1/7. Disuse osteoporosis as evidence of brachial plexus palsy due to intrauterine fetal maladaptation. We report what may be overlooked evidence of the effects of intrauterine maladaptation as a cause of brachial plexus palsy. A case of total brachial plexus palsy in the posterior arm associated with Horner's syndrome and severe demineralization of the bones of the affected arm is analyzed. In this litigated case, a report of marked demineralization of the bones of the affected arm was analyzed by the plaintiff's radiology expert as diagnostic of disuse osteoporosis. The presence of clear-cut evidence of disuse osteoporosis during the early neonatal period is compelling evidence of an intrauterine onset of brachial plexus palsy. ( info) |
2/7. Spontaneous external auditory canal cholesteatoma complicated by rheumatoid arthritis--case report and review of the literature. A 63-year-old woman with rheumatoid arthritis sought medical assistance for dull and chronic pain in her left ear two and half years after her initial diagnostic examination. Otoscopic examination revealed that the posteroinferior wall of the bony external ear canal was eroded and that the small cavity was filled with squamous debris. The condition was diagnosed as external auditory canal cholesteatoma (EACC). The existence of EACC might suggest complications of bone disease, aging cerumen gland, or a low migratory rate of the epithelium. ( info) |
3/7. Case report: the management of bone demineralization associated with long-term treatment of multiple paraphilias with long-acting LHRH agonists. A patient with multiple paraphilias had been successfully treated for 10 years with a long-acting LHRH agonist with complete suppression of deviant sexual activity. However, during treatment, he demonstrated bone demineralization, as documented by serial bone densitometry studies. A treatment regimen was instituted, which resulted in the cessation or partial reversal of bone loss. ( info) |
4/7. mandible and maxilla bone mineral density and threshold analysis studies by pQCT in two edentulous women receiving pamidronate. The mandible and maxilla of two edentulous women, treated during 25 weeks with oral pamidronate, were monitored by peripheral quantitative tomography (pQCT). Whole bone volumetric mineral density failed to show meaningful variations after treatment. However, an analysis of separated cortical and medullar areas disclosed focal bone loss at the right mandible cortex of patient #1 and at the left maxilla cortex of patient #2. These and other bone sub-regions were further studied by clustering the internal sites with a different degree of bone mineral density, resorting to the mineral threshold analysis provided by the system. Where bone loss was detected, it corresponded to increased loss of the most osteopenic sites, while medium and high-density portions tended to remain unchanged within the region. There were no significant variations in all other regions, or alternatively, minor losses at osteopenic sites were compensated by an increase at high-density portions. Hence, the pQCT system allowed monitoring volumetric bone mineral density at particular sites of interest, discriminating variations at portions with a dissimilar degree of bone volume. Further studies should confirm whether pamidronate exerts a protective effect on sub-regions with previous medium and high degrees of bone mineralization, as suggested by our present findings. ( info) |
| Atypical presentations are common when spondyloarthropathy develops in older patients. We report two cases initially mistaken for reflex sympathetic dystrophy syndrome (RSDS). Both the patients were men, aged 62 and 75 years, respectively, with marked painful edema of a foot. One patient reported a moderate-energy trauma as the triggering event. Severe diffuse demineralization was noted on radiographs and diffuse hyperactivity on bone scans starting at the early vascular phase. These findings suggestive of RSDS led to treatment with calcitonin, griseofulvin, and pamidronate, all of which were ineffective. Laboratory tests showed severe inflammation, promoting investigations for other conditions. Spondyloarthropathy was diagnosed based on oligoarthritis with sacroiliitis, presence of HLA B27, and a favorable response to non-steroidal antiinflammatory therapy. In older patients, edema of the foot with severe demineralization and the laboratory evidence of inflammation should suggest a spondyloarthropathy. ( info) |
6/7. New patients: should children be treated differently? Inflammatory bowel disease (IBD) in childhood is often diagnosed at a vulnerable time of growth and development, and is recognized as one of the most significant chronic gastrointestinal diseases to affect children. Children and adolescents with IBD are at increased risk of complications as a result of malnutrition secondary to reduced appetite, increased metabolism and decreased absorptive capacity. The most common and serious complications are growth failure, bone demineralization and impaired psychosocial development. These issues add to the complexity of childhood IBD management and it is essential that adequate medical management is in place to prevent these long-term complications. Current treatment options include 5-aminosalicylic acid, antibiotics, corticosteroids, nutritional therapy and immunomodulators used to induce and maintain remission; some are specifically employed to maintain a steroid free long-term remission. As a general rule, long-term corticosteroid use should be avoided to reduce the risk of bone demineralization and growth failure. Newer treatment options such as infliximab have been shown to be effective for inducing and prolonging remission of Crohn's disease in children and paediatric use of infliximab is likely to increase in the near future. A recent case report, involving a 15-year old boy presenting with abdominal pain and bloody diarrhoea, illustrates the difficulty in correctly diagnosing IBD in children and the need for optimizing therapy to achieve treatment success. ( info) |
7/7. Skeletal demineralization and fractures caused by fetal magnesium toxicity. Two surviving female infants, born from a triplet pregnancy at 30 weeks gestation, were noted to have severe osteopenia and multiple fractures diagnosed at 20 days of age. Their mother had been treated for preterm labor with intravenous magnesium sulfate from week 22 until their birth at 30 weeks gestation. At birth, the triplets exhibited craniotabes with enlarged fontanelles and sutures. All developed Respiratory Distress syndrome (RDS) and the two surviving infants required prolonged respiratory support. serum calcium and phosphate levels were normal and alkaline phosphatase levels were increased. The infants were treated with supplements of calcium and phosphorous, with resultant healing of the multiple fractures without deformity. Fetal magnesium toxicity impairs bone mineralization and can lead to serious bone demineralization that may cause fractures in the newborn period that complicate recovery from respiratory disease. Early recognition and treatment may minimize complications related to osteopenia caused by fetal magnesium toxicity. ( info) |