Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0027497 (
nausea
)
23,468
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Gastrointestinal complications of diabetes include gastroparesis, intestinal enteropathy (which can cause diarrhea, constipation, and fecal incontinence), and nonalcoholic fatty liver disease. Patients with gastroparesis may present with early satiety,
nausea
, vomiting, bloating, postprandial fullness, or upper abdominal pain. The diagnosis of diabetic gastroparesis is made when other causes are excluded and postprandial gastric stasis is confirmed by gastric emptying scintigraphy. Whenever possible, patients should discontinue medications that exacerbate gastric dysmotility; control blood glucose levels; increase the liquid content of their diet; eat smaller meals more often; discontinue the use of tobacco products; and reduce the intake of insoluble dietary fiber, foods high in fat, and alcohol. Prokinetic agents (e.g., metoclopramide, erythromycin) may be helpful in controlling symptoms of gastroparesis. Treatment of diabetes-related constipation and diarrhea is aimed at supportive measures and symptom control. Nonalcoholic fatty liver disease is common in persons who are obese and who have diabetes. In persons with diabetes who have elevated hepatic transaminase levels, it is important to search for other causes of liver disease, including hepatitis and
hemochromatosis
. Gradual weight loss, control of blood glucose levels, and use of medications (e.g., pioglitazone, metformin) may normalize hepatic transaminase levels, but the clinical benefit of aggressively treating nonalcoholic fatty liver disease is unknown. Controlling blood glucose levels is important for managing most gastrointestinal complications.
...
PMID:Gastrointestinal complications of diabetes. 1861 80
A 58-year-old female patient was transferred by her general practitioner with fatigue,
nausea
and icterus which had begun 2 weeks prior to admission. Laboratory results revealed acute hepatitis (ALAT [alanine aminotransferase] 3,871 U/l, ASAT [aspartate aminotransferase] 2,004 U/l, bilirubin 6.7 mg/dl, gamma-GT [gamma-glutamyl transferase] 503 U/l). The patient's medical history included genetic
hemochromatosis
(without cirrhosis). Hepatitis A to C, infection with herpesviruses or Leptospira interrogans were excluded by serologic and molecular biological tests. There was no diagnostic evidence for underlying autoimmune or additional metabolic liver disease. Due to a trip to Africa 5 months earlier, the patient was tested for hepatitis E, leading to positive anti-hepatitis E-IgM and negative anti-hepatitis E-IgG. PCR (polymerase chain reaction) detection of hepatitis E virus (HEV) was positive as well. In conclusion, acute HEV infection was diagnosed. After close reconsideration, the nonfitting incubation period precluded a travel-associated infection. Additionally, there was no evidence for current HEV infections within the patient's social environment, so that a zoonotic origin has to be discussed.
...
PMID:[Rare acute hepatitis in a female patient with hemochromatosis: a zoonosis?]. 2045 55
Ferroportin disease is a rare type of autosomal dominantly inherited
hemochromatosis
caused with mutations in the ferroportin gene (SLC40A1). The patients characteristically have hyperferritinemia but normal transferin saturations. Herein, we present a 15-year-old female whose chief complaint was persistent
nausea
for the last one year. Extensive work-up including brain imaging revealed nothing to explain the etiology of
nausea
. The serum ferritin level of 1474ng/mL was suggestive for
hemochromatosis
syndromes and the molecular testing revealed de-novo c.485_487delTTG (P.Val162del) ferroportin gene mutation. Mild hepatic iron loading, in addition to the cumbersome
nausea
were accepted as indications for chelation treatment in this particular patient and deferasirox was initiated (10mg/kg/day) since family did not consent for phlebotomy. Deferasirox was stopped by the 9th month of initiation, since
nausea
subsided and hepatic iron content was normalized, in order to prevent over chelation. There are no well-established guidelines for the chelation of patients with hereditary hemochromatosis syndromes. However, lifelong monitorization for iron loading and re-initiation of chelation when necessary was planned in our patient.
...
PMID:Iron chelation with deferasirox in a patient with de-novo ferroportin mutation. 2574 2