MYH9 nephropathy

MYH9-related disorder is an autosomal dominant disease caused by a mutation in the MYH9 gene, which encodes nonmuscle myosin heavy chain IIA (NMMHC-IIA). This disease is characterized by giant platelets, thrombocytopenia, granulocyte inclusion bodies, proteinuria, and high-pitch sensorineural deafness. Nephropathy has been observed in 30% of patients with MYH9-related disorder. The characteristic features are early onset proteinuria and rapidly progressing renal disorder. However, the prognosis of MYH9 nephropathy remains unclear. Herein, we describe a 36-year-old woman who presented with proteinuria and was diagnosed with MYH9 nephropathy via renal biopsy and gene analysis. Her proteinuria improved after administration of an angiotensin II receptor blocker, but was aggravated after changing to a calcium channel blocker.

Incidental Findings with Technetium-99m Methoxyisobutrlisonitrile Imaging of Ectopic Parathyroid Hyperplasia in Patient with Intrathyroidal Parathyroid Hyperplasia

We report a case of intrathyroidal and ectopic parathyroid hyperplasia in a 47-year-old female patient with secondary hyperparathyroidism. During evaluation for end stage renal disease, hypercalcemia and hyperparathyroidism were detected in laboratory exam and thyroid nodules were found in computed tomography, and thyroid ultrasonography. In subsequent dual-phase technetium-99m methoxyisobutrlisonitrile (Tc-99m MIBI) scan, delayed focal uptakes were found in thyroid gland and the upper mediastinum. I-123 scan showed photon defects in thyroid gland and no uptake in the upper mediastinum. The imaging findings indicate intrathyroidal and mediastinal ectopic parathyroid hyperplasia. The intrathyroidal and ectopic parathyroid hyperplasia were confirmed by surgical approach. Tc-99m MIBI scan was useful for detecting ectopic parathyroid hyperplasia concomitant intrathyroidal parathyroid lesion.

Guided bone regeneration with beta-tricalcium phosphate and poly Llactide-co-glycolide-co-epsilon-caprolactone membrane in partial defects of canine humerus

This study was performed to evaluate the effect of betatricalcium phosphate and poly L-lactide-co-glycolide-coepsilon- caprolactone (TCP/PLGC) membrane in the repair of partial bone defects in canine proximal humerus. Three adult mixed-breed dogs were used during the experimental period. The length of the defect was quarter of the full length of humerus, and width of the defect was quarter of middle diameter of the lateral aspect of humerus. The humeri of each dog were divided into treatment (TCP/ PLGC) and control groups. The defect was covered with TCP/PLGC membrane in treatment group. To evaluate regeneration of the bone, computerized tomography (CT) and histopathologic examination were performed. The radiopaque lines were appeared at the original defect sites in TCP/PLGC group but below the original site in control at 4th week. Radiopacity and thickness of the defect sites, and radiopaque lines were more increased at 8th week than those of 4th week. Histopathologic findings revealed fibrous connective tissue migration into the defect and the migration inhibited the structure of new cortex to be placed in the original level in control whereas new cortex growth was found in the level of original line in TCP/ PLGC group. However, the new cortical bone in the TCP/ PLGC group was thinner and less organized than the adjacent intact cortex, and the amount of new cancellous bones were also scanty. The result suggested that TCP/ PLGC membrane is a good guided bone regeneration material to restore the original morphology of humerus in partial defect.