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)

During treatment of four type-1 diabetics (aged 20-46 years) by continuous subcutaneous insulin infusion (CSII) a leak developed in the system which caused severe ketoacidosis. The gastrointestinal symptoms (nausea, vomiting and abdominal pain) were misdiagnosed by both the patients and their doctors because there was only mild hyperglycaemia. These observations highlight the importance of carefully instructing and supervising patients at the beginning of CSII and point to the need of frequent urine testing by the patients, also for urinary keto bodies.
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PMID:[Diabetic ketoacidosis during insulin pump therapy]. 249 65

The metabolic effects of the anti-fungal drug fluconazole were investigated in 18 women, 10 of whom were taking oral contraceptives, to examine whether this steroid antagonist has any effects primarily on hormone systems. The women, aged 29-40, took 50 mg fluconazole orally from Day 1 of their menstrual cycle for 21-28 days. Subjects kept a symptom diary, were tested weekly for hematological and liver function, and were checked for compliance by analyzing blood for drug by GLC. 5 women reported side effects: somnolence, dizziness, fatigue, increased appetite, headache (1) and nausea (1). No effects on liver function or menses were noted. The only significant findings were increases in serum thyroxine and testosterone in fluconazole-only subjects, and increases in insulin and apo-lipoprotein B in fluconazole-oral contraceptive subjects. Pills containing levonorgestrel were used by 9 women, desogestrel by 1. No significant differences were seen in estradiol, progesterone, sex-hormone-binding globulin, thyroid function, cortisol, glucose, C-peptide, cholesterol, triglycerides, lipoproteins. Thus it is unlikely that the short-term use of fluconazole for treatment of superficial mycoses, such as vulvovaginal candidiasis, will adversely affect steroid metabolism in women.
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PMID:Metabolic effects of low-dose fluconazole in healthy female users and non-users of oral contraceptives. 254 10

In this pilot clinical trial conducted in 10 postmenopausal women with advanced breast cancer, we evaluated the endocrine effects and toxicity of combined somatostatin analog and dopaminergic therapy in the attempt to suppress both growth hormone (GH) and prolactin (PRL) secretion. The patients' mean age was 63 years (range: 54-77) and the average number of previous treatments was 4.8 +/- 2 (SD). All patients were treated with the somatostatin analog SMS 201-995 (100-200 micrograms s.c. in a.m. and h.s.) and bromocriptine (2.5 mg orally twice a day). During treatment, GH levels following provocative testing (either L-DOPA or insulin-induced hypoglycemia) were suppressed in 7/9 patients. Basal somatomedin-S (Sm-C) levels declined in 6/9 women. Both GH and Sm-C levels decreased in 4 patients, while in the remaining 5 only one of the two parameters was lowered on treatment. PRL secretion (during provocative TRH testing) was almost totally abolished in 8/9 patients. The treatment did not affect circulating levels of FSH, LH, E1, E2, E1-S, T4, T3RU, or cortisol. Seven patients experienced no side effects. Nausea occurred in 3, but was severe enough in only one to require discontinuation of therapy. One patient experienced disease stabilization consisting of less than 50% regression of skin nodules and pleural effusion, a decline in CEA titer, and an improved performance status lasting 7 months. We conclude that combined SMS 201-995 and bromocriptine therapy is safe and frequently suppresses GH and PRL secretion. Its role in the treatment of metastatic breast cancer should be tested in patients with less advanced disease.
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PMID:Endocrine effects of combined somatostatin analog and bromocriptine therapy in women with advanced breast cancer. 257 6

Headaches affecting 117 insulin-dependent diabetic patients were studied. 50 developed 3 varieties of headaches associated with clinical hypoglycaemic episodes: (1) Brief headaches, contemporaneous with cerebral and autonomic symptoms, were relieved within minutes of ingesting carbohydrates (8 patients). (2) Prolonged headaches outlasting hypoglycaemic symptoms by 1-48 (average 4.3) hours, not relieved by food, occurred in 36 patients; 12 of these also had nausea, vomiting or photophobia. (3) Migraine headache. 11 of the 117 patients were migraineurs: in 6 of the 11 their typical migraines (2 classical and 4 common) were induced by hypoglycaemic episodes. 9 of the 50 had 2 types of headaches, easily distinguished by each subject. In the whole series of 117 patients, 9 had never had a headache in their life. The remainder had headaches associated with premenstrual tension, anxiety, alcohol or other causes.
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PMID:Headaches in insulin-dependent diabetic patients. 261 15

Pancreatic beta cell function was measured in 15 nondiabetic controls, 10 insulin-dependent diabetics (IDD) and 19 non-insulin-dependent diabetics (NIDD), aged 18 to 45 years, by means of the peripheral serum C-peptide response to 1 mg of glucagon. The fasting serum C-peptide (FCP) in IDD was lower than in the controls and NIDD (p less than 0.01), but there was no significant difference between the controls and NIDD (p greater than 0.05). The maximal in crement of serum C-peptide (delta CP) after glucagon stimulation in the controls was higher than in IDD and NIDD (p less than 0.01), and there was a gap between IDD (less than or equal to 0.69 ng/ml) and NIDD (1.20 ng/ml). During the glucagon test, serum C-peptide concentrations were highest in the first 15 minutes unlike plasma glucose which reached its highest value between 20 and 40 minutes. NIDD, either obese or nonobese, had a lower mean delta CP value than did controls. In the controls, IDD and NIDD, the FCP was correlated well with delta CP (r = 0.61, 0.93 and 0.59) but not with fasting plasma glucose (r = 0.19, -0.08 and 0.23). During the glucagon test, the mean maximal increments of plasma glucose were between 52.5 and 62.5 mg/dl. Nausea was the main complaint in 19 (43%) of the subjects but it was mild and transient. In conclusion, measuring serum C-peptide response after glucagon stimulation is a simple and safe test which may be a discriminative method to establish insulin dependency in young diabetic patients.
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PMID:C-peptide response to glucagon in young diabetics. 267 32

Octreotide is an analogue of somatostatin. Like endogenous somatostatin, it exerts a potent inhibitory effect on the release of anterior pituitary growth hormone and thyroid-stimulating hormone, and peptides of the gastroenteropancreatic endocrine system, while overcoming some of the shortcomings of exogenously administered somatostatin, namely a short duration of action, a need for intravenous administration and postinfusion rebound hypersecretion of hormone. Clinical studies have shown that octreotide is effective in the treatment of acromegaly and thyrotrophinomas. In comparative trials octreotide was significantly superior to bromocriptine in patients with acromegaly. Octreotide also appears to provide a significant advantage over existing therapies in the management of the carcinoid syndrome and offers considerable therapeutic potential in reversing carcinoid crises which may be life-threatening. Trials in patients with tumours producing vasoactive intestinal peptide demonstrated that octreotide may be an effective first-line choice for this condition, which has usually metastasised and become refractory to traditional symptomatic therapy. In limited studies in patients with high-output secretory diarrhoea, including cryptosporidium-related diarrhoea associated with AIDS and in patients with small bowel fistulas, octreotide has been shown to be effective in reducing stool/fistula output. However, well-designed clinical trials are still required to confirm its long term usefulness in these disorders. Similarly, although the use of octreotide in other conditions such as neonatal hypoglycaemia caused by nesidioblastosis, reactive pancreatitis, insulin-dependent diabetes mellitus, postprandial hypotension and the dumping syndrome has provided encouraging preliminary results, more studies are needed to clarify the place of octreotide in their treatment. Overall, octreotide appears to be well tolerated with the most frequently reported reactions being pain at the site of injection and gastrointestinal symptoms such as abdominal cramps, nausea, bloating, flatulence, diarrhoea and steatorrhoea. These adverse effects usually abate with time. Additionally, octreotide, like endogenous somatostatin, may also result in cholelithiasis, presumably by altering fat absorption and possibly by decreasing motility of the gallbladder. Thus, octreotide represents a new departure from traditional therapies in the treatment of various pathophysiological states associated with excessive peptide production and secretion. It offers a significant advantage over existing therapies in the medical management of patients with acromegaly, thyrotrophinomas, the carcinoid syndrome, tumours producing vasoactive intestinal peptide and severe secretory diarrhoea in whom conventional management options have either become exhausted or have provided suboptimal symptomatic relief.
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PMID:Octreotide. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in conditions associated with excessive peptide secretion. 268 36

Potassium is one of the most abundant ions in the human body and yet it is difficult to assess potassium balance. Potassium chloride is extensively used as a potassium supplement, both by physicians as a therapeutic modality and by the general public, mostly in the form of salt substitute. Therapeutically, both the oral and intravenous forms of potassium are utilised. Overdose of potassium is not as frequently encountered in clinical practice as hyperkalaemia (excess potassium in the body) due to acute or chronic renal disease. Potassium homeostasis is maintained very delicately and is governed by the daily consumption of potassium and the renal excretion mechanisms. Any change in these or related factors can present as hyperkalaemia. However, potassium overdoses leading to serious consequences do occur. Orally, the dose of potassium has to be large enough so that the normal excretory mechanisms for potassium are overcome and clinical toxicity occurs. It takes a much bigger dose of ingested potassium to produce toxicity in a person with normal renal function than in patients with compromised renal function. Potassium toxicity manifests in significant, characteristic, acute cardiovascular changes with ECG abnormalities. Besides cardiovascular effects, neuromuscular manifestations in the form of general muscular weakness and ascending paralysis occur. Gastrointestinal symptoms manifest as nausea, vomiting, paralytic ileus, and local mucosal necrosis which may lead to perforation. It is imperative when treating hyperkalaemia that the whole clinical picture is taken into account rather than the numerical potassium values. Only the extracellular potassium can be measured in the laboratory, yet 98% of the body potassium is intracellular and cannot be measured. In acute overdose situations due to ingestion of potassium salt, the general principles of treatment for overdoses should be followed. Calcium chloride infusion, dextrose and insulin in water, and correction of acidosis with sodium bicarbonate are helpful in controlling the acute, life-threatening cardiac arrhythmias. These modalities do not remove the excess potassium from the body. That is achieved either by utilising ion-exchange resins or by mechanically removing potassium via haemodialysis. To curtail inadvertent or accidental potassium overdoses, physicians should prescribe any potassium supplements very carefully to their patients and monitor the plasma potassium periodically.
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PMID:Clinical features and management of poisoning due to potassium chloride. 268 36

We reported the clinical results in 13 cases of hypercortisolism treated with amino-glutethimide (AG), which was developed by Tiantsin Research Institute of Medical Industry. Of the thirteen cases nine were confirmed by surgery and histology, and the others were diagnosed clinically. Clinical improvements have been achieved in ten of the thirteen cases over a therapeutic course of 8 to 12 wk with a daily dosage of 1.0 to 2.0 g of AG. Plasma and urinary corticosteroids, as well as plasma testosterone levels were significantly decreased after one-month treatment followed, however, by somewhat return and fluctuation. The high levels of blood glucose and serum insulin were declined after therapy consistent with the decrement of corticoids. Serum potassium levels in hypokalemic patients returned to normal after one month of therapy. Radial bone mineral contents in patients with low bone density returned or closed to normal after three-month treatment. The main side effects of AG are anorexia, nausea, drowsy, tierdness, skin rashes, etc, which are mild and transient. Adrenal hypofunction was seen in one case after treatment.
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PMID:[Clinical observation on hypercortisolism treated with amino-glutethimide]. 279 46

A case of benign intracranial hypertension associated with generalized oedema is reported in a normotensive pregnant patient with long-standing insulin-treated diabetes mellitus. Following treatment with bed rest, chlorthalidone and dexamethasone the condition resolved and a healthy infant was delivered. This condition, not previously reported in a diabetic pregnancy, must be differentiated from other causes of bilateral optic nerve abnormalities associated with retinal haemorrhages and oedema, including diabetic retinopathy, diabetic optic neuropathy, accelerated hypertension and cerebral mass lesions. Treatment is required to prevent permanent visual impairment due to pressure on the susceptible optic nerve of the diabetic patient and to avoid the metabolic consequences to both mother and fetus of poor nutritional intake due to nausea.
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PMID:Retinal haemorrhages and papilloedema due to benign intracranial hypertension in a pregnant diabetic. 295 Dec 4

In 10 healthy men, we have compared the respective effects of an intravenous injection of glucagon (1 mg) and an oral glucose load (75 G) in eliciting the release of C-peptide and insulin from the pancreas. Serum C-peptide and insulin concentrations increased respectively to median values of 190% and 500% at 6 minutes after glucagon injection, and 344% and 794% at 30 minutes and 268% and 278% at 60 minutes following glucose ingestion. The oral glucose load was as effective as glucagon injection in testing beta cell function and was free from the unpleasant side effects (nausea, vomiting, syncope) commonly associated with glucagon. We conclude that oral glucose loading is probably the test of choice to elicit C-peptide release when screening populations of normal subjects for adequacy of beta cell function.
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PMID:Comparison of oral glucose loading and intravenous glucagon injection as stimuli to C-peptide secretion in normal men. 295 15


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