PubMed · 7806824
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M A Wehbé. 1994. Reflex sympathetic dystrophy.. https://doi.org/10.1016/0363-5023(94)90207-0
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BACKGROUND: In most developed countries, survivors of physical torture inflicted for political, religious, or ethnic reasons face ever more stringent review when seeking asylum. In Austria, asylum seekers are required by immigration authorities to undergo medical examination as part of the review. Bone scintigraphy can detect bone lesions that are not detectable clinically or radiologically. We assessed the value of bone scintigraphy as corroboration of alleged injuries. METHODS: Human-rights organisations referred 25 asylum seekers to us from countries where torture is practised. We included patients who claimed to have been beaten by the security forces in their home country because of political or religious conviction or ethnic origin. Injuries had been inflicted 4 months to 5 years earlier. The patients (three women, 22 men) from 12 countries were categorised retrospectively into two groups: group A (n=12), tortured with blows from hard objects, and group B (n=13), tortured with blows from fists and kicks. We also used a control group of 25 individuals with the same age and sex distribution from the same countries who had no history of torture. FINDINGS: In group A, bone scans showed abnormalities in the area of alleged injury in all patients, whereas radiography was positive in only five patients. In group B, bone scans in the alleged areas of damage were positive in seven patients, but radiography yielded no positive outcomes. Among the controls there was one abnormal scan due to a known coxarthrosis. INTERPRETATION: Our preliminary results suggest that bone scintigraphy is a sensitive, non-invasive tool to document trauma some years after the actual injury.
BACKGROUND: Timely diagnosis and continued monitoring of patients with type I Gaucher disease is critical because skeletal involvement can permanently disable patients and visceral organ involvement can lead to abdominal pain and secondary hematologic and biochemical complications. OBJECTIVE: To seek clinical consensus for minimum recommendations for effective diagnosis and monitoring of patients with type I Gaucher disease. PARTICIPANTS, EVIDENCE, AND CONSENSUS PROCESS: Contributing authors collaborated in quarterly meetings over a 2-year period to synthesize recommendations from peer-reviewed publications and their own medical experiences. These physicians care for most patients with Gaucher disease in the United States and serve as the US Regional Coordinators for the International Collaborative Gaucher Group Registry, the world's largest database for this disorder. CONCLUSIONS: The definitive method of diagnosis is enzyme assay of beta-glucocerebrosidase activity. Schedules differ for monitoring complications of type I Gaucher disease, depending on symptoms and whether enzyme replacement therapy is used. Hematologic and biochemical involvement should be assessed by complete blood cell count, including platelets, acid phosphatase, and liver enzymes, at baseline and every 12 months in untreated patients and every 3 months and at enzyme replacement therapy changes in treated patients. Visceral involvement should be assessed at diagnosis using magnetic resonance imaging or computed tomographic scans. Skeletal involvement should be assessed at diagnosis using T1- and T2-weighted magnetic resonance imaging of the entire femora and plain radiography of the femora, spine, and symptomatic sites. Follow-up skeletal and visceral assessments are recommended every 12 to 24 months in untreated patients, and every 12 months and at enzyme replacement therapy changes in treated patients.
The parathyroid hormone (PTH)/PTH-related peptide (PTHrP) receptor (PTHR) functions in skeletal development and mediates an array of other physiological responses modulated by PTH and PTHrP. PTHR gene transcription in mouse is controlled by two promoters: P1, which is highly and selectively active in kidney; and P2, which functions in a variety of tissues. P1 and P2 are conserved in human tissue; however, P1 activity in kidney is weak. We have now identified a third human promoter, P3, which is widely expressed and accounts for approximately 80% of renal PTHR transcripts in the adult. No P3 activity was detected in mouse kidney, indicating that renal PTHR gene expression is controlled by different signals in human and mouse. During development, only P2 is active at midgestation in many human tissues, including calvaria and long bone. This strongly suggests that factors regulating well conserved P2 control PTHR gene expression during skeletal development. Our results indicate that human PTHR gene transcription is upregulated late in development with the induction of both P1 and P3 promoter activities. In addition, P2-specific transcripts are differentially spliced in a number of human cell lines and adult tissues, but not in fetal tissues, giving rise to a shorter and less structured 5' UTR. Thus, our studies show that both human PTHR gene transcription and mRNA splicing are developmentally regulated. Moreover, our data indicate that renal and nonrenal PTHR gene expression are tightly coordinated in humans.