Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical and laboratory features and risk factors for diabetic gastroparesis (DGP) were investigated in 226 diabetics on chronic dialysis; 106 subjects (43%) had DGP diagnosed by persistent vomiting improved with the use of prokinetic agents and 120 (control group) had no clinical DGP. Type 1 diabetics had DGP more frequently than type 2 diabetics (70 vs. 37%). The DGP group had longer duration of diabetes (21 +/- 8 vs. 13 +/- 6 years), higher frequency of diabetic orthostatic hypotension (95 vs. 33%), enteropathy (49 vs. 5%), blindness (52 vs. 23%), myocardial infarction (86 vs. 42%), extremity gangrene (54 vs. 27%) and cerebrovascular accidents (43 vs. 25%), lower serum albumin 32.3 +/- 3.9 vs. 35.4 +/- 3.8 g/l), urea (24.0 +/- 5.5 vs. 25.5 +/- 5.5 mmol/l) and creatinine (710 +/- 210 vs. 820 +/- 220 mumol/l), and higher serum TCO2 (20.9 +/- 3.1 vs. 19.8 +/- 2.7 mmol/l) than the control group (all differences significant at p +/- 0.004). Glycemic control was adequate in 24% of the DGP group subjects and 83% of the control subjects (p < 0.001). Annual hospitalization rate was 49 +/- 48 days/patient in the DGP group and 16 +/- 27 days/patient in the control group (p < 0.001). Median patient survival was 24 +/- 2 months in the DGP group and 61 +/- 9 months in the control group (p < 0.0001). Logistic regression identified long duration of diabetes and poor glycemic control as risk factors for DGP. In diabetics on dialysis, DGP is associated with high frequency of other diabetic complications, low serum albumin and creatinine, and high morbidity and mortality.(ABSTRACT TRUNCATED AT 250 WORDS)
Nephron 1995
PMID:Gastroparesis in diabetics on chronic dialysis: clinical and laboratory associations and predictive features. 747 16

Although serologic studies have identified hantaviral infection in the United States, acute disease has not been recognized. This study describes 3 cases of domestically acquired hemorrhagic fever with renal syndrome (HFRS) in the United States. Infection was due to a local strain of Seoul virus (Baltimore rat virus). A review of the clinical features indicated a mild illness characterized by nausea, vomiting, renal and liver failure similar to HFRS described elsewhere for rat-borne viruses. Follow-up of 2 patients identified persistent hypertension and renal disease providing further evidence of an association between past hantaviral infection and hypertensive renal disease.
Nephron 1994
PMID:Domestic cases of hemorrhagic fever with renal syndrome in the United States. 799 Oct 40

Ten cases of acute renal failure (ARF) were seen in the period from July 1990 to August 1991 in the Nephrology Department of the SIMS Hospital, Srinagar. All were males in the age group of 18-28 years and in apparent good health when apprehended by the police. There was alleged history of physical torture of different types. All had been beaten on the buttocks, back and limbs; in addition, 2 cases had been given repeated electric shocks and 1 case put to 'sit-and-stand' exercise for about 3 h. The interval between the first day of torture till they came to our observation varied from 4 to 11 days. The main clinical features at the time of presentation were generalized aches and weakness (10), oligoanuria (9), vomiting (8), hypertension (6), acidosis (10), facial puffiness and pedal edema (6), fever and shivering (3), pulmonary edema (2), stupor (4), and hyperkalemia (5). All the cases had an established ARF (serum creatinine 668-1,997 mumol/l and serum urea 21.8-71.8 mmol/l) when first seen. Muscle enzymes, creatine phosphokinase, lactic dehydrogenase and serum glutamic oxaloacetic transaminase were all significantly raised indicating rhabdomyolysis. All showed evidence of myoglobin casts in urine. Nine had oliguric and 1 had nonoliguric ARF. All except the 1 case with nonoliguric ARF were managed with peritoneal dialysis and/or hemodialysis. All recovered. Early recognition of ARF is important since the main attention in such cases is directed towards the surgical aspect.
Nephron 1993
PMID:Acute renal failure following physical torture. 845 79

A case of isolated ACTH deficiency with hyporeninemic hypoaldosteronism, presenting severe hyponatremia, is described. A 57-year-old man complaining of nausea, vomiting and fatigability was admitted to our hospital because of hyponatremia (114 mEq/I). The low levels of serum cortisol and urinary 17-OHCS suggested glucocorticoid deficiency, and that the glucocorticoid deficiency was due to isolated ACTH deficiency was confirmed by a continuous ACTH loading test and pituitary gland stimulation tests. Although the low level of serum sodium was normalized after the administration of cortisone acetate (50 mg/day) combined with an increase in oral salt intake, urinary sodium loss persisted by the results of hypertonic saline infusion test. Treatment led to improvement of impairment of water diuresis due to hypersecretion of ADH. Hyporeninemic hypoaldosteronism persisted after treatment. We have shown that severe hyponatremia that occurs with combined deficiency of glucocorticoids and mineralocorticoids can be corrected with high salt intake and glucocorticoid replacement without correcting mineralocorticoid deficiency.
Nephron 1996
PMID:A case of isolated ACTH deficiency with hyporeninemic hypoaldosteronism. 877 60

Acute interstitial nephritis with severe acute renal failure is reported following tetracycline treatment in a 22-year-old male medical student. Acute renal failure developed within 48 h of a single repeated tetracycline dose and presented 2 days after taking the drug when there was oliguria, nausea, vomiting and bilateral loin pain without rash and fever. The serum creatinine concentration was 8.6 mg/dl and blood urea nitrogen 84 mg/dl. Examination of the urinary sediment revealed 15-20 RBCs per high-power field, and occasional granular and hyaline casts. Percutaneous renal biopsy performed immediately after admission revealed acute interstitial nephritis with immune complexes along the tubular basement membrane and intact glomeruli and was consistent with type 2 interstitial nephritis. Within 4 days of commencement of steroid treatment and hemodialysis, the urine output started to increase with improvement in serum creatinine and BUN levels and after 2 weeks of therapy hemodialysis was discontinued. He remains well 1 year following his illness with complete normalization of his renal function. Although a number of renal side effects of tetracycline antibiotics have been reported, acute interstitial nephritis is rarely caused by tetracycline treatment having been reported just twice following systemic use of minocycline.
Nephron 1999 Jan
PMID:Tetracycline-induced acute interstitial nephritis as a cause of acute renal failure. 988 23

To clarify the role of autonomic nervous function in motion sickness, the effect of agents that act on the autonomic nervous system on the motion stimuli-induced emesis was studied in two strains of Suncus murinus (Jic:SUN-Her and Jic:SUN-Ler) with congenitally different sensitivity to veratrine sulfate. We demonstrated significant differences between the two strains in sensitivity to motion stimuli. Isoproterenol (2.5 mg kg(-1), s.c.) significantly prolonged the latency to the first emetic episode induced by motion stimuli and significantly decreased the number of emetic episodes in Jic:SUN-Her suncus. Hexamethoium (2.0 mg kg(-1), s.c.) tended to shorten the latency in Jic:SUN-Ler. Acetylcholine (1.2 mg kg(-1), s.c.) enhanced the emetic response in Jic:SUN-Ler, but atropine (4.0 mg kg(-1), s.c.) suppressed motion stimuli-induced emetic response in Jic:SUN-Her. These results suggest that the predominance of parasympathetic nervous activity is relevant to the enhancement of motion stimuli-induced emetic response, whereas the predominance of sympathetic nervous activity suppresses motion stimuli-induced emetic response. Norepinephrine (0.8 mg kg(-1), s.c.) enhanced motion stimuli-induced emesis contrary to isoproterenol in Jic:SUN-Ler although both drugs are adrenergic agents. However, atropine pretreatment (4.0 mg kg(-1), s.c.) inhibits norepinephrine-induced emetic response. It was considered that norepinephrine-induced emetic response might be dependent on a secondary increase of parasympathetic nervous activity due to bororeflex. Moreover, the different emetic response in Jic:SUN-Her and Jic:SUN-Ler suncus to motion stimuli and drug administration mentioned above indicated that different participation of autonomic nervous activity and/or afferent information from the baroreceptor in the emetic response may exist between these animal groups.
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PMID:Role of autonomic nervous system for development and suppression of motion sickness in Suncus murinus. 1177 7

Bismuth subcitrate is a known nephrotoxic agent that may lead to acute oliguric renal failure when ingested in toxic doses. We report a 17-year-old girl who was admitted to the emergency room with complaints of nausea, vomiting, and anuria. She had taken 25 tablets containing 300 mg bismuth subcitrate (total 7.5 g). The patient was managed with hemodialysis started a week after ingestion. Bismuth subcitrate nephrotoxicity should be considered in the differential diagnosis of acute renal failure.
Nephron 2002 Apr
PMID:Bismuth subcitrate nephrotoxicity. A reversible cause of acute oliguric renal failure. 1196 12

The antiemetic and emetic actions of the anticancer drug cyclophosphamide injected intracerebroventricularly (i.c.v.) and intravenously (i.v.) through chronically implanted cannulae were investigated in unanaesthetized cats. Cyclophosphamide in single doses was injected into the cerebral ventricles and intravenously for 5 consecutive days. The antiemetic effect was regularly obtained, whereas the emetic effect was unpredictable and of low incidence. The antiemetic effect of i.c.v. and i.v. cyclophosphamide was assessed, when the neurotoxic (mydriasis, restlessness, emesis, ataxia, muscular weakness) signs subsided, against i.c.v. noradrenaline- and clonidine-induced emesis. Noradrenaline-induced emesis was dose-dependently and dose-independently inhibited with i.c.v. and i.v. cyclophosphamide. On the other hand, i.c.v. cyclophosphamide inhibited the clonidine-induced emesis in dose-independent manner, while i.v. injection of the anticancer drug had no significant effect on the emesis. The inhibition of emesis was consistently obtained and no significant differences in the antiemetic potency were found between 1 and 5 consecutive days of treatment with cyclophosphamide. However, the inhibition of noradrenaline-induced emesis was dose-dependent only after first administration of i.c.v. cyclophosphamide. It is assumed that noradrenaline acts at alpha-adrenoceptors within the area postrema and clonidine at alpha-adrenoceptors within and outside the area postrema as well as at muscarinic cholinoceptors, 5-hydroxytryptamine, dopamine and histamine H1 and H2 receptors, outside the area postrema, of multitransmitter system subserving the central regulation of emesis. It is suggested, therefore, that the antiemetic effect of cyclophosphamide at the receptors of the multitransmitter central emetic system is non-specific. In general, the antiemetic effect, even non-specific, of an anticancer drug could have practical implication. Namely, when a combination of two or more anticancer drugs are used for chemotherapy, the emesis could not occur if one of them could antagonize the emesis induced by other anticancer drug/s. Finally, cyclophosphamide injected i.c.v., but not i.v., evoked shortlasting emesis in about 20% of cats. Since the emesis was unpredictable and of low incidence it was not possible to study the mechanism/s and site/s of action of the anticancer drug.
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PMID:Emesis: antiemetic effect of cyclophosphamide at central receptors of multitransmitter system in the cat. 1241 47

Postoperative pain after laparoscopic cholecystectomy is an ongoing problem. To relieve this pain, practitioners have used many anesthetic and analgesic drugs. This study was undertaken to assess the effects of incisional and intraperitoneal administration of ropivacaine on postoperative pain and stress response in patients undergoing laparoscopic cholecystectomy. In this prospective, single-blinded, randomized study, 45 patients with ASA (American Society of Anesthesiologists) scores I and II who were about to undergo laparoscopic cholecystectomy were divided into 3 groups. After cholecystectomy, a total of 40 mL of 3.75% ropivacaine was administered pre-incisionally and intraperitoneally to patients in group 1 (n=14); pre-incisionally and intraperitoneally to patients in group 2 (n=17); and intraperitoneally and locally at incision sites to patients in group 3 (n=14). Blood levels of epinephrine and norepinephrine were examined preoperatively, 15 min after insufflation, and at the end of the operation. Visual analog pain scale scores and analgesic requirements were used for 24-h postoperative follow-up of pain levels reported by patients. No statistically significant difference was found among the 3 groups with respect to visual analog pain scale scores, total analgesic requirements, and accompanying pain, nausea, and vomiting. The earliest analgesic requirements were seen in group 2 (P<.005), and less shoulder pain was noted in group 3 (P<.005). Norepinephrine and epinephrine levels showed no statistically significant differences between the 3 groups. Administration of ropivacaine preoperatively and postoperatively for laparoscopic cholecystectomy has similar effects on postoperative pain and the stress response of patients.
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PMID:Effects of ropivacaine on pain after laparoscopic cholecystectomy: a prospective, randomized study. 1756 14

Opioids are effective analgesics used clinically for both acute and chronic pain management. However, repeated opioid treatment can induce serious side effects such as nausea, vomiting, drowsiness, respiratory depression, euphoria, dependence, hyperalgesia, and tolerance. The mechanism of noxious information transmission in the central nervous system following dependence is still not clear. Norepinephrine (NE), an important neurotransmitter, participates both in the process of opioid dependence and also pain modulation in the central nervous system. In this study, we examined the role of NE on the evoked discharges of pain-excitation neurons (PENs) and pain-inhibition neurons (PINs) in the nucleus accumbens (NAc) of rats, following the development of morphine dependence. Our results revealed that NE inhibited the evoked discharges of PENs and attenuated the inhibition of PINs, while phentolamine enhanced the evoked discharges of PENs and facilitated the inhibition of PINs. These results indicate that the inhibitory action of NE on pain modulation acts via alpha adrenoceptors in the NAc of morphine-dependent rats.
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PMID:The involvement of norepinephrine in pain modulation in the nucleus accumbens of morphine-dependent rats. 2544 69


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