Diagnostic imaging in pediatric renal inflammatory disease.
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Biomedical subjects
Publications and source records attributed to R G Wells.
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Technetium 99m pertechnetate thyroid scans were performed on 57 infants referred for evaluation of suspected congenital hypothyroidism. Thyroid anatomy may be characterized by four general types, based on the scintigraphic findings: (1) normal size and location; (2) ectopic location; (3) no detectable thyroid activity; (4) normal location with increased size or uptake. There are diverse etiologies of congenital hypothyroidism. Correlation of thyroid scintigraphy with blood T4 and TSH levels allows specific etiological diagnosis in the majority of cases of congenital hypothyroidism.
A case demonstrating the radionuclide cardioangiographic appearance of a coronary artery fistula is presented. The correct definitive diagnosis of this disorder has generally been made by angiography since clinical findings and noninvasive diagnostic studies can be nonspecific. We report the diagnosis and shunt quantification of a right coronary artery fistula to the right ventricle by radionuclide cardioangiography.
In immunocompromised patients with cerebral toxoplasmosis, the tachyzoite forms rather than cystic and bradyzoite forms of the protozoon are commonly seen. These tachyzoites are minute, scattered among cellular debris, sometimes lodged inside macrophages and neutrophils, and difficult to visualize by light microscopy, even with special stains. Immunodiagnostic tests may be falsely negative due to inability of the host to produce appropriate antibodies. Isolation of the organism is dangerous because Toxoplasma gondii is highly infective. In this situation, transmission electron microscopy (EM) may be a diagnostic tool of choice. It demonstrates the fine definitive features of the protozoon and can be expedited to give results in five hours. Further evaluation of EM for diagnosing possible toxoplasmosis in immunocompromised patients is indicated.
Although suprarenal abscess in a newborn is rare, a prompt diagnosis is essential for proper patient management. The findings obtained with Tc-99m glucoheptonate renal imaging in a newborn with a right adrenal abscess are reported. A radionuclide renal imaging sequence over a 15-hour period demonstrated a "rim sign" which can be used to suggest the diagnosis. Radionuclide and ultrasound imaging of neonatal adrenal masses is discussed.
A case of a large plasma-cell granuloma of the left upper lobe in a 5-year-old girl is presented. Uptake of Tc-99m MDP by the soft tissue mass was demonstrated with bone imaging. Plasma cell granuloma should be included in the gamut of extraosseous uptake of bone-seeking radionuclide in the pediatric chest.
A 3-week-old male neonate with heart failure associated with Coxsackie virus infection was imaged with Tc-99m PYP and TI-201. The abnormal imaging pattern suggested myocardial infarction. Autopsy findings indicated that the cause was myocardial necrosis secondary to an acute inflammatory process. Causes of abnormal myocardial uptake of Tc-99m PYP in pediatrics include infarction, myocarditis, cardiomyopathy, bacterial endocarditis, and trauma. Myocardial imaging cannot provide a specific cause diagnosis. Causes of myocardial infarction in pediatrics are listed in Table 1.
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Congenital lymphangioma is a relatively common cause of childhood soft tissue masses of the extremities. Radionuclide pedal lymphangiography is a simple and rapid technique for the diagnosis of lymphangiomas of the lower extremities. A case of congenital lymphangioma of the thigh in an eight-year-old child is illustrated.
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Intervertebral disk calcification in childhood probably occurs secondary to disk inflammation or trauma. Images obtained in the evaluation of a six-year-old boy with cervical disk calcification demonstrate the typical findings with radiography, bone scintigraphy, and computed tomography.
The gamma delta resolvase, product of the transposon's tnpR gene, mediates a site-specific recombination between two copies of gamma delta directly repeated on the same replicon. The site at which the recombination occurs, res, lies between the tnpA and tnpR genes. Within this same region lie the promoters for expression of tnpA and tnpR and the operator sites through which resolvase regulates the transcription. In order to determine the extent of the res site we have constructed in vitro a series of deletions that terminate within the tnpA-tnpR intergenic region, and have analyzed their effect on site-specific recombination. Our results indicate that a fully functional res site is about 115 base-pairs (bp) and runs from a position 15 bp to the left (tnpA-proximal) side of the crossover point to 100 bp to the right. This segment corresponds precisely to the region defined by the three resolvase binding sites that we have demonstrated previously. Alterations of the nucleotide sequence around the crossover point indicate the importance of all or part of the central palindrome 5' T-T-A-T-A-A within which the breakage--reunion reaction takes place. Taken together, our results strengthen our earlier conclusion that resolvase recognizes the 9 bp segment 5' T-G-T-C-Y-N-N-T-A that occurs (in slightly degenerate form) in each half of the three binding sites. Using the deletions we have confirmed that the tnpA promoter spans the crossover site and have shown that the major tnpR promoter in vivo coincides with resolvase binding site II, although a second promoter for tnpR transcription lies across site I.
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The tnpR gene product, resolvase, of the transposable element gamma delta mediates site-specific recombination between two copies of gamma delta directly repeated on the same replicon, and it negatively regulates transcription of the tnpA (transposase) gene and its own gene. The recombinational site, res, and the regulatory region both are located in the tnpA-tnpR intercistronic region. In studying the interaction of purified resolvase with DNA fragments derived from gamma delta and the related transposon, Tn3, that span this region, we have demonstrated that three sites specifically bind resolvase. Site I overlaps the recombinational crossover point and both transcriptional promoters. Sites II and III cover most of the DNA between the crossover point and the translational start of the tnpR gene. These are the only binding sites we have detected in a region of about 400 base pairs centered on the crossover point. Studies of cointegrates that contain only part of the region that binds resolvase indicate that site I is not sufficient for efficient site-specific recombination and suggest that all three sites are probably required.
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