A Case of Panhypopituitarism with Rhabdomyolysis / 대한내분비학회지

Rhabdomyolysis is the consequence of extensive muscle injury with the release of muscle cell constituents into plasma. It can arise from trauma and also from a variety of nontraumatic causes. Trauma, drugs, toxins and infection are the major causes of rhabdomyolysis, but it is rarely associated with metabolic disorders such as severe electrolyte disturbance, diabetic ketoacidosis, hyperosmolar nonketotic coma, hypothyroidism and thyrotoxicosis. There have been several reported cases of metabolic rhabdomyolysis, but panhypopituitarism as a cause has never been identified. We experienced a case of acute rhabdomyolysis associated with panhypopituitarism. Thus, So we report this case with the review of related literature. Metabolic disorder is a rare cause of rhabdomyolysis, but it should always be considered in a patient having and unexplained increased of the creatine kinase concentration

A Case of Kallmann's Syndrome with Unilateral Renal Aplasia and Diabetes Mellitus / 대한내분비학회지

Kallmann's syndrome is defined as the combination of hypogonadotropic hypogonadism and anosmia/hyposmia. The syndrome is a result of defect in the embryonic migratory pathway of gonadotropin-releasing hormone, which synthesizes neurons and olfactory axons. The hypogonadotropic hypogonadism results due to absence of or incomplete pubertal development and may be associated with anosmia, hyposmia, midline defect(color blindness, cleft-lip, cleft-palate, unilateral renal agenesis, sensorineural deafness), cryptorchidism and skeletal anomaly. Till date in Korea, few cases of Kallmann's syndrome have been reported but there are no available reports on cases of Kallmann's syndrome with unilateral renal aplasia and diabetes mellitus. We handled a case of Kallmann's syndrome associated with unilateral renal agenesis and diabetes mellitus. In the current work, we present a peculiar case as afore mentioned with the review of related literature.

A Case of Thyrotoxic Paraplegia / 대한내분비학회지

Hyperthyroidism may be associated or present with a variety of neuromuscular disorders, including thyrotoxic myopathy, exophthalmic ophthalmoplegia, periodic paralysis and myasthenia gravis. In contrast to muscle, peripheral nerve involvement in hyperthyroidism is exceedingly rare, and has received little attention. Paraplegia-like weakness during severe hyperthyroidism was first described by Charcot in 1889, and called Basedow's paraplegia' by Joffory in 1894. However, there has been no reported case in Korea. A 38-year-old woman was admitted for evaluation of progressive weakness and a gait disturbance. Her endocrinological results were compatible with hyperthyroidism. The polyneuropathy was also confirmed with sequential electrophysiological studies of the nerves and muscles. Drug therapy for hyperthyroidism resulted in resolution of the clinical neurological symptoms and progressive improvement of electrophysiological findings. Hyperthyroidisms are common medical disorders, which are often accompanied by diverse types of neurological and neuromuscular dysfunctions. All of these neurological manifestations are important, as they can serve as important clues to the diagnosis of a thyroid disorder. Furthermore, they are often related to the patient's presenting complaint. Therefore, the physician must be alert to the diverse manifestations of thyroid dysfunction, as they can lead to the diagnosis of potentially serious but treatable disorders. Herein is reported a case of myopathy and neuropathy associated with hyperthyroidism (Basedow's paraplegia), with a review of the literature

A Case of Thyrotoxic Paraplegia / 대한내분비학회지

Hyperthyroidism may be associated or present with a variety of neuromuscular disorders, including thyrotoxic myopathy, exophthalmic ophthalmoplegia, periodic paralysis and myasthenia gravis. In contrast to muscle, peripheral nerve involvement in hyperthyroidism is exceedingly rare, and has received little attention. Paraplegia-like weakness during severe hyperthyroidism was first described by Charcot in 1889, and called Basedow's paraplegia' by Joffory in 1894. However, there has been no reported case in Korea. A 38-year-old woman was admitted for evaluation of progressive weakness and a gait disturbance. Her endocrinological results were compatible with hyperthyroidism. The polyneuropathy was also confirmed with sequential electrophysiological studies of the nerves and muscles. Drug therapy for hyperthyroidism resulted in resolution of the clinical neurological symptoms and progressive improvement of electrophysiological findings. Hyperthyroidisms are common medical disorders, which are often accompanied by diverse types of neurological and neuromuscular dysfunctions. All of these neurological manifestations are important, as they can serve as important clues to the diagnosis of a thyroid disorder. Furthermore, they are often related to the patient's presenting complaint. Therefore, the physician must be alert to the diverse manifestations of thyroid dysfunction, as they can lead to the diagnosis of potentially serious but treatable disorders. Herein is reported a case of myopathy and neuropathy associated with hyperthyroidism (Basedow's paraplegia), with a review of the literature

Increased Expression of Focal Adhesion Kinase in Thyroid Cancer: Immunohistochemical Study

Focal adhesion kinase (FAK) is a tyrosine kinase that is found in cellular structures called focal adhesions. FAK appears to be a key element in signal transduction pathways involved in cell adhesion and locomotion. FAK is overexpressed in various tumors, including tumors derived from regions of the head and neck, colon, breast, prostate, and liver. In this study, we investigated immunohistochemically whether FAK expression was increased in thyroid cancers. FAK staining was not seen in any of the 20 normal thyroid tissues or the 6 nodular hyperplasia specimens. In contrast, FAK staining was observed in all of 17 papillary carcinomas, 9 follicular carcinomas, 8 medullary carcinomas, and 2 anaplastic carcinomas. Nine of 17 follicular adenomas showed FAK immunoreactivity. FAK was not expressed in normal tissue and nodular hyperplasia, but was expressed in some of the follicular adenoma, and all of the follicular, papillary, medullary and anaplastic thyroid carcinoma. This result indicates that the up-regulation of FAK may play a role in the development of thyroid carcinogenesis.

Immunohistochemical Expression of COX-2 in Thyroid Nodules

BACKGROUND: Recent evidence indicates that elevated COX-2 expression is associated with the carcinogenesis of numerous neoplasms. In this study, we investigated COX-2 expression in various thyroid specimens in order to elucidate its physiological role in pathologic conditions, and to evaluate the efficiency of COX-2 protein expression as a molecular marker of malignancy in the thyroid gland. METHODS: COX-2 expression was studied immunohistochemically in 19 papillary carcinomas, 8 follicular carcinomas, 14 follicular adenomas, 2 H rthle cell carcinomas, 4 H rthle cell adenomas, 8 nodular hyperplasias, 3 Graves' diseases, 3 Hashimoto's thyroiditis, 2 medullary carcinomas, 1 anaplastic carcinoma, and 20 normal thyroid tissues. RESULTS: COX-2 staining was not seen in any of the normal thyroid, Graves' disease, or nodular hyperplasia specimens. In contrast, COX-2 staining was observed in all of papillary carcinomas, Hashimoto's thyroiditis, H rthle cell carcinomas, and H rthle cell adenomas tissues. Moreover, 7 of 8 follicular carcinomas and 11 of 14 follicular adenomas showed COX-2 staining. CONCLUSION: These results indicate that COX-2 is not useful as a marker of malignancy. Since COX-2 expression was evident in follicular adenomas and in papillary and follicular carcinomas. Thus, the enzyme may be involved in the early process of thyroid tumorigenesis.