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Forearm nonunion caused by hyperparathyroidism with 7 years follow up: A case report.

ABSTRACT: We report a patient who developed nonunion of both bones of the forearm associated with hyperparathyroidism (HPT).The patient was a 71-year-old female who previously fell and hit her left hand on the ground. At 2 years after injury the patient visited our hospital, since she became aware of instability of the left forearm without an inducer due to nonunion of the radioulnar diaphysis. The patient was surgically treated to acquire forearm support. Surgery for nonunion was applied only to the ulna. To acquire an elbow joint flexion angle, an about 30° angle was added to the false joint region. At one year after surgery, blood testing suggested HPT, however, the parathyroid mass was not excised following the current guidelines for management of HPT. At 7 years after surgery, the elbow range of motion, VAS and the Q-DASH score were improved. Weight-bearing by the forearm became possible, and the patient can perform pronation and supination at the radial nonunion.We learned from this case that it is necessary to immediately perform close examination to identify the presence or absence of primary disease causing insufficiency fracture, such as HPT. For treatment of nonunion of the 2 forearm bones in this elderly female, osteosynthesis of the ulna alone achieved sufficient osteal support without osteosynthesis of the radius, and the postoperative course was favorable.We presented here a rare case of nonunion of both bones of the forearm associated with HPT.

SUBMITTER: Kinoshita M

PROVIDER: S-EPMC5537439 | biostudies-other | 2017

REPOSITORIES: biostudies-other

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Project description:BackgroundWe present the disease course and long-term follow-up of two patients who were phenotypically diagnosed with atypical Leber Hereditary Optic Neuropathy (LHON) 14 and 12 years ago, respectively, whereby whole exome sequencing revealed recently described recessive DNAJC30:c.152G>A 152 A>G (p.Tyr51Cys) homozygous pathogenic variant with significant spontaneous visual acuity recovery in one.Case presentationTwo presented unrelated males with atypical LHON with sequential visual acuity (VA) loss were followed for many years. Both patients had negative family history. At the presentation at ages 17 (Case 1) and 18 years (Case 2), both had reduced visual acuity (Snellen): (Case 1) right eye (RE):CF 3m, left eye (LE):0.6, (Case 2) RE:0.2, LE:0.15; and color vision (Ishihara): (Case 1) 1/15 and 13/15; (Case 2) 2/15 and 3/15. Both had hyperemic optic disks (PNO) and central scotoma in their visual fields. Electrophysiology in the acute phase showed reduced and delayed visually evoked potentials (VEP) P100 in both patients, with reduced N95 amplitude in Case 2, and initially normal N95 amplitude in Case 1. Fluorescein angiography showed no early leakage with some late pooling at optic disks. Extensive clinical workout, including brain magnetic resonance imaging (MRI), aquaporin 4 (Aq4), and anti-myelin oligodendrocyte protein (anti-MOG) antibodies, was negative. Intravenous corticosteroids did not improve vision. Both experienced further deterioration several months after the onset accompanied by thinning of the peripapillary retinal nerve fiber layer (RNFL). Genetic testing for typical LHON pathogenic variants and whole mitochondrial DNA (mtDNA) sequencing was negative. 1 year after the onset, modest VA improvement began in Case 2 and continued over the next 3 years. VA improved bilaterally to 0.7, color vision 15/15, and islands of vision appeared within the visual field scotoma. VEP P100 peak time shortened, and amplitude increased, despite further RNFL thinning on optical coherent tomography (OCT). The patient's visual function remained stable during the entire 12-year follow-up period. Case 1 experienced modest VA improvement to 0.1 with some improvement in the visual field seven years after the disease onset, remaining stable during the entire 14-year follow-up period. VEP P100 wave remained undetectable.ConclusionsPresented are two autosomal recessive LHON (arLHON, OMIM:619382) cases with the same DNAJC30:c.152G>A pathogenic variant and different degrees of spontaneous visual recovery despite progressive RNFL thinning during a long-term follow-up. This mutation should be screened in every atypical LHON patient.

Project description:BackgroundSagliker syndrome is caused by severe secondary hyperparathyroidism in hemodialysis patients with chronic renal failure. It is mainly manifested by disturbances of calcium and phosphorus metabolism and bone changes, which eventually lead to abnormal changes in facial appearance and morphology, seriously affecting the quality of life of patients. With the improvement of management mode and technology for hemodialysis in chronic renal failure, the incidence of severe secondary hyperparathyroidism related to hemodialysis is relatively reduced. Therefore, Sagliker syndrome is more rare. How to early identify and choose the appropriate treatment for Sagliker syndrome is particularly important.Case descriptionA 34-year-old female patient with uremia, who underwent regular hemodialysis at the Blood Purification Center of Tianjin Third Central Hospital, developed Sagliker syndrome. The general data, clinical symptoms, height changes, biochemical indicators (serum calcium, phosphorus, alkaline phosphatase, parathyroid hormone, hemoglobin, and hematocrit), and parathyroid emission computerized tomography (ECT) were collected and analyzed. The patient had a history of hemodialysis with chronic renal failure for 6 years, and presented with bone pain for 2 years. Laboratory tests showed parathyroid hormone was 2,269 pg/mL and ECT showed 3 parathyroid hyperplasia. Finally, total parathyroidectomy and forearm transplantation were performed. The level of parathyroid hormone was significantly lower than that before the operation. On the first postoperative day, the level of parathyroid hormone decreased to 28.3 pg/mL. Four months later, the bone pain symptoms of the patient were significantly improved compared with those before the operation.ConclusionsSagliker syndrome is a special syndrome in maintenance hemodialysis patients with refractory secondary hyperparathyroidism. Early monitoring and standardized treatment of secondary hyperparathyroidism may prevent the occurrence of Sagliker syndrome. Early identification and diagnosis of Sagliker syndrome and the choice of appropriate treatment will have an important impact for the prognosis.

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Forearm nonunion caused by hyperparathyroidism with 7 years follow up: A case report.

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