RESUMEN
The association between malignancies and autoimmunity had been well-established. The proposed pathophysiology and causality can be bidirectional. For example, a paraneoplastic syndrome can be triggered by an underlying malignancy or vice versa, where chronic inflammation of organs affected by autoimmunity can induce malignant transformation such as the case with inflammatory bowel disease and colorectal cancer or primary sclerosing cholangitis and hepatobiliary cancer. This report presents a case of autoimmune phenomena, namely, autoimmune hemolytic anemia, pernicious anemia, and Graves disease associated with newly diagnosed breast cancer. We also highlight the postulated pathophysiologic mechanisms in an attempt to answer the question of whether the occurrence of these autoimmune phenomena in our patient is a result of the law of parsimony (Occam's razor), where clinical variables are pathogenically related, or the counterargument, where random events and diseases can take place simultaneously (Hickam's dictum).
RESUMEN
Severe hypoglycemia occurs with different types of tumors, including islet cell and non-islet cell tumors. Non-islet cell tumor hypoglycemia (NICTH) is a rare and potentially life-threatening complication of malignancy. The primary underlying mechanism of NICTH proposed in the literature includes paraneoplastic overproduction of insulin-like growth factor-2 (IGF-2), the production of autoantibodies against insulin or its receptors, or the presence of extensive metastatic burden replacing hepatic tissue or adrenal glands. In this report, we propose a potentially novel mechanism underlying NICTH involving stimulation of the insulin signaling pathway in a 58-year-old woman with a rare ovarian tumor of Müllerian origin that carries a duplication of the AKT2 gene. AKT2 is a molecular mediator of insulin signaling. To our knowledge, this is the first reported case of tumor-induced hypoglycemia associated with AKT2 gene duplication. In this report also, we discuss the currently available diagnostic modalities and highlight the therapeutic rationale in patients with NICTH, a highly vulnerable population.
RESUMEN
Unlike hyperparathyroidism, hypoparathyroidism is rarely encountered in clinical practice. Usually, it results from surgical resection, an autoimmune phenomenon, or an infiltrative process. Under certain circumstances, one may encounter a genetic etiology of hypoparathyroidism, often combined with myriad other syndromic manifestations. We report a case of a young female with congenital deafness and subacute visual loss. Hypocalcemia and primary hypoparathyroidism were subsequently discovered, and the cause of the vision loss was diagnosed as idiopathic intracranial hypertension, likely secondary to severe primary hypoparathyroidism. The patient was also found to have small bilateral kidneys, with tubular loss of magnesium and calcium, yet with a normal glomerular filtration rate. The constellation of congenital deafness, hypoparathyroidism, and renal dysfunction suggests Barakat syndrome, one of the less common causes of syndromic primary hypoparathyroidism.
RESUMEN
While the milk-alkali syndrome is traditionally viewed as the sole cause of exogenous hypercalcemia, the wide use of calcium sulfate (CS) in orthopedic procedures introduced another important item to be considered in the differential diagnosis. Calcium sulfate beads are increasingly used as void fillers and prophylactic measures to prevent postoperative hardware infections. However, hypercalcemia secondary to rapid calcium absorption from calcium sulfate beads is generally an underrecognized adverse effect and likely underreported. Furthermore, with calcium sulfate beads, hypercalcemia can dramatically present with alteration in mental status. In this report, we present a case of a 67-year-old female who underwent two orthopedic procedures, where calcium sulfate beads were used in both. The patient, on both occasions, developed significant hypercalcemia, manifested as agitation and suicidal thoughts, with each episode resolving after proper hydration and lowering of serum calcium. Also, in this report, we examined the literature and highlighted the female predominance in the reported cases, often manifesting in postoperative day (POD) 4. Given the acuity and severity of hypercalcemia, it is paramount to anticipate hypercalcemia, monitor serum calcium postoperatively to allow timely interventions, and avoid potentially serious complications.
RESUMEN
Dexmedetomidine is a preferred agent for light sedation with minimal adverse effects. We report a case of acute colonic pseudo-obstruction following dexmedetomidine use in a patient with alcohol withdrawal. He was treated with benzodiazepines first to control the withdrawal symptoms, then escalated to dexmedetomidine once delirium tremens ensued. Later on, the patient developed abdominal distension and vomiting. Imaging showed dilated bowel loops and absence of peristalsis on ultrasound. Decompression with the nasogastric (NG) tube was done, with high output from the NG tube. Dexmedetomidine infusion was used twice, and once it was stopped, the NG tube output was reduced, with the resumption of gastrointestinal motility and improvement of the abdominal distension. Recent similar reports of functional intestinal obstruction following alpha-2 (α2) agonist use necessitate further studies of intestinal motility following dexmedetomidine use and awareness of the possible side effect of dexmedetomidine on intestinal motility.
RESUMEN
Diabetes is one of the most common chronic diseases affecting over 400 million patients worldwide, many of which are affected with devastating macrovascular and microvascular complications. Diabetes affects both the peripheral and the central nervous systems. One of the unusual effects of hyperglycemia is involuntary movement, termed hyperglycemia-induced involuntary movement (HIIM). Here, we present a case of a middle-aged woman with neck dystonia as the initial manifestation of type 2 diabetes. Achieving euglycemia with insulin alone resulted in complete resolution of the neck dystonia.