Central Diabetes Insipidus in the Setting of Acute Myelogenous Leukemia

Acute myeloid leukemia with diabetes insipidus and hypophyseal infiltration

“…It has been reported that the pathogenesis may include leukemic infiltrate in the hypothalamus‐pituitary area, and our case highlights this etiology. Interestingly, peri‐pituitary leukemic infiltrates have been identified at postmortem in AML patients who did not have clinical CDI . As previously reported, clinical CDI has also been described in patients without abnormal radiological findings or cerebrospinal fluid abnormalities suggestive of leukemic infiltration .…”

“…Interestingly, peri‐pituitary leukemic infiltrates have been identified at postmortem in AML patients who did not have clinical CDI . As previously reported, clinical CDI has also been described in patients without abnormal radiological findings or cerebrospinal fluid abnormalities suggestive of leukemic infiltration . These patients are reported commonly in association with a rare AML with the recurrent cytogenetic abnormality t(3;3)(q21;q26) with approximately half of the cases having monosomy 7 .…”

“…It seems increasingly likely that the pathogenetic mechanism of the two most commonly reported etiologies for CDI in AML, infiltrative and t(3;3)(q21;q26) and/or monosomy 7, may be different. Both etiologies appear to carry a poor prognosis and whether the etiology has treatment implications has not yet been explored. Our case highlights that CDI is a rare presentation of AML and these patients may present with either the “typical” karyotypic or radiographic abnormalities.…”

The Available Clinical Approaches to the Management of Patients with Acute and Chronic Hypernatremia

“…Faje et al [28] concluded that, although the prevalence of central diabetes insipidus is rare, it may be referred to as a reversible side effect of treatment with temozolomide. This type of diabetes insipidus is relevant to acute myelogenous leukemia, as well [30].…”

Diabetes Insipidus: Little-Known Facts

“…У обоих отмечались полиурия и полидипсия, снижение потребления жидкости приводило к развитию гипернатриемии; оба пациента хорошо реагировали на лечение десмопрессином. Таким образом, гематологические нарушения у пациентов с ЦНД должны побуждать клиницистов рассматривать возможность сочетания обеих патологий или подозревать рецидив ОМЛ у пациентов с ранее диагностированным лейкозом даже в стадии ремиссии [25]. K. Yamagami и соавт.…”