Cases reported "Femur Head Necrosis"

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1/142. The prevalence and clinicopathological appearance of extension of osteonecrosis in the femoral head.

    In about 50% of cases, osteonecrosis of the femoral head is known to occupy more than one site. There is controversy as to whether a single focus may increase in size. We have reviewed 606 consecutive femoral heads which had been surgically removed for osteonecrosis. Extension of osteonecrosis was observed in only two (0.3%) and was confirmed histopathologically by the enlargement of the necrotic segment beyond the repair zone formed for the primary necrosis into the adjacent, previously uninvolved bone. In both cases, the necrotic regions were wedge-shaped and occupied over 80% of the femoral head. It appears that an increase in size is extremely rare and that osteonecrosis is due to a single event. Our findings may be of value in assessing the use of joint-salvage procedures for osteonecrosis of the femoral head.
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2/142. A clinicopathologic study of transient osteoporosis of the hip.

    OBJECTIVE: It has been proposed that transient osteoporosis of the hip (TOH) may represent the early reversible phase of osteonecrosis of the femoral head (ON). The purpose of this study was to investigate the clinicopathologic characteristics of three cases of TOH. DESIGN AND patients: A bone biopsy was performed on three patients who had been diagnosed as having TOH based on the clinical course, radiograph, bone scintigram, and MR images. The biopsy specimens were studied histopathologically by light and electron microscopy. RESULTS: The most characteristic feature of TOH was focal areas of thin and disconnected bone trabeculae covered by osteoid seams and active osteoblasts. The surrounding bone marrow tissue showed edematous changes and mild fibrosis, frequently associated with vascular congestion and/or interstitial hemorrhage. No osteonecrotic region was observed in either the bone trabeculae or the bone marrow tissue. All patients have improved clinically and in the 3.5-9 years of follow-up have shown no evidence of ON. CONCLUSIONS: This study supports the concept that transient osteoporosis of the hip is a distinct entity.
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3/142. Aseptic bone necrosis in Japanese divers.

    Medical examination was performed on the divers in Ohura for 7 years from 1969 to 1972. Aseptic bone necrosis was found in 268 of 450 divers (59.5%). Men with over 5 years of experience in diving were highly affected (more than 54.4%). These bone lesions were found most frequently in the proximal end of the femur and the humerus. There was a significantly higher incidence of bone lesions in the men who dived over 30 meters. In the group of men with one or more bone lesions, 73.1% were known to have been treated for bends. The bone, once exposed to a certain compression of air, would have a tendency to develop bone lesions even after cessation of diving. Type A2 (linear opacity) led to the structural failure of the joint surface of the femur and the humerus. Histopathological study was carried out on the sections of bone obtained from three autopsy cases and four operated cases. Formation of air bubbles in the bone marrow cavity seemed to be the most important as the cause for the occurrence of aseptic bone necrosis, and local circulatory disturbance might be the most responsible for the progression of the bone lesion.
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4/142. indomethacin induced avascular necrosis of head of femur.

    Chemically induced avascular necrosis of bone is a well documented entity. indomethacin is one of the causes of this condition but is often difficult to recognise. review of the literature shows that only one case of indomethacin induced avascular necrosis has been reported in the English language between 1966 and the present.The case of a young healthy man, who developed avascular necrosis of head of femur after prolonged administration of indomethacin, is reported here.
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5/142. Aseptic necrosis in hiv seropositive patients: a possible etiologic role for megestrol acetate.

    The association between pharmacologic doses of corticosteroids and the development of aseptic bone necrosis has been well documented. Recent reports have described the corticosteroid activity of megestrol acetate. A retrospective review of adverse events reported to the U.S. food and Drug Administration identified three human immunodeficiency virus (hiv) seropositive patients who developed avascular necrosis of the femoral head during treatment with megestrol acetate. All were males, ages 34, 36, and 55 years, and were on therapy for 6, 1.5, and 18 months, respectively, when symptoms of aseptic necrosis occurred in the absence of antecedent trauma. megestrol acetate doses were 640, 320, and 600-1200 mg/d, respectively. Two patients had no history of corticosteroid use whereas the third had taken an undisclosed dose and duration of corticosteroids concurrent with pentamidine administration. Notably, despite the predominant use of megestrol in women for hormone sensitive malignancies, none of the reports of aseptic necrosis occurred in this population. megestrol acetate may be associated with the development of avascular necrosis via its glucocorticoid-like effects. Cachectic acquired immunodeficiency syndrome (AIDS) patients may have additional risk factors that predispose them to aseptic necrosis when receiving megestrol acetate.
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6/142. Avascular necrosis of head of femur in a patient with acute promyelocytic leukemia.

    Avascular necrosis (AVN) of head of the femur is associated with various pathological conditions and treatment modalities. We present a case of acute promyelocytic leukemia who was treated with all-transretinoic acid (ATRA), daunomycin, cytarabine and a short course of dexamethasone. He developed AVN of bone after 2 years of treatment. Whether this is related to ATRA is dealt with in the discussion.
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7/142. Concomitant sickle cell disease and skeletal fluorosis.

    Skeletal fluorosis typically manifests as a diffuse increase in bone density, whereas avascular necrosis of the epiphyses and diaphyseal marrow are the main skeletal manifestations of sickle cell disease. The diagnostic and therapeutic challenges raised when both disorders are present are illustrated by two cases in Senegalese patients from an area characterized by high fluoride contents in the water and soil. Both had SS sickle cell disease. Skeletal fluorosis was diagnosed during evaluation for avascular necrosis in one patient and in the wake of septic arthritis in the other. Femoral head necrosis is difficult to identify in a patient with skeletal fluorosis. The bone lesions due to sickle cell disease and those due to fluorosis can mimic other bone diseases, most notably metastases. The combination of sickle cell disease and fluorosis results in significant medullary canal narrowing due to cortical thickening and to accumulation of necrotic bone. When performing hip replacement surgery, careful reaming of the medullary canal may reduce the risk of iatrogenic femoral fracture and inappropriate stem placement.
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8/142. Pathological fracture of the femoral neck as the first manifestation of osteonecrosis of the femoral head.

    We describe two cases of pathological fracture of the femoral neck occurring as the first manifestation of osteonecrosis of the femoral head (ONFH). No abnormal findings suggestive of ONFH were identified on the radiographs for either of the patients, and the fractures occurred like spontaneous fractures without any trauma or unusually increased activity. The patients' medical history, age, and good bone quality suggested ONFH as a possible underlying cause of the fractures. If we had not suspected ONFH as a predisposing condition, these minimally displaced fractures might have been fixed internally with multiple pins, and this would have led to nonunion or collapse of the femoral head. To avoid inappropriate treatment, ONFH should be considered as a predisposing factor in pathological fractures of the femoral neck.
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9/142. Non-traumatic osteonecrosis of the femoral head treated with transtrochanteric anterior rotational osteotomy combined with vascularized iliac bone grafting.

    A 49-year-old Japanese man who had non-traumatic osteonecrosis of the femoral head with a wide necrotic lesion received transtrochanteric anterior rotational osteotomy combined with vascularized iliac bone grafting. After the bone graft (6 x 1.5 cm) was collected, the femoral head was anteriorly rotated by 90 degrees. A bone tunnel of 1.2 cm in diameter was prepared on the necrotic lesion adjacent to the intact area from the anterior part of the femoral neck to inside the femoral head. The bone graft was trimmed to the size of this bone tunnel, and inserted up to immediately below the articular surface. In the monitoring using T1-weighted magnetic resonance imaging (MRI), the low signal-intensity area between the bone graft and intact area had disappeared, and a high signal-intensity area on the weight-bearing portion of the femoral head had extended. With modifications on the insertion point of the bone graft, transtrochanteric anterior rotational osteotomy combined with vascularized iliac bone graft would be a useful means to preserve the femoral head in large non-traumatic osteonecrosis of the femoral head.
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10/142. Avascular necrosis in the femoral head secondary to bone marrow infarction in a patient with graft-versus-host disease after unrelated bone marrow transplantation.

    We previously reported a case of bone marrow infarction attributable to acute graft-versus-host disease (GVHD) in a patient with acute lymphoblastic leukemia after unrelated bone marrow transplantation (BMT). Although the bone marrow infarction-induced arthralgia in this patient improved, severe arthralgia appeared again with exacerbation of chronic GVHD, and the arthralgia was strongly correlated with the clinical course of chronic GVHD, i.e., the course of symptoms such as dermal and hepatic GVHD and ocular dryness. Finally, the patient developed avascular necrosis (AVN) in the right femoral head. serum interleukin (IL)-6 and IL-10 levels were high at the onset of arthralgia but low during remission, and levels of interferon-gamma were undetectable throughout the period of arthralgia. Based on the clinical course and these data, chronic GVHD was thought to have been the major cause of the AVN. Since IL-10 antagonizes various other cytokines that induce GVHD, the increase in IL-10 might have inhibited the development of GVHD.
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