Diagnosis and Treatment > Signs and Symptoms
Search for other papers by Raku Son in
Google Scholar
PubMed
Search for other papers by Masahiko Nagahama in
Google Scholar
PubMed
Search for other papers by Fumiaki Tanemoto in
Google Scholar
PubMed
Search for other papers by Yugo Ito in
Google Scholar
PubMed
Search for other papers by Fumika Taki in
Google Scholar
PubMed
Search for other papers by Ryosuke Tsugitomi in
Google Scholar
PubMed
Search for other papers by Masaaki Nakayama in
Google Scholar
PubMed
Summary
The etiology of hyponatremia is assessed based on urine osmolality and sodium. We herein describe a 35-year-old Asian man with pulmonary tuberculosis and perforated duodenal ulcer who presented with hyponatremia with hourly fluctuating urine osmolality ranging from 100 to 600 mosmol/kg, which resembled urine osmolality observed in typical polydipsia and SIADH simultaneously. Further review revealed correlation of body temperature and urine osmolality. Since fever is a known non-osmotic stimulus of ADH secretion, we theorized that hyponatremia in this patient was due to transient ADH secretion due to fever. In our case, empiric exogenous glucocorticoid suppressed transient non-osmotic ADH secretion and urine osmolality showed highly variable concentrations. Transient ADH secretion-related hyponatremia may be underrecognized due to occasional empiric glucocorticoid administration in patients with critical illnesses. Repeatedly monitoring of urine chemistries and interpretation of urine chemistries with careful review of non-osmotic stimuli of ADH including fever is crucial in recognition of this etiology.
Learning points:
-
Hourly fluctuations in urine osmolality can be observed in patients with fever, which is a non-osmotic stimulant of ADH secretion.
-
Repeated monitoring of urine chemistries aids in the diagnosis of the etiology underlying hyponatremia, including fever, in patients with transient ADH secretion.
-
Glucocorticoid administration suppresses ADH secretion and improves hyponatremia even in the absence of adrenal insufficiency; the etiology of hyponatremia should be determined carefully in these patients.
Search for other papers by Runa Acharya in
Google Scholar
PubMed
University of Iowa, Carver College of Medicine, Iowa City, Iowa, USA
Medicine and Endocrinology, University of Iowa, Iowa City, Iowa, USA
Des Moines University, Des Moines, Iowa, USA
Search for other papers by Udaya M Kabadi in
Google Scholar
PubMed
Summary
Diabetic ketoacidosis (DKA) is commonly encountered in clinical practice. The current case is a unique and rare presentation of DKA as the initial manifestation of Cushing’s disease secondary to ACTH-secreting pituitary adenoma. Appropriate management as elaborated in the article led to total remission of diabetes as well as the Cushing’s disease.
Learning points:
-
DKA is a serious and potentially life-threatening metabolic complication of diabetes mellitus.
-
Some well-known precipitants of DKA include new-onset T1DM, insulin withdrawal and acute illness.
-
In a patient presenting with DKA, the presence of a mixed acid–base disorder warrants further evaluation for precipitants of DKA.
-
We present a rare case of DKA as an initial manifestation of Cushing’s disease secondary to ACTH-producing pituitary adenoma.
