Cerebral malaria: an unusual case of central diabetes insipidus

Central diabetes insipidus is an uncommon feature of malaria. A previously healthy 72-year-old man presented with fever, rigors, and altered mental status after a recent trip to Liberia, a country known for endemic falciparum malaria. Investigations confirmed plasmodium falciparum parasitemia. Within one week after admission, the serum sodium rose to 166 mEq/L and the urine output increased to 7 liters/day. Other labs were notable for a high serum osmolality, low urine osmolality, and low urine specific gravity. The hypernatremia did not respond to hypotonic fluids. Diabetes insipidus was suspected and parenteral desmopressin was started with a prompt decrease in urinary output and improvement in mental status. Additional testing showed normal anterior pituitary hormones. The desmopressin was eventually tapered off with complete resolution of symptoms. Central diabetes insipidus occurred likely as a result of obstruction of the neurohypophyseal microvasculature. Other endocrinopathies that have been reported with malaria include hyponatremia, adrenal insufficiency, hypothyroidism, hypocalcemia, hypophosphatemia, hyper-, and hypoglycemia, but none manifested in our patient. Though diabetes insipidus is a rare complication of malaria, clinicians need to be aware of this manifestation, as failure to do so may lead to fatality particularly if the patient is dehydrated

Cerebral Malaria: An Unusual Cause of Central Diabetes Insipidus

Central diabetes insipidus is an uncommon feature of malaria. A previously healthy 72-year-old man presented with fever, rigors, and altered mental status after a recent trip to Liberia, a country known for endemic falciparum malaria. Investigations confirmed plasmodium falciparum parasitemia. Within one week after admission, the serum sodium rose to 166 mEq/L and the urine output increased to 7 liters/day. Other labs were notable for a high serum osmolality, low urine osmolality, and low urine specific gravity. The hypernatremia did not respond to hypotonic fluids. Diabetes insipidus was suspected and parenteral desmopressin was started with a prompt decrease in urinary output and improvement in mental status. Additional testing showed normal anterior pituitary hormones. The desmopressin was eventually tapered off with complete resolution of symptoms. Central diabetes insipidus occurred likely as a result of obstruction of the neurohypophyseal microvasculature. Other endocrinopathies that have been reported with malaria include hyponatremia, adrenal insufficiency, hypothyroidism, hypocalcemia, hypophosphatemia, hyper-, and hypoglycemia, but none manifested in our patient. Though diabetes insipidus is a rare complication of malaria, clinicians need to be aware of this manifestation, as failure to do so may lead to fatality particularly if the patient is dehydrated

New-Onset Diabetes Mellitus With Exposure to Ledipasvir and Sofosbuvir.

The combination therapy of ledipasvir/sofosbuvir was approved by the Food and Drug Administration in 2014 for the treatment of chronic hepatitis C. Although hyperglycemia is not well known to occur with its use, we present 2 cases of new-onset diabetes mellitus and a review of the literature suggesting an adverse event association. In the first patient with HIV, we postulate that ledipasvir/sofosbuvir increased the levels of tenofovir and thereby potentiated hyperglycemia. In the second case of a patient with prediabetes, ledipasvir/sofosbuvir appeared to increase insulin resistance. A literature review further supported an association of hyperglycemia and the use of ledipasvir/sofosbuvir. Hence, clinicians should be cautious about worsening of glucose intolerance, and more studies are warranted to explore the underlying mechanism

Lipid Profile Changes Associated with SGLT-2 Inhibitors and GLP-1 Agonists in Diabetes and Metabolic Syndrome

The introduction of sodium glucose transporter-2 inhibitors and glucagon-like peptide-1 receptor agonists in type 2 diabetes mellitus treatment has shown an unexpectedly significant improvement in heart disease outcome trials. Although they have very different modes of action, a portion of the salutary cardiovascular disease improvement may be related to their impact on diabetic dyslipidemia. As discussed in this focused review, the sodium glucose transporter-2 inhibitors as a class show a mild increase in low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol levels, while triglycerides (TG) decrease inconsistently. In particular, the rise in LDL appears to be related to the less atherogenic, large buoyant LDL particles. The glucagon-like peptide-1 receptor agonists show more of an impact on weight loss and improvement in the underlying low HDL and high TG dyslipidemia. The effect of sodium glucose transporter-2 inhibitors and glucagon-like peptide 1 receptor agonists when used in combination remains largely unknown. Also unexplored is difference in effect of these medications among various ethnicities and metabolic syndrome