrophic cardiomyopathy (HCM): In this type, there is abnormal thickening of the heart muscle, particularly in the septum between the two ventricles, which can obstruct blood flow and increase the risk of arrhythmias.
3. Restrictive cardiomyopathy (RCM): This is a rare form of cardiomyopathy characterized by stiffness of the heart muscle, impaired relaxation, and diastolic dysfunction, leading to reduced filling of the ventricles and heart failure.
4. Arrhythmogenic right ventricular cardiomyopathy (ARVC): In this type, there is replacement of the normal heart muscle with fatty or fibrous tissue, primarily affecting the right ventricle, which can lead to arrhythmias and sudden cardiac death.
5. Unclassified cardiomyopathies: These are conditions that do not fit into any of the above categories but still significantly affect the heart muscle and function.
Cardiomyopathies can be caused by genetic factors, acquired conditions (e.g., infections, toxins, or autoimmune disorders), or a combination of both. The diagnosis typically involves a comprehensive evaluation, including medical history, physical examination, electrocardiogram (ECG), echocardiography, cardiac magnetic resonance imaging (MRI), and sometimes genetic testing. Treatment depends on the type and severity of the condition but may include medications, lifestyle modifications, implantable devices, or even heart transplantation in severe cases.
Antinuclear antibodies (ANA) are a type of autoantibody that target structures found in the nucleus of a cell. These antibodies are produced by the immune system and attack the body's own cells and tissues, leading to inflammation and damage. The presence of ANA is often used as a marker for certain autoimmune diseases, such as systemic lupus erythematosus (SLE), Sjogren's syndrome, rheumatoid arthritis, scleroderma, and polymyositis.
ANA can be detected through a blood test called the antinuclear antibody test. A positive result indicates the presence of ANA in the blood, but it does not necessarily mean that a person has an autoimmune disease. Further testing is usually needed to confirm a diagnosis and determine the specific type of autoantibodies present.
It's important to note that ANA can also be found in healthy individuals, particularly as they age. Therefore, the test results should be interpreted in conjunction with other clinical findings and symptoms.
Glucuronidase is an enzyme that catalyzes the hydrolysis of glucuronic acid from various substrates, including molecules that have been conjugated with glucuronic acid as part of the detoxification process in the body. This enzyme plays a role in the breakdown and elimination of certain drugs, toxins, and endogenous compounds, such as bilirubin. It is found in various tissues and organisms, including humans, bacteria, and insects. In clinical contexts, glucuronidase activity may be measured to assess liver function or to identify the presence of certain bacterial infections.
Phosphorus is an essential mineral that is required by every cell in the body for normal functioning. It is a key component of several important biomolecules, including adenosine triphosphate (ATP), which is the primary source of energy for cells, and deoxyribonucleic acid (DNA) and ribonucleic acid (RNA), which are the genetic materials in cells.
Phosphorus is also a major constituent of bones and teeth, where it combines with calcium to provide strength and structure. In addition, phosphorus plays a critical role in various metabolic processes, including energy production, nerve impulse transmission, and pH regulation.
The medical definition of phosphorus refers to the chemical element with the atomic number 15 and the symbol P. It is a highly reactive non-metal that exists in several forms, including white phosphorus, red phosphorus, and black phosphorus. In the body, phosphorus is primarily found in the form of organic compounds, such as phospholipids, phosphoproteins, and nucleic acids.
Abnormal levels of phosphorus in the body can lead to various health problems. For example, high levels of phosphorus (hyperphosphatemia) can occur in patients with kidney disease or those who consume large amounts of phosphorus-rich foods, and can contribute to the development of calcification of soft tissues and cardiovascular disease. On the other hand, low levels of phosphorus (hypophosphatemia) can occur in patients with malnutrition, vitamin D deficiency, or alcoholism, and can lead to muscle weakness, bone pain, and an increased risk of infection.
A centromere is a specialized region found on chromosomes that plays a crucial role in the separation of replicated chromosomes during cell division. It is the point where the sister chromatids (the two copies of a chromosome formed during DNA replication) are joined together. The centromere contains highly repeated DNA sequences and proteins that form a complex structure known as the kinetochore, which serves as an attachment site for microtubules of the mitotic spindle during cell division.
During mitosis or meiosis, the kinetochore facilitates the movement of chromosomes by interacting with the microtubules, allowing for the accurate distribution of genetic material to the daughter cells. Centromeres can vary in their position and structure among different species, ranging from being located near the middle of the chromosome (metacentric) to being positioned closer to one end (acrocentric). The precise location and characteristics of centromeres are essential for proper chromosome segregation and maintenance of genomic stability.
Osteopontin (OPN) is a phosphorylated glycoprotein that is widely distributed in many tissues, including bone, teeth, and mineralized tissues. It plays important roles in various biological processes such as bone remodeling, immune response, wound healing, and tissue repair. In the skeletal system, osteopontin is involved in the regulation of bone formation and resorption by modulating the activity of osteoclasts and osteoblasts. It also plays a role in the development of chronic inflammatory diseases such as rheumatoid arthritis, atherosclerosis, and cancer metastasis to bones. Osteopontin is considered a potential biomarker for various disease states, including bone turnover, cardiovascular disease, and cancer progression.
In medical terms, fingers are not specifically defined as they are common anatomical structures. However, I can provide you with a general anatomy definition:
Fingers are the terminal parts of the upper limb in primates, including humans, consisting of four digits (thumb, index, middle, and ring fingers) and one opposable thumb. They contain bones called phalanges, connected by joints that allow for movement and flexibility. Each finger has a nail, nerve endings for sensation, and blood vessels to supply nutrients and oxygen. Fingers are crucial for various activities such as grasping, manipulating objects, and tactile exploration of the environment.
Autoantibodies are defined as antibodies that are produced by the immune system and target the body's own cells, tissues, or organs. These antibodies mistakenly identify certain proteins or molecules in the body as foreign invaders and attack them, leading to an autoimmune response. Autoantibodies can be found in various autoimmune diseases such as rheumatoid arthritis, lupus, and thyroiditis. The presence of autoantibodies can also be used as a diagnostic marker for certain conditions.
In medical terms, the skin is the largest organ of the human body. It consists of two main layers: the epidermis (outer layer) and dermis (inner layer), as well as accessory structures like hair follicles, sweat glands, and oil glands. The skin plays a crucial role in protecting us from external factors such as bacteria, viruses, and environmental hazards, while also regulating body temperature and enabling the sense of touch.
A biopsy is a medical procedure in which a small sample of tissue is taken from the body to be examined under a microscope for the presence of disease. This can help doctors diagnose and monitor various medical conditions, such as cancer, infections, or autoimmune disorders. The type of biopsy performed will depend on the location and nature of the suspected condition. Some common types of biopsies include:
1. Incisional biopsy: In this procedure, a surgeon removes a piece of tissue from an abnormal area using a scalpel or other surgical instrument. This type of biopsy is often used when the lesion is too large to be removed entirely during the initial biopsy.
2. Excisional biopsy: An excisional biopsy involves removing the entire abnormal area, along with a margin of healthy tissue surrounding it. This technique is typically employed for smaller lesions or when cancer is suspected.
3. Needle biopsy: A needle biopsy uses a thin, hollow needle to extract cells or fluid from the body. There are two main types of needle biopsies: fine-needle aspiration (FNA) and core needle biopsy. FNA extracts loose cells, while a core needle biopsy removes a small piece of tissue.
4. Punch biopsy: In a punch biopsy, a round, sharp tool is used to remove a small cylindrical sample of skin tissue. This type of biopsy is often used for evaluating rashes or other skin abnormalities.
5. Shave biopsy: During a shave biopsy, a thin slice of tissue is removed from the surface of the skin using a sharp razor-like instrument. This technique is typically used for superficial lesions or growths on the skin.
After the biopsy sample has been collected, it is sent to a laboratory where a pathologist will examine the tissue under a microscope and provide a diagnosis based on their findings. The results of the biopsy can help guide further treatment decisions and determine the best course of action for managing the patient's condition.
Calcium is an essential mineral that is vital for various physiological processes in the human body. The medical definition of calcium is as follows:
Calcium (Ca2+) is a crucial cation and the most abundant mineral in the human body, with approximately 99% of it found in bones and teeth. It plays a vital role in maintaining structural integrity, nerve impulse transmission, muscle contraction, hormonal secretion, blood coagulation, and enzyme activation.
Calcium homeostasis is tightly regulated through the interplay of several hormones, including parathyroid hormone (PTH), calcitonin, and vitamin D. Dietary calcium intake, absorption, and excretion are also critical factors in maintaining optimal calcium levels in the body.
Hypocalcemia refers to low serum calcium levels, while hypercalcemia indicates high serum calcium levels. Both conditions can have detrimental effects on various organ systems and require medical intervention to correct.
Chronic kidney failure, also known as chronic kidney disease (CKD) stage 5 or end-stage renal disease (ESRD), is a permanent loss of kidney function that occurs gradually over a period of months to years. It is defined as a glomerular filtration rate (GFR) of less than 15 ml/min, which means the kidneys are filtering waste and excess fluids at less than 15% of their normal capacity.
CKD can be caused by various underlying conditions such as diabetes, hypertension, glomerulonephritis, polycystic kidney disease, and recurrent kidney infections. Over time, the damage to the kidneys can lead to a buildup of waste products and fluids in the body, which can cause a range of symptoms including fatigue, weakness, shortness of breath, nausea, vomiting, and confusion.
Treatment for chronic kidney failure typically involves managing the underlying condition, making lifestyle changes such as following a healthy diet, and receiving supportive care such as dialysis or a kidney transplant to replace lost kidney function.
Calcinosis
Tumoral calcinosis
Calcinosis cutis
Dystrophic calcinosis cutis
Iatrogenic calcinosis cutis
Milia-like calcinosis
Idiopathic scrotal calcinosis
Metastatic calcinosis cutis
Traumatic calcinosis cutis
Normophosphatemic familial tumoral calcinosis
Joseph Harold Sheldon
Hypercalcaemia
List of OMIM disorder codes
Indrajit Prasad
Dystrophic calcification
Hypervitaminosis A
Progeroid syndromes
Fiddler's neck
SAMD9
Nierembergia rivularis
GALNT3
Subepidermal calcified nodule
Primrose syndrome
Shapiro Senapathy algorithm
Primary familial brain calcification
Nicholas Theodore
Juvenile dermatomyositis
Calcification
Trisetum flavescens
American lobster
Calcinosis - Wikipedia
Hyperphosphatemic familial tumoral calcinosis: MedlinePlus Genetics
Calcinosis Cutis: Background, Pathophysiology, Etiology
Calcinosis - Gluten Free Works: TREATMENT GUIDE
Uremic tumoral calcinosis causing atlantoaxial subluxation and spinal cord compression in a patient on continuous ambulatory...
Evaluation of crystals in formalin-fixed, paraffin-embedded tissue sections for the differential diagnosis of pseudogout, gout,...
Juvenile dermatomyocitis with calcinosis
Calcinosis cutis - A series of 59 consecutive cases confined among women | East African Medical Journal
Petrified Ear - A Case of Calcinosis Cutis | HTML | Acta Dermato-Venereologica
Dermoscopic features of milia-like calcinosis cutis - Giornale Italiano di Dermatologia e Venereologia 2019 December;154(6):724...
Calcinosis Involving Multiple Paws in a Cat with Chronic Renal Failure and in a Cat with Hyperthyroidism | Advanced Veterinary...
Scrotal Calcinosis
Calcinosis cutis: Management
Calcinosis (medical condition) - Chemwatch
Diffuse Soft-Tissue Calcinosis
Calcinosis Cutis: Background, Pathophysiology, Epidemiology
575: Pathology⎪Tumoral Calcinosis - Orthohub
metastatic calcinosis cutis histopathology - Loma Linda Dermatopathology
Subcutaneous calcinosis revealed by an elbow trauma
Calcinosis Cutis in Lacey, WA | Dermatology Clinic for Animals
hyperphosphataemic
Scrotum, Idiopathic scrotal calcinosis [LMP53298] | LMP - Digital Laboratory Medicine Library
Idiopathic calcinosis cutis universalis | International Journal of Pediatric Endocrinology | Full Text
Live Action Mafia • View topic - Even arteries faints boys, calcinosis guidance communicated
Calcinosis cutis in Albright hereditary osteodystrophy: Pseudohypoparathyroidism Type Ia - Fingerprint - University of...
AJOU Open Repository: Obesity and calcinosis cutis: characteristic early signs of infantile pseudohypoparathyroidism.
View of Idiopathic giant scrotal calcinosis: a rare case report and literature review
G Jones | West Indian Medical Journal
Tumoral calcinosis of the temporomandibular joint: CT and MR findings<...
Resolution of calcinosis using bisphosphonates in overlap syndrome - a case report | BMC Rheumatology | Peer Review
Cutis25
- Calcinosis Cutis. (wikipedia.org)
- Calcinosis cutis complicating adult-onset dermatomyositis. (medscape.com)
- Calcinosis cutis universalis with joint contractures complicating juvenile dermatomyositis. (medscape.com)
- Marzano AV, Kolesnikova LV, Gasparini G, Alessi E. Dystrophic calcinosis cutis in subacute lupus. (medscape.com)
- Miteva L, Pramatarov K, Vassileva S. Calcinosis cutis in childhood systemic lupus erythematosus. (medscape.com)
- Extensive calcinosis cutis with systemic lupus erythematosus. (medscape.com)
- Tristano AG, Villarroel JL, Rodriguez MA, Millan A. Calcinosis cutis universalis in a patient with systemic lupus erythematosus. (medscape.com)
- Solitary milialike idiopathic calcinosis cutis: a case unassociated with Down syndrome. (medscape.com)
- Sais G, Jucglà A, Moreno A, Peyrí J. Milia-like idiopathic calcinosis cutis and multiple connective tissue nevi in a patient with Down syndrome. (medscape.com)
- Larralde M, Giachetti A, Kowalczuk A, D'Agostino D, Galimberti R. Calcinosis cutis following liver transplantation in a pediatric patient. (medscape.com)
- Uncommon localization of calcinosis cutis after liver transplantation. (medscape.com)
- Moss J, Syrengelas A, Antaya R, Lazova R. Calcinosis cutis: a complication of intravenous administration of calcium glucanate. (medscape.com)
- Tc-99m MDP scintigraphy in a case of idiopathic calcinosis cutis. (medscape.com)
- Dermal uptake of technetium-99m MDP in calcinosis cutis. (medscape.com)
- He responded very well to high doses of steroids that are used to treat these conditions, but shortly before starting to taper the dose, erupted in lesions of Calcinosis cutis all over the body. (leicesterskinvet.co.uk)
- This photo was taken 4 weeks after the start of his Calcinosis cutis and having a total body clip. (leicesterskinvet.co.uk)
- The next photo shows him virtually fully recovered from his Calcinosis cutis with thankfully, no relapse of his pemphigus or otitis. (leicesterskinvet.co.uk)
- Calcinosis cutis can occur with or without extravasation of Calcium Gluconate Injection. (nih.gov)
- If extravasation occurs or clinical manifestations of calcinosis cutis are noted, immediately discontinue intravenous administration at that site and treat as needed. (nih.gov)
- The most common adverse events with Calcium Gluconate Injection are local soft tissue inflammation and necrosis, calcinosis cutis and calcification that are related to extravasation. (nih.gov)
- Calcinosis Cutis in the Setting of Chronic Skin Graft-Versus-Host Disease. (nih.gov)
- Calcinosis cutis, calcium growth that appear as very hard nodules under the surface of the skin. (hss.edu)
- The patient signs and symptoms of pitting fingertips (i.e. calcinosis cutis), burning chest pain, dysphasia, telangiectasia and hard thickening of fingers (i.e. sclerodactyly), make the diagnosis of CREST syndrome the most likely one (Answer E) . CREST syndrome is a localized variant of systemic sclerosis characterized by the presence of Calcinosis, Raynaud's phenomenon (i.e. three-color change of fingers and toes), esophageal dysmotility, sclerodactyly and telangiectasias. (acc.org)
- Although the patient presents with some dermatological manifestations (sclerodactyly and calcinosis cutis), no lesions indicating psoriasis are revealed by the clinical examination. (acc.org)
- Metastatic calcinosis cutis refers to the deposition of calcium salts in normal tissue secondary to an underlying defect in calcium and/or phosphate metabolism. (koreamed.org)
Tumoral26
- The cause of the rare condition of tumoral calcinosis is not entirely understood. (wikipedia.org)
- Tumoral calcinosis with vitamin D deficiency. (medscape.com)
- Hyperphosphatemic familial tumoral calcinosis (HFTC) is a condition characterized by an increase in the levels of phosphate in the blood (hyperphosphatemia) and abnormal deposits of phosphate and calcium (calcinosis) in the body's tissues. (medlineplus.gov)
- Hyperphosphatemic Tumoral Calcinosis: Pathogenesis, Clinical Presentation, and Challenges in Management. (nih.gov)
- Tumoral calcinosis: case report and review. (nih.gov)
- The clinical diagnosis of HFTC is established by the presence of tumoral calcinosis and/or characteristic laboratory findings of hyperphosphatemia in the setting of inappropriately increased renal tubular reabsorption of phosphorus (TRP), elevated or inappropriately normal 1,25-dihydroxyvitamin D 3 (1,25D) levels, and elevated C-terminal FGF23 fragments. (nih.gov)
- Surgical resection of tumoral calcinosis lesions - generally reserved for those patients with significant pain or functional impairment - has variable success. (nih.gov)
- 1. Hyperphosphatemic tumoral calcinosis: a 10-year follow-up. (nih.gov)
- 2. Recurrent primary hyperphosphatemic tumoral calcinosis: a case report. (nih.gov)
- 3. Complete resolution of tumoral calcinosis after renal transplantation. (nih.gov)
- 4. Hyperphosphatemic familial tumoral calcinosis secondary to fibroblast growth factor 23 (FGF23) mutation: a report of two affected families and review of the literature. (nih.gov)
- 7. Dialysis as a Treatment Option for a Patient With Normal Kidney Function and Familial Tumoral Calcinosis Due to a Compound Heterozygous FGF23 Mutation. (nih.gov)
- 8. Successful treatment of hyperphosphatemic tumoral calcinosis with long-term acetazolamide. (nih.gov)
- 9. Tumoral calcinosis, diaphysitis, and hyperphosphatemia. (nih.gov)
- 10. Familial tumoral calcinosis caused by a novel FGF23 mutation: response to induction of tubular renal acidosis with acetazolamide and the non-calcium phosphate binder sevelamer. (nih.gov)
- 11. Clinical and genetic analysis of idiopathic normophosphatemic tumoral calcinosis in 19 patients. (nih.gov)
- 12. Tumoral calcinosis: report of a case and brief review of the literature. (nih.gov)
- 13. A case of familial tumoral calcinosis/hyperostosis-hyperphosphatemia syndrome due to a compound heterozygous mutation in GALNT3 demonstrating new phenotypic features. (nih.gov)
- 14. Nonfamilial hyperphosphatemic tumoral calcinosis with ulnar neuropathy. (nih.gov)
- 15. Tumoral calcinosis in two infants. (nih.gov)
- 16. Autoimmune hyperphosphatemic tumoral calcinosis in a patient with FGF23 autoantibodies. (nih.gov)
- 17. High dietary phosphate intake induces development of ectopic calcifications in a murine model of familial tumoral calcinosis. (nih.gov)
- 18. [Familial tumoral calcinosis in three patients in the same family]. (nih.gov)
- 19. Familial tumoral calcinosis: a forty-year follow-up on one family. (nih.gov)
- 20. Tumoral calcinosis: serial images to monitor successful dietary therapy. (nih.gov)
- Thus, some may resemble tumoral calcinosis, whereas others are similar to a rheumatoid nodule or osteoma. (ajnr.org)
Lesions4
- Five investigators examined DM/JDM calcinosis lesions by durometry, optimally recording three readings per site, as well as control readings unaffected by calcinosis in similar anatomic areas. (nih.gov)
- Durometry readings of calcinosis lesions were statistically higher than control lesions in the following locations: upper neck/clavicle, upper arms/forearms, elbows, hand/wrists, buttocks, thigh, calf and foot. (nih.gov)
- Calcinosis lesions overall were harder compared to control lesions. (nih.gov)
- Conclusion: Our study identifies durometry as a reliable tool in assessing targeted lesions of calcinosis lesions in DM/JDM patients. (nih.gov)
Dermatomyositis6
- Valenzuela A, Chung L, Casciola-Rosen L, Fiorentino D. Identification of clinical features and autoantibodies associated with calcinosis in dermatomyositis. (medscape.com)
- This study is aiming to find out more about calcinosis, the development of calcium deposits in various parts of the body, in people with dermatomyositis (DM) and juvenile dermatomyositis (JDM). (nih.gov)
- Rapid improvement of calcinosis in juvenile dermatomyositis with alendronate therapy. (jrheum.org)
- A 6-year-old boy with improving juvenile dermatomyositis (JDM) developed severe and debilitating calcinosis, unresponsive to diltiazem and probenecid. (jrheum.org)
- Is Anti-NXP2 Autoantibody a Risk Factor for Calcinosis and Poor Outcome in Juvenile Dermatomyositis Patients? (unige.it)
- Children and adults with dermatomyositis may develop calcium deposits, which appear as hard bumps under the skin or in the muscle (calcinosis). (nih.gov)
Raynaud's1
- It has also been known to cause complications like calcinosis, Raynaud's phenomenon, esophageal dysfunction, sclerodactyl and telangiectadias. (home-remedies-for-you.com)
Dystrophic3
- The most common type of calcinosis is dystrophic calcification. (wikipedia.org)
- After 58 years, she was diagnosed with dystrophic calcinosis in the burn scar, which was confirmed through biopsy and histopathological analysis. (rbcp.org.br)
- The anatomopathological examination of January 2019 indicated hyperkeratosis, hypergranulosis, and lymphoplasmacytic infiltrate in the papillary dermis associated with fibrinoleukocyte crust and dermal fibrosis, concluding the examination with no signs of malignancy and diagnosis of dystrophic calcinosis. (rbcp.org.br)
Autoantibodies1
- It has been published that the presence of anti-NXP2 autoantibodies presents a risk for calcinosis in patients with JDM. (unige.it)
Calcium deposits2
- Calcinosis is the formation of calcium deposits in any soft tissue. (wikipedia.org)
- People with DM and JDM can develop calcium deposits in places they should not, known as calcinosis. (nih.gov)
Sodium thiosulfate2
Burn scar1
- Calcinosis in a burn scar. (nih.gov)
Systemic1
- Bullous systemic lupus erythematosus with milia and calcinosis. (medscape.com)
Cutaneous1
- Cutaneous calcinosis is a rare disease characterized by the precipitation of calcium crystals in the skin tissue. (rbcp.org.br)
Complication1
- Calcinosis, a known complication of DM/JDM, is associated with significant morbidity. (nih.gov)
Deposits1
- Calcinosis typically develops in early childhood to early adulthood, although in some people the deposits first appear in infancy or in late adulthood. (medlineplus.gov)
Severe1
- People ages 7 and older who have moderate or severe calcinosis. (nih.gov)
Lumps1
- Hardened lumps or sheets of calcium (calcinosis) under the skin. (gillettechildrens.org)
Elbows1
- Calcinosis usually occurs in and just under skin tissue around the joints, most often the hips, shoulders, and elbows. (medlineplus.gov)
Occurs2
- Rarely, calcinosis occurs in blood vessels or in the brain and can cause serious health problems. (medlineplus.gov)
- Calcinosis most often occurs one to three years after disease onset but may occur many years later. (nih.gov)
Prone2
- In conclusion, JDM patients with anti-NXP2 are prone to develop calcinosis, especially if they present with the disease early, before 5 years of age. (unige.it)
- For example, if you don't have enough magnesium, you will be more prone to calcinosis. (thenourishinggourmet.com)
Measurements2
Skin2
Presentation2
- Patients were divided into two groups (A and B) based on the presence of calcinosis, which occurred in 42% of anti-NXP2 positive JDM patients (group A). Four patients already had calcinosis at presentation, one developed calcinosis after 4 months, and 6 developed calcinosis later in the disease course (median 2 years, range 0.8-7.8). (unige.it)
- The mean age at disease presentation (5.2/7.5 years) trended toward being younger in group A. Children with calcinosis were treated with several combinations of drugs. (unige.it)
Inflammation1
- Calcinosis can be localized (tissue damage due to trauma, inflammation, infection, necrosis or neoplasia) or generalized (associated with collagenosis, genodermatoses and some types of panniculitis) 2 . (rbcp.org.br)
Virtually1
- Alendronate produced dramatic improvement within 1 month and by 12 months calcinosis had virtually resolved. (jrheum.org)
Vitamin2
- The Effect of Vitamin K 2 on Experimental Calcinosis. (thenourishinggourmet.com)
- 18 They gave rats calcinosis by giving them way too much vitamin D 2 . (thenourishinggourmet.com)
Outcomes1
- The development of calcinosis is associated with worse disease outcomes. (unige.it)
Patients4
- Tools to assess calcinosis in DM/JDM patients have been inadequately validated. (nih.gov)
- We aimed to investigate the prevalence of calcinosis and response to the treatment in JDM patients with anti-NXP2. (unige.it)
- however, there are no evidence-based therapies for treating calcinosis in JDM patients. (unige.it)
- Anti- EA was present more frequently in SSc patients with calcinosis compared to those without (75% vs 27.5%, p=0.014) and tended to be more frequent in patients with pulmonary fibrosis compared to those without (47.8% vs 25%, p=0.071). (bmj.com)
Soft1
- Calcinosis may also develop in the soft tissue of the feet, legs, and hands. (medlineplus.gov)