1.Bilateral primary pigmented nodular adrenocortical disease: a case of report describing a rare cause of Cushing's syndrome.
Yong Koo PARK ; Youn Wha KIM ; Jin Woo KIM ; Young Kil CHOI ; Young Tae KO ; Seok Whan KO ; Moon Ho YANG
Journal of Korean Medical Science 1994;9(6):450-457
A case of Cushing's syndrome due to bilateral pigmented nodular adrenal disease in a 35-year-old male is presented. The adrenals showed multiple, black, variable sized nodules. Histologically the cells contained lipofuscin and either had a clear cytoplasm or an eosinophilic cytoplasm with a prominent nucleus. Lymphocytic infiltration and fatty metaplasia within the nodules are two of the prominent histological features. There is extreme internodular atrophy which suggests that primary pigmented nodular adrenocortical disease is a non-adrenocorticotropic hormone dependent condition. Since the disorder appears to involve primarily the cortex of both adrenals, the treatment of choice is bilateral adrenalectomy followed by steroid replacement. The characteristic clinicopathological manifestations that separate this diagnosis from other types of adrenal disease are also discussed. This is the first reported case in Korea to be documented with the pertinent clinicopathological findings.
Adipose Tissue/pathology
;
Adrenal Cortex/chemistry/*pathology/radiography/secretion/ultrasonography
;
Adrenalectomy
;
Adult
;
Atrophy
;
Case Report
;
Cushing Syndrome/*etiology/surgery
;
Dexamethasone/diagnostic use
;
Furosemide/diagnostic use
;
Human
;
Hydrocortisone/secretion
;
Inflammation
;
Lipofuscin/*analysis
;
Male
;
Metaplasia
;
Organelles/ultrastructure
2.Attenuated Renal Excretion in Response to Thiazide Diuretics in Gitelman's Syndrome: A Case Report.
Chung Ho YEUM ; Soo Wan KIM ; Seong Kwon MA ; Jung Hee KO ; Myong Yun NAH ; Nam Ho KIM ; Ki Chul CHOI
Journal of Korean Medical Science 2002;17(4):567-570
Gitelman's syndrome is a variant of Bartter's syndrome characterized by hypocalciuria and hypomagnesemia. The administration of thiazide diuretics may induce a subnormal increase of urinary Na+ and Cl- excretion in patients with Gitelman's syndrome, consistent with the hypothesis that less Na+ and Cl- than normal is reabsorbed by the thiazide-inhibitable transporter in Gitelman's syndrome. Specific mutations of NaCl cotransporter, coupled with mutant NaCl cotransporter expression studies clearly demonstrated that many of the characteristics of individuals with Gitelman's syndrome are explained by lack of function of NaCl cotransporter. We recently diagnosed a patient with Gitelman's syndrome by performing the thiazide and furosemide tests, and it is suggested that the clearance studies by diuretic administration may be of diagnostic help in Gitelman's syndrome.
Adolescent
;
Bartter Syndrome/*diagnosis/metabolism/physiopathology
;
*Benzothiadiazines
;
Chlorides/blood/urine
;
Diuretics/diagnostic use
;
Electrolytes/blood/urine
;
Female
;
Furosemide/diagnostic use
;
Humans
;
Kidney/*physiopathology
;
Kidney Function Tests
;
Sodium/blood/urine
;
Sodium Chloride Symporter Inhibitors/*diagnostic use
;
Sodium Chloride Symporters
;
Symporters/metabolism
;
Syndrome