Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 54-year-old white female with hypothyroidism presented with abdominal pain, nausea, vomiting, and diarrhea. She was found to have diabetic ketoacidosis (DKA) and admitted to our hospital for treatment. Laboratory workup revealed positive antiglutamic acid decarboxylase antibodies and subsequently she was diagnosed with latent onset autoimmune diabetes in adult (LADA). She was successfully treated with insulin with clinical and laboratory improvement. Diagnosis of LADA has been based on three criteria as given by The Immunology of Diabetes Society: (1) adult age of onset (>30 years of age); (2) presence of at least one circulating autoantibody (GADA/ICA/IAA/IA-2); and (3) initial insulin independence for the first six months. The importance of this case is the unlikely presentation of LADA. We believe that more research is needed to determine the exact proportion of LADA patients who first present with DKA, since similar cases have only been seen in case reports. Adult patients who are obese and have high blood sugar may deserve screening for LADA, especially in the presence of other autoimmune diseases. Those patients once diagnosed with LADA need extensive diabetic education including potentially serious events such as diabetic ketoacidosis.
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PMID:Diabetic ketoacidosis as first presentation of latent autoimmune diabetes in adult. 2583 74

Autoimmune polyglandular syndrome type 2 (APS 2) is defined by the presence of Addison's disease (AD) associated with autoimmune thyroid disease and/or Type 1 diabetes mellitus (T1DM). It is a rare disease, affecting about 1.4-2 cases/100,000 inhabitants. Its less frequent clinical presentation is the combination of AD, Graves' disease, and T1DM. We present the case of a 42-year-old woman with a history of total thyroidectomy due to Graves' disease, type 2 diabetes mellitus, and hypertension, who sought the ED due to asthenia, dizziness, nausea, and vomiting. She reported having stopped antihypertensive therapy due to hypotension and presented a glycemic record with frequent hypoglycemia. On physical examination, she had cutaneous hyperpigmentation. She had no leukocytosis, anemia, hypoglycemia, hyponatremia or hyperkalemia, and a negative PCR. Serum cortisol <0.5 ug/dl (4,3-22,4), urine free cortisol 9 ug/24h (28-214), ACTH 1384 pg/mL (4,7-48,8), aldosterone and renin in erect position of 0 pg/ml (41-323) and 430.7 uUI/ml (4.4-46.1) respectively. Quantiferon TB was negative; computerized axial tomography of the adrenals showed no infiltrations, hemorrhage, or masses. The 21-hydroxylase antibody assay was positive. B12 vitamin was normal, anti-GAD antibodies were positive, anti-insulin, anti-IA2, and anti-transglutaminase antibodies were all negative. The patient started insulin therapy and treatment for AD with prednisolone and fludrocortisone with good clinical response. This case aims to alert to the need for high clinical suspicion in the diagnosis of AD. Since this is a rare autoimmune disease, it is important to screen for other autoimmune diseases in order to exclude APS.
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PMID:Autoimmune Polyglandular Syndrome type 2. 3199 21