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)

The acute hepatic porphyrias include four disorders: acute intermittent porphyria [AIP], hereditary coproporphyria [HCP], variegate porphyria [VP], and the rare porphyria due to severe deficiency of ALA dehydratase [ADP]. In the USA, AIP is the most severe and most often symptomatic. AIP, HCP, and VP are due to autosomal dominant genetic abnormalities, in which missense, nonsense, or other mutations of genes of normal hepatic heme biosynthesis, in concert with other environmental, nutritional, hormonal and genetic factors, may lead to a critical deficiency of heme, the end-product of the pathway, in a small but critical 'regulatory pool' within hepatocytes. This deficiency leads to de-repression of the first and normally rate-controlling enzyme of the heme synthetic pathway, delta- or 5-aminolevulinic acid [ALA] synthase-1, and thus to marked up-regulation of this key enzyme and to marked hepatic overproduction of ALA. In addition, except for ADP, there is marked overproduction as well of porphobilinogen [PBG], the intermediate immediately downstream of ALA in the synthetic chain, and, especially in HCP and VP, also porphyrinogens and porphyrins farther down the pathway. The major clinical features of the acute porphyrias are attacks of severe neuropathic-type pain. Pain is felt first and foremost in the abdomen but may also occur in the back, chest, and extremities. Attacks are more common in women than in men [ratio of about 4:1], often accompanied by nausea, vomiting, constipation, tachycardia, and arterial hypertension. Hyponatremia may also occur. Some patients also describe chronic symptoms of pain, anxiety, insomnia, and others.
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PMID:Pathogenesis and clinical features of the acute hepatic porphyrias (AHPs). 3098 16

Poly-ADP ribose polymerase inhibitors (PARPi) are a promising new treatment option for patients with ovarian cancer and are moderately emetogenic. Tolerance of therapy is paramount, and uncontrolled nausea and vomiting may limit use. Although most patients will experience improvement in nausea and vomiting after one to two months, approximately one in twenty patients will discontinue therapy due to unrelieved symptom burden. Three cases of olaparib-related nausea and vomiting mitigated by primary pyridoxine use are reported. Case 1 demonstrates successful use of pyridoxine in breakthrough nausea. Case 2 details the use of pyridoxine following refractory nausea and vomiting requiring hospitalization. Case 3 describes a prophylactic approach for a patient with significant anticipatory nausea. All three patients tolerated olaparib after starting and continuing pyridoxine. Vitamin B6, or pyridoxine, was successful as both a therapeutic and prophylactic option for significant treatment-related nausea and vomiting with PARPi use.
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PMID:Pyridoxine for prevention and treatment of PARP inhibitor induced nausea and vomiting. 3151 11


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