Gout, unspecified. The 2019 edition of ICD-10-CM M10.9 became effective on October 1, 2018. This is the American ICD-10-CM version of M10.9 - other international versions of ICD-10 M10.9 may differ.
In 1999, Möller and colleagues concluded, "The Gorham-Stout syndrome may be, essentially, a monocentric bone disease with a focally increased bone resorption due to an increased number of paracrine – or autocrine – stimulated hyperactive osteoclasts. The resorbed bone is replaced by a markedly vascularized fibrous tissue.
Often, Gorham's disease is not recognized until a fracture occurs, with subsequent improper bone healing. The diagnosis essentially is one of exclusion and must be based on combined clinical, radiological, and histopathological findings.
M10 Gout. Gout is a common, painful form of arthritis. It causes swollen, red, hot and stiff joints. Gout occurs when uric acid builds up in your blood. This happens if your body produces extra acid or does not eliminate enough, or if you eat too many foods with purines, such as liver and dried beans.
Gorham-Stout disease (GSD), which is also known as vanishing bone disease, disappearing bone disease, massive osteolysis, and more than a half-dozen other terms in the medical literature, is a rare bone disorder characterized by progressive bone loss (osteolysis) and the overgrowth (proliferation) of lymphatic vessels.
Gorham's disease is extremely rare and may occur at any age, though it is most often recognized in children and young adults. It strikes males and females of all races and exhibits no inheritance pattern. The medical literature contains case reports from every continent.
Gorham's disease is a rare bone disorder characterized by bone loss (osteolysis), often associated abnormal blood vessel growth (angiomatous proliferation). Bone loss can occur in just one bone, or spread to soft tissue and adjacent bones. Symtoms may include pain, swelling, and increased risk of fracture.
Gorham's disease is a rare bone disorder characterized by bone loss (osteolysis), often associated abnormal blood vessel growth (angiomatous proliferation). Bone loss can occur in just one bone, or spread to soft tissue and adjacent bones. Symtoms may include pain, swelling, and increased risk of fracture.
Diagnosis of Gorham-Stout disease is made by exclusion, and its clinical presentation varies widely, from spontaneous remission to a fatal outcome.
The clinical presentation of a patient suffering from vanishing bone disease includes, most frequently, pain, functional impairment and swelling of the affected region, although asymptomatic cases have been reported, as well as cases in which the diagnosis was made after a pathologic fracture[20].
The first case of Gorham-Stout disease was already reported in 1838 and described a patient with a vanishing of the complete humerus bone over 11 years (19). After more than a century, in 1955, Gorham and Stout investigated the characteristic histopathological findings of the massive osteolysis based on 8 cases.
Boneitis is a deadly disease that cripples the bones, ultimately resulting in death. Steve Castle, who was from the 20th century, was stricken with the disease. Symptoms include bone twisting, bone breaking and bone loss.
Low bone density and osteoporosis, which make your bones weak and more likely to break. Osteogenesis imperfecta makes your bones brittle. Paget's disease of bone makes them weak. Bones can also develop cancer and infections.
The medical treatment for Gorham's disease includes radiation therapy, anti-osteoclastic medications (bisphosphonates), and alpha-2b interferon. Surgical treatment options include resection of the lesion and reconstruction using bone grafts and/or prostheses.
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To date around 300 cases have been reported in the literature. GSD does not display a clear race, sex predilection (1.6:1; male: female ratio) or geographic distribution.
GSD can present at any age, but is commonly diagnosed in children and young adults (average 13 years). GSD may affect any bone in the body but most commonly affects the ribs, followed by the cranium, clavicle and cervical spine. Additional affected areas include maxillofacial bones (mostly the mandible), sternum, humerus, hand, femur, and foot.
Etiology of GSD is still elusive. The pathological process is the benign vascular proliferation of endothelial channels adjacent to or within bone, leading to extreme thinning of bony trabecula, osteoclast-mediated resorption, and replacement of bone with fibrous tissue.
Diagnosis relies on radiographic findings revealing progressive osteolysis and cortical destruction. Magnetic resonance imaging shows complete resorption of bone and replacement with infiltrative soft tissue that is of low signal intensity on T1-weighted imaging and high signal intensity on T2, with intense enhancement on contrast imaging.
Differential diagnosis includes generalized lymphatic anomaly (the major distinguishing characteristic is the progressive osteolysis seen in GSD), acroosteolysis dominant type, multicentric carpo-tarsal osteolysis with or without nephropathy, autosomal recessive carpotarsal osteolysis, hereditary sensory and autonomic neuropathy type 2, Farber lipogranulomatosis, Torg-Winchester syndrome, and idiopathic phalangeal acro-osteolysis (see these terms).
Treatment of GSD includes drugs (bisphosphonates and/or interferon alpha 2b, sirolimus is also being studied) to stabilize progressive disease, and supportive procedures that may reduce or halt chylothorax (pleurectomy, pleurodesis, thoracentesis, and thoracic duct embolization or ligation), or may stabilize affected regions of the skeleton.
The following clinical terms are approximate synonyms or lay terms that might be used to identify the correct diagnosis code:
The General Equivalency Mapping (GEM) crosswalk indicates an approximate mapping between the ICD-10 code M89.8X9 its ICD-9 equivalent. The approximate mapping means there is not an exact match between the ICD-10 code and the ICD-9 code and the mapped code is not a precise representation of the original code.
Your bones help you move, give you shape and support your body. They are living tissues that rebuild constantly throughout your life. During childhood and your teens, your body adds new bone faster than it removes old bone. After about age 20, you can lose bone faster than you make bone.
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It may affect any part of the skeleton, but the most common sites of disease are the shoulder, skull, pelvic girdle, jaw, ribs, and spine. In some cases, no symptoms are seen until a fracture occurs either spontaneously or following minor trauma, such as a fall.
In many cases, the end result of Gorham's disease is severe deformity and functional disability. Symptoms such as difficulty breathing and chest pain may be present if the disease is present in the ribs, scapula, or thoracic vertebrae. These may indicate that the disease has spread from the bone into the chest cavity.
The specific cause of Gorham's disease remains unknown. Bone mass and strength are obtained and maintained through a process of bone destruction and replacement that occurs at the cellular level throughout a person's life. Cells called osteoclasts secrete enzymes that dissolve old bone, allowing another type of cells called osteoblasts to form new bone. Except in growing bone, the rate of breakdown equals the rate of building, thereby maintaining bone mass. In Gorham's disease, that process is disrupted.
Recognition of the disease requires a high index of suspicion and an extensive workup. Because of its serious morbidity, Gorham's must always be considered in the differential diagnosis of osteolytic lesions.
To date, no known interventions are consistently effective for Gorham's, and all reported interventions are considered experimental treatments, though many are routine for other conditions. Some people may require a combination of these approaches. Unfortunately, some people will not respond to any intervention.
Treatment of Gorham's disease is for the most part palliative and limited to symptom management. Sometimes, the bone destruction spontaneously ceases and no treatment is required, but when the disease is progressive, aggressive intervention may be necessary.
The disease may stabilize after a number of years , go into spontaneous re mission, or in cases involving the chest and upper spine, prove fatal. Recurrence of the disease following remission can also occur. Involvement of the spine and skull base may cause a poor outcome from neurological complications. In many cases, the end result of Gorham's ...
Gouty tophus of right olecranon bursa. Clinical Information. A condition marked by increased levels of uric acid in the blood, joints, and tissue. The buildup of uric acid in the joints and tissues causes arthritis and inflammation. Gout is a common, painful form of arthritis.
It causes swollen, red, hot and stiff joints. Gout occurs when uric acid builds up in your blood. This happens if your body produces extra acid or does not eliminate enough, or if you eat too many foods with purines, such as liver and dried beans. Pseudogout has similar symptoms and is sometimes confused with gout.
Disease. Gorham-Stout disease (GSD) is a rare, progressive angiomatous disorder characterized by osteolysis and vascular anomalies . GSD, also known as “vanishing bone disease,” frequently involves a bone of the axial skeleton . The disorder is characterized by resorption, cortical loss, and progressive osteolysis of bone with an angiomatosis ...
Epidemiology. GSD, first characterized in the 1950s, has both congenital and acquired forms . Although GSD primarily affects children and young adults, there is a bimodal distribution pattern and some patients present after the age of 50 years . GSD shows no predilection for gender or race .
GSD is a rare disorder characterized by progressive osteolysis and angiomatosis of blood vessels and lymphatic vessels. Although ocular manifestations of GSD are rare, the ophthalmologist can play an important role in the diagnosis of GSD if a patient presents with proptosis with cortical resorption, massive osteolysis, and angiogenic malformations. Medication, surgery, and radiation are available treatment options, but appropriate management on a case-by-case basis would lead to favorable results in GSD patients.
Signs/Symptoms. Localized pain is the most common symptom, while other symptoms include weakness, swelling, and functional impairment of affected limbs . GSD patients may be asymptomatic until they experience a minor trauma or a fracture .
The pathophysiology of GSD is not entirely known . Angiogenic and osteoclastogenic cytokine production, including vascular endothelial growth factor (VEGF) and interleukin-6 (IL-6), are hypothesized to drive the disease processes . VEGF and VEGF-C are overexpressed in GSD patients, indicating their implications in the pathologic endothelial cell proliferation . Furthermore, VEGF and VEGF-C are also involved in disease activity and response to interferon-α (IFN-α) therapy in some patients . Amounts of IL-6, VEGF-A, and tumor necrosis factor-α (TNF-α) are elevated in ex vivo cells from a patient’s soft-tissue lesion .
GSD may be a likely diagnosis if a patient presents an early asymptomatic clinical course, positive biopsy of angiomatous tissue, progressive osteolysis of a bone in the axial skeleton, and osteolytic radiographic pattern with negative hereditary, metabolic, immunologic, infectious, or neoplastic etiology .