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Overview Acute myeloid leukemia (AML) is a cancer that occurs in the blood and the marrow of the bones. Mycobacterial culture is a test to look for tuberculosis or a related organism in the body. What is Multiple Myeloma?Multiple myeloma (from ''myelo-'', bone marrow), also known as MM, myeloma, plasma cell myeloma, or as Kahler's disease (after Otto Kahler) is a cancer of the white blood cells known as plasma cells. November 1, 2013In the article Bone Tumors - Differential diagnosis we discussed a systematic approach to the differential diagnosis of bone tumors and tumor-like lesions. The differential diagnosis mostly depends on the age of the patient and the findings on the conventional radiographs. In this article we will discuss the differential diagnosis of sclerotic bone tumors and tumor-like lesions in more detail. In the table the most common sclerotic bone tumors and tumor-like lesions in different age-groups are presented.
Fibrous dysplasia and eosinophilic granuloma more commonly present as osteolytic lesions, but they can be sclerotic. Notice that many benign osteolytic lesions that are frequently seen in younger age groups may heal and appear as sclerotic lesions in the middle aged group. Another approach to the differential diagnosis of sclerotic bone lesions is to use the mnemonic I VINDICATE, which means 'I clear myself from accusation'.
The mnemonic I VINDICATE is a commonly used mnemonic for the differential diagnostis of any radiological lesion. Typical presentation: central lesion in metaphysis or diaphysis with a well defined serpentiginous border. Causes: corticosteroid use, sickle cell disease, trauma, Gaucher's disease, renal transplantation.
If the osteonecrosis is located in the epiphysis, the term avascular osteonecrosis is used.
The radiograph shows typical bone infarcts in diaphysis and metaphysis of femur and tibia.. On MR imaging bone infarcts are characterized by irregulair serpentiginous margins with low signal intensity on both T1 and T2 WI and with intermediate to high fat signal in the center part. At the periphery of the infarct a zone of relative high signal intensity on T2WI may be found.
Differentiating a bone infarct from an enchondroma or low-grade chondrosarcoma on plain films can be difficult or even impossible. Cartilaginous tumors in particular chondrosarcoma may show endosteal scalloping, while a bone infarct does not.
Benign lesion consisting of well-differentiated mature bone tissue within the medullary cavity.
Typical presentation: well-defined osteolytic lesion in tarsal bone, patella or epiphysis of a long bone in a 20-year old with pain and swelling in a joint. Radiological hallmark: formation of a chondroid (cartilagenous) matrix, which presents as punctuated, stippled or popcorn-like calcifications. The chondroid matrix is of a variable amount from almost absent to dens compact chondroid matrix.
Disappearane of calcifications in a pre-existing enchondroma should raise the suspicion of malignant transformation. There were other features that favored the diagnosis of a low-grade chondrosarcoma like a positive bone scan and endosteal scalloping of the cortical bone on an MRI (not shown). Here a 44-year old male with a mixed lytic and sclerotic mass arising from the fifth metacarpal bone. T2-weighted axial MR image demonstrates high signal intensity of the tumor in the metacarpal bone with extension of a lobulated soft tissue mass. Because of the large dimensions with soft tissue extension on plain radiograph and axial T2-weighted MR image, a high grade chondrosarcoma was suspected. The sclerotic lesion in the humeral head could very well be a benign enchondroma based on the imaging findings.
Symptoms are usually absent, however, in adult patients with a chondroid lesion in a long bone, particularly of larger size, always consider low-grade chondrosarcoma. Plain radiograph and coronal T1-weighted contrast-enhanced fat-suppressed MR image of a mixed lytic and sclerotic lesion of the distal femoral diaphysis. The homogeneous enhancement in the upper part with edema and cortical thickening are not typical for a low-grade chondrosarcoma.
Development in centrally located osteochondromas like the pelvis, hip and shoulder is most common. Consider peripheral chondrosaroma in growing osteochondromas with or without pain after closure of the physeal plate. Consider progression of osteohondroma to chondrosarcoma when cartilage cap measures > 10 mm.
A juxtacortical chondrosarcoma has be considered in the differential diagnosis when a mineralized lesion adjacent to the cortical bone is seen.
Here a partially calcified mass against the proximal humerus with involvement of the cortical bone on an axial CT image. A periosteal chondroma may have the same imaging characteristics, however, these are almost always much smaller.
Plain radiograph in another patient shows irreglar mineralized lesion with elevation of the periosteum and cortical involvement. Enchondroma is a fairly common benign cartilaginaous lesion which may present as an entirely lytic lesion without any calcification, as a dense calcified lesion or as a mixed leson with osteolysis and calcifications. Enchondromas aswell as low-grade chondrosarcomas are frequently encountered as coincidental findings in patients who have a MRI or bone scan for other reasons. In the active phase there is multilaminar periosteal reaction and bone and soft tissue edema. Eosinophilic granuloma like osteomyelitis, can be a serious mimicker of malignancy (particularly Ewing sarcoma). Should be included in the differential diagnosis of young patient with multiple lucent lesions (Langerhans cell histiocytosis).
If the patient had fever and a proper clinical setting, osteomyelitis would be in the differential diagnosis. Adamantinoma in case of a sclerotic lesion with several lucencies of the tibia in a young patient. The signal intensity on MR depends on the amount of calcifications and ossifications and fibrous tissue (low SI) and cystic components (high SI on T2). Melorrheostosis is a dysplasia of the bone, characterized by apposition of mature bone on the outer or inner surface of cortical bone. Axial T1-weighted MR image shows homogeneous low signal intensity due to the compact bone apposition. Sclerotic osteoblastic metastases must be included in the differential diagnosis of any sclerotic bone lesion in a patient > 40 years. Most commonly originate from prostate and breast cancer and less frequently from lung cancer, lymphoma or carcinoid. In breast cancer, metastases may present as lytic lesions that may become sclerotic expressing a favourable response to chemotherapy. There is a metastasis, which presents as a subtle sclerotic lesion in the humerus metaphysis. This could be an osteoblastic metastasis or an osteolytic metastasis that responded to chemotherapy. Here a radiograph of the pelvis with a barely visible osteoblastic metastasis in the left iliac bone (blue arrow). Non-ossifying fibroma (NOF) can be encoutered occasionally as a partial or completely sclerotic lesion.
Typically a NOF presents as an eccentric well-defined lytic lesion, usually found as a coincidental finding.


Other benign lesions, like solitary bone cyst, fibrous dysplasia, chondroblastoma and other benign bone tumors may become inert and may also become sclerotic. The image on the right is of a different patient who has an old NOF that shows complete fill in. Growth of the osteochondroma takes place in the cap, corresponding with normal enchondral growth at the growth plates. Accordingly, growth of osteochondromas is allowed until a patient reaches adulthood and the physeal plates are closed. Growth of osteochondromas at adult ages, which is characterized by a thick cartilaginous cap (high SI on T2WI) should raise the suspicion of progression to a peripheral chondrosarcoma.
Here a patient with a broad-based osteochondroma with extension of the cortical bone into the stalk of the lesion. Surrounded by a prominent zone of reactive sclerosis due to a periosteal and endosteal reaction, which may obscure the central nidus. There is reactive sclerosis with a nidus that is barely visible on the radiograph (blue arrow), but clearly visible on the CT (red arrows).
CT scan is usually very helpful in detecting the nidus and differentiating osteoid osteoma from other sclerotic lesions like osteoblastoma, osteomyelitis, arthritis, stress fracture and enostosis.
In most cases of osteoid osteoma the radiographic appearance is determined by the reactive sclerosis.
It is most commonly located in the outer table of the neurocranium or in a paranasal sinus. Osteomyelitis is a mimicker of various benign and malignant bone tumors and reactive processes that may be accompanied by reactive sclerosis. Sometimes a more solid periosteal reaction is present combined with cortical thickening and broadening of the bone. Plain films typically reveal lesions with moth-eaten or permeative pattern of the transition zone with irregular cortical destruction and an interrupted periosteal reaction with soft tissue extension.
A periosteal reaction known as Codman's triangle appears as tumor elevates periosteum from underlying bone. The sagittal T1WI and Gd-enhanced T1W-image with fatsat show a large tumor mass infiltrating a large portion of the distal femur and extending through the cortex into the soft tissues. It grows primarily into the surrounding soft tissues, but may also infiltrate into the bone marrow.
It is nost commonly located on the posterior side of the distal meta-diaphysis of the femur. Ossification in parosteal osteosaroma is usually more mature in the center than at the periphery. Paget disease is a chronic disorder of unknown origin with increased breakdown of bone and formation of disorganized new bone. In this case we see the pathognomonic triad of bone expansion, cortical thickening and trabecular bone thickening in the mixed lytic and sclerotic phase of Paget's disease of right hemipelvis. Notice that the mineralization is predominantly in the periphery of the mass and that there is a lucent zone between the mass and the cortical bone.
Contrast-enhanced T1-weighted MR image demonstrates heterogeneous enhancement of the mass with extensive surrounding edema. Stress fractures occur in normal (fatigue fractures) or metabolically weakened (insufficiency fractures) bones. Uncommonly it can be difficult to differentiate a stress fracture from a pathologic fracture, that occurs at the site of a bone tumor.
Uncommonly it can be difficult to differentiate a stress fracture from a bone tumor like an osteoid osteoma or from a pathologic fracture, that occurs at the site of a bone tumor.
Notice the resemblance to a juxtacortical mass in another patient (right), which was a biopsy proven parosteal osteosarcoma. This shows that differentiating a tumor from a reactive proces scan be quite difficult in some cases.
When a reactive process is more likely based on history and imaging features, follow-up is sometimes still needed. Subungual exostoses are bony projections which arise from the dorsal surface of the distal phalanx, most commonly of the hallux. Here two patients with a bizar parosteal osteochondromatous proliferation (BPOP), also called Nora's lesion.
This benign reactive process is most commonly found adjacent to the cortex of phalanges of hands or feet (75%). Distinction of Long Bone Stress Fractures from Pathologic Fractures on Cross-Sectional Imaging: How Successful Are We? Some contexts promote anemia, such as repeated pregnancies and closely spaced, malnutrition, alcoholism, chronic gynecological or digestive bleeding, treatment with antifolate drugs. A type of B cell, plasma cells are a crucial part of the immune system responsible for the production of antibodies in humans and other vertebrates. Cortical soft tissue extension may produce radiating spicules of bone called sunray appearance.
This is opposed to myositis ossificans which may present very close to the cortical bone, but maturation develops from the center to the periphery. AML specifically affects the white blood cells of the body, causing them to form abnormally.
Leukemia is divided into four major types:- Acute myeloid leukemia (AML) Chronic myeloid leukemia (CML) Acute lymphoblastic leukemia (ALL) Chronic lymphoblastic leukemia (CLL) This article focuses on the Acute lymphoblastic leukemia (ALL) type of leukemia. Myeloma is generally thought to be incurable, but remissions may be induced with steroids, chemotherapy, thalidomide and stem cell transplants. According to the National Bone Marrow Program, there are nearly 11,900 new cases of AML each year.
Some doctors believe it may be related to exposure to certain chemicals, radiation, and even drugs used for chemotherapy. In leukemia, the affected bone marrow fails to release adult and mature cells and releases a large number of immature white blood cells that are known as blast cells. A doctor will request protein electrophoresis of the blood and urine, which might show the presence of a paraprotein (monoclonal protein, or M protein) band, with or without reduction of the other (normal) immunoglobulins (known as immune paresis). One type of paraprotein is the Bence Jones protein which is a urinary paraprotein composed of free light chains (see below). Quantitative measurements of the paraprotein are necessary to establish a diagnosis and to monitor the disease.
Shortage of adult and mature white blood cells means an increased risk of infections as well. If you work in an industry where you may have been exposed to chemicals like benzene you are also at risk. In addition, light and or heavy chains (the building blocks of antibodies) may be secreted in isolation: I?- or I»-light chains or any of the five types of heavy chains (I±-, I?-, I?-, Iµ- or I?-heavy chains). Your risk also goes up if you have a blood disorder like myelodysplasia or a genetic disorder like Down syndrome. The majority of cases of ALL are of B-cell origin, but it can also arise from T-cell precursors.
Close inspection revealed a lytic lesion in the left temporal bone (right side of image), and focused reconstructions of the petrous temporal bones confirmed a lytic lesion involving the mastoid segment of the facial nerve canal.
It can be diagnosed and differentiated from other forms of leukemia and lymphomas by the immunophenotype of the cells, cytochemistry and cytogenetic markers. The lytic lesion was one of many in the skull and is consistent with a myeloma deposit.]]The workup of suspected multiple myeloma includes a skeletal survey. Other symptoms include: bone pain frequent nosebleeds bleeding and swollen gums bruising shortness of breath unexplained weight loss heavier than normal periods in women How Is AML Diagnosed?
Magnetic resonance imaging (MRI) is more sensitive than simple X-ray in the detection of lytic lesions, and may supersede skeletal survey, especially when vertebral disease is suspected. Your doctor will also order blood tests to check for anemia and to determine your white blood cell levels.


Bone scans are typically not of any additional value in the workup of myeloma patients (no new bone formation, lytic lesions not well visualized on bone scan).A bone marrow biopsy is usually performed to estimate the percentage of bone marrow occupied by plasma cells.
Immunohistochemistry (staining particular cell types using antibodies against surface proteins) can detect plasma cells which express immunoglobulin in the cytoplasm but usually not on the surface; myeloma cells are typically CD56, CD38, CD138 positive and CD19 and CD45 negative. In MM, lack of a proliferative clone makes conventional cytogenetics informative in only ~30% of cases. Your doctor may also do a spinal tap, or lumbar puncture, which involves withdrawing fluid from the spine with a small needle. Array-based karyotyping cannot detect balanced translocations, such as t(4;14) seen in ~15% of MM. Multiple myeloma develops in B lymphocytes after they have left the part of the lymph node known as the germinal center.
The normal cell line most closely associated with MM cells is generally taken to be either an activated memory B cell or the precursor to plasma cells, the plasmablast.The immune system keeps the proliferation of B cells and the secretion of antibodies under tight control. Often, a promoter gene moves (or translocates) to a chromosome where it stimulates an antibody gene to overproduction.
A chromosomal translocation between the immunoglobulin heavy chain gene (on the fourteenth chromosome, locus 14q32) and an oncogene (often 11q13, 4p16.3, 6p21, 16q23 and 20q11) is frequently observed in patients with multiple myeloma. This mutation results in dysregulation of the oncogene which is thought to be an important initiating event in the pathogenesis of myeloma. A transplant of your own stem cells however, has a higher risk for relapse because some old leukemia cells may be present in the sample retrieved from your body. The result is proliferation of a plasma cell clone and genomic instability that leads to further mutations and translocations. Deletion of (parts of) the thirteenth chromosome is also observed in about 50% of cases.Production of cytokines) (especially IL-6) by the plasma cells causes much of their localised damage, such as osteoporosis, and creates a microenvironment in which the malignant cells thrive. Angiogenesis (the attraction of new blood vessels) is increased.The produced antibodies are deposited in various organs, leading to renal failure, polyneuropathy and various other myeloma-associated symptoms. The symptoms are usually slow in onset but may rapidly get severe as the number of immature white blood cells (blast cells) rises and overcrowd other cells in the blood. Once all signs and symptoms of AML have disappeared, you are considered to be in remission.
Due to the rise in number of blast cells in blood the red blood cells are lowered in number and this may result in anemia. In recent years, high-dose chemotherapy with hematopoietic stem-cell transplantation has become the preferred treatment for patients under the age of 65.
Prior to stem-cell transplantation, these patients receive an initial course of induction chemotherapy.
The most common induction regimens used today are thalidomidea€“dexamethasone, bortezomib based regimens, and lenalidomidea€“dexamethasone.
Autologous stem cell transplantation, the transplantation of a patienta€™s own stem cells after chemotherapy, is the most common type of stem cell transplantation for multiple myeloma. Some of them may be simple infections that take longer to go away and sometimes with more severe immunity-depression there may be life threatening infections.
Allogeneic stem cell transplantation, the transplantation of a healthy persona€™s stem cells into the affected patient, has the potential for a cure, but is only available to a small percentage of patients.
Treatment with bortezomib, melphalan and prednisone had an estimated overall survival of 83% at 30 months, lenalidomide plus low-dose dexamethasone an 82% survival at 2 years and melphalan, prednisone and lenalidomide had a 90% survival at 2 years.
Head-to-head studies comparing these regimens have not been performed.RelapseThe natural history of myeloma is of relapse following treatment.
This may be a reversible effect, In MM, lack of a proliferative clone makes conventional cytogenetics informative in only ~30% of cases. There may be bruises caused by minor injuries and severe and uncontrolled bleeding caused by injuries. Therefore, FISH for this translocation should also be performed if using SNP arrays to detect genome-wide copy number alterations of prognostic significance in MM. Although the peak age of onset of multiple myeloma is 65 to 70 years of age, recent statistics indicate both increasing incidence and earlier age of onset. African Americans and Native Pacific Islanders have the highest reported incidence of this disease in the United States and Asians the lowest.
In addition due to increased number of cell death and formation there may be raised uric acid levels.
It helps identify those patients in whom ALL begins as the lymphoblastic phase of chronic myeloid leukaemia (CML). This may be positive in patients in whom the cancer has spread to the central nervous system. Exposure of an unborn baby to radiation within the first months of development may also raise the risk of acute leukemia.
These include Down syndrome, Klinefelter syndrome, Fanconi’s anemia, Ataxia-telangiectasia, Bloom syndrome, Neurofibromatosis etc. These tumor suppressor genes slow down cell growth and division or cause them to die at appropriate times.
A translocation means that DNA from one chromosome breaks off and becomes attached to another chromosome.
This break off at a chromosome can turn on oncogenes or turn off tumor suppressor genes leading to cancers. There may deletions where part of a chromosome is lost or inversion where a segment is rearranged and placed wrongly. This is mainly due to advances in chemotherapy and efficacy and safety of novel therapies like bone marrow transplantation and stem cell transplants. Caucasians are also more likely to respond to therapy and have a better prognosis than others. This includes:- Those with a bad prognosis or outlook - these patients usually have a set of one or more criteria.
Translocation between 4:11 occurs rarely in about 4% of cases and is most common in infants under 12 months. Unclassified ALL is considered to have an intermediate prognosis Acute Lymphoblastic Leukemia Classification There are several systems of classification of Acute lymphoblastic leukemia. The classification is commonly used to determine treatment and predict the prognosis of the cancer.
In this type the cells are large and uniform with vacuoles (bubble like features) in the cytoplasm overlying the nucleus.
This includes ALL with cytoplasmic granules, aplastic form of ALL, ALL with eosinophilia, secondary ALL and relapse of ALL or lymphoblastic leukemia. The team includes: an oncologist (cancer specialist) an haematologist (one who specializes in blood and related disorders) a pathologist a radiotherapist a neurologist (if there is involvement of the central nervous system) a paediatrician (childhood disease specialists since ALL is common among children) a social worker a clinical oncology nurse a counsellor Three phases of treatment Treatment is given in three main phases. This includes nausea, vomiting, diarrhea, loss of appetite, mouth sores, fatigue, rashes, hair loss etc. It involves taking regular doses of chemotherapy tablets along with regular follow ups and check-ups.
It is useful in advanced cases of ALL that has spread to the brain or central nervous system or before a bone marrow transplant.
The treatment basically involves use of very high dose aggressive chemotherapy to kill of all the cancer cells and some of the healthy cells of the bone marrow.
Following this healthy bone marrow or stem cells are transfused to replace the destroyed cells of the bone marrow.
The best candidate to provide a donation is usually a brother or sister with the same tissue type.



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