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

Twenty-eight patients with histologically proven metastatic or invasive, unresectable pheochromocytomas, which were shown to concentrate and retain tracer doses of [131I]metaiodobenzylguanidine (131I-MIBG), were treated with therapeutic quantities of this radiopharmaceutical. Between one and six doses ranging from 97 to 301 mCi (cumulative dose 111-916 mCi) were administered. Partial response in tumor size was achieved in 8/28 patients and partial biochemical responses in 12/28 patients. No pharmacological toxicity was observed. Mild radiation sickness (nausea, vomiting, anorexia) occurred in 21/28. Minor degrees of leukopenia and thrombocytopenia were observed in 3/28. There were three cases of hypothyroidism but no significant hepatic, renal, adrenocortical or autonomic nervous dysfunction. We conclude that therapeutic 131I-MIBG can achieve significant therapeutic responses in some cases of malignant pheochromocytoma without pharmacological toxicity and only mild radiotoxicity.
 ...
PMID:Radiopharmaceutical therapy of malignant pheochromocytoma with [131I]metaiodobenzylguanidine: results from ten years of experience. 182 34

A multicentre study of IL2 and IFN alpha has been performed in 58 patients with metastatic melanoma. The scheme consisted of IL2 3.0 BRMP MU/m2/d as a continuous infusion for 4 d combined with subcutaneous administration of IFN alpha 6 MU/m2/d, day 1 + 4. The cycle was repeated every 2 weeks for a maximum duration of 26 weeks. 54 patients were evaluable for response. One (2%) achieved a complete and 10 (19%) a partial response. 19 (35%) patients were stable and 24 (44%) showed progressive disease. Common side-effects included fever, chills, fatigue, skin rash, anorexia, nausea and diarrhoea. Hypothyroidism was noted in 10% of the patients. These results show that this regimen of IL2 and IFN alpha is active but, in contrast to what could be expected, not superior to IL2 alone possibly due to suboptimal dosing. In an ongoing study in Rotterdam and Nijmegen, a more intense schedule was chosen, consisting of three daily i.v. doses of IL2 4.5 BRMP MU/m2 and IFN alpha 3.0 MU/m2 for 5 d. This regimen is repeated at intervals of 3 weeks for a total of three cycles. Presently, nine patients have been entered. One patient achieved a complete response, four a partial response (overall 56%), three had stable disease and one progressed. Toxicity was severe and treatment was prematurely stopped in five patients: myocardial infarction (one patient), atrial fibrillation (one patient), negative T waves and myocardial hypokinesia (one patient) and psychosis (two patients). This regimen can only be justified if the therapeutic results are superb, which has yet to be awaited.
 ...
PMID:Clinical experience with the combined use of recombinant interleukin-2 (IL2) and interferon alfa-2a (IFN alpha) in metastatic melanoma. 193 17

Primary hypothyroidism may be associated with enlargement of the sella turcica, due to thyrotroph hyperplasia, in its turn due to the lack of feedback control by thyroid hormones. It may develop independently of the severity or of the duration of thyroid failure. A 42-year-old woman was referred to us. She presented us with a CT scan compatible with a pituitary microadenoma, in the left part of the sella. The patient showed obvious signs of myxedema, due to subtotal thyroidectomy which had been performed 14 months before, because of the presence of multinodular goiter. After operation, the patient has been discontinuously and inappropriately treated with desiccated thyroid. She complained of headache, nausea, galactorrhea without amenorrhea. Serum T4 (0.8 micrograms/dl), serum T3 (47 ng/dl) and TSH (174.5 +/- 60.1 mU/l: M +/- SD of 4 assays) were compatible with primary hypothyroidism as confirmed by TSH hyper-response to i.v. TRH (200 micrograms) and i.v. domperidone (10 mg), and by the normal TSH decrease after orally administered 2.5 mg bromocriptine or 90 min continuously infused 800 micrograms GHIRH. Moreover, an abnormal GH response to TRH was observed, whereas basal and appropriately stimulated PRL levels were normal. Serum alpha-subunit was marginally high (5.92 ng/ml), but alpha-subunit/TSH molar ratio fell within the normal range (0.1 molar ratio). Complete suppression of basal and TRH stimulated TSH values was achieved after a 14-day L-T3 (120 micrograms per day) and 4-month L-T4 (200 micrograms per day) administration. L-T4 treatment, first administered at suppressive doses (200 micrograms per day for 4 months) and subsequently at substitutive doses (150 micrograms per day for 2 months), induced complete remission of symptoms along with normalization of the CT scan picture.
 ...
PMID:Pituitary enlargement in post-surgical hypothyroidism misdiagnosed as thyrotroph neoplasia. Report of a case. 262 26

14 normal volunteers, 23 patients with euthyroid goiter, 9 patients with hypothyroidism and 17 patients with hyperthyroidism were injected with 400 micrograms thyroliberin (thyrotropin releasing hormone, TRH). The documented side effects were the same in all the 4 groups studied. Subjective symptoms such as flushing, nausea, urinary urgency, dizziness and headache in decreasing sequence were mentioned by 86% of subjects. Shortly after thyroliberin injection, a mean increase of 26 +/- 13 mm Hg for systolic and 14 +/- 6 mm Hg for diastolic blood pressure as well as an increased heart rate by 7.2 +/- 6.6 min-1 was demonstrated. Plasma catecholamines were lowered in patients with euthyroid goiter and hyperthyroidism and raised in patients with hypothyroidism, compared with the controls. Thyroliberin administration was associated with an activation of the sympathoadrenal system. The increments in plasma epinephrine and norepinephrine concentrations were proportional to initial values, but were insufficient to affect blood pressure. The mean increase of 28% for plasma epinephrine and 21% for norepinephrine were maximal in the second to the forth minute, where subjective symptoms, blood pressure and heart rate were already decreasing. In view of the rapid onset of the subjective symptoms as well as the chronotropic and the pressor response, thyroliberin may partly exert these effects centrally or directly on the vascular system, independently of catecholamines. Since individual systolic blood pressure increased by as much as 64 mm Hg, caution is advised in selecting patients with risk factors for testing.
 ...
PMID:[Adverse reactions and changes in norepinephrine and epinephrine in the plasma after intravenous thyroliberin in persons with normal and abnormal thyroid function]. 311 48

We describe a 47 year old woman with a 30-year history of generalized myasthenia gravis whose condition had been stable and well controlled on a combination of pyridostigmine and ephedrine until she presented. At this time she gave a 2 month history of weakness, nausea, vomiting and more recently intermittent confusion. Investigations confirmed both primary hypothyroidism and primary adrenal failure (Schmidt syndrome). The autoimmune aetiology of these three conditions was confirmed by positive acetylcholine receptor, adrenal and thyroid microsomal antibodies.
 ...
PMID:Myasthenia gravis and Schmidt syndrome. 325 19

Synthetic thyrotropin-releasing hormone (TRH) was administered intravenously in a dose of 7 mug/kg to 20 normal children ages 4-13 yr. Serum thyroid-stimulating hormone (TSH) was measured by radioimmunoassay and rose from a mean value of 1.7 muU/ml (range = < 1.25-7.2) to a mean peak value of 21.5 muU/ml (5.2-33.2) at 15 or 30 min after administration.13 patients with idiopathic hypopituitarism and apparent normal thyroid function, ages 3-19 yr, responded to TRH in a manner very similar to the control subjects: TSH rose from a mean value of 1.8 muU/ml (range < 1.25-4.3) to a mean peak value of 18.5 muU/ml (range = 9.5-45.0) which occurred between 15 and 60 min after TRH.13 idiopathic hypopituitary patients with documented thyroid deficiency were tested after thyroid therapy had been discontinued for a minimum of 10 days. The serum TSH values in 10 of 13 patients rose from a mean base line level of 2.2 muU/ml (< 1.25-5.3) to a peak mean value of 32.5 muU/ml (9.6-61.3) between 30 and 120 min after TRH. In three patients, however, little or no TSH response was detected, even when serum thyroxine levels were extremely low. Similar to the latter group, three of five patients with hypopituitarism secondary to craniopharyngiomas had undetectable or barely measurable TSH levels before and after TRH. Two of these five patients had significant responses which were compatible with hypopituitarism resulting from damage to the hypothalamus or hypothalamic vessels instead of the pituitary. Side effects were experienced in 41 of 54 patients (76%). The effects were limited to a mild nausea-like sensation in 63% of the patients and occurred within the first 5 min after receiving TRH. No evidence of serious toxicity or long-term side effects was noted. The TRH test is a safe, effective way to measure TSH reserve in children. The positive response in 10 of 13 patients with secondary hypothyroidism supports data previously accumulated that most patients with idiopathic hypopituitarism have an abnormality of their hypothalamic-releasing hormone function, whereas the remaining minority probably have primary pituitary disease.
 ...
PMID:Serum thyrotropin responses to synthetic thyrotropin-releasing hormone in normal children and hypopituitary patients. A new test to distinguish primary releasing hormone deficiency from primary pituitary hormone deficiency. 462 44

In outlining the pathology of various electrolyte metabolism abnormalities in cancer patients we considered the main clinical points between pathologies and emergency treatment. In regard to sodium (Na+) metabolism, one pathologic state that requires our attention is hypernatremia. Hypernatremia is accompanied with dehydration and is due to water loss, vomiting, diarrhea and renal insufficiency. One of the major causes of this condition is lack of the antidiuretic hormone due to intracranial metastasis of the tumor. When hypernatremia becomes severe, it is accompanied with circulatory failure, muscular asthenia, disorientation, convulsions, coma and other cerebral symptoms. Treatment consists of replenishing the water content by infusion of electrolyte solutions which should be carefully conducted after complete diagnose of the severity of the patient's pathological condition. Hyponatremia, like sick cell syndrome, is observed relatively frequently in cancer patients. When the serum Na level falls markedly, it induces cerebral edema and causes disorders of consciousness. The major treatment consists of providing both water and sodium supplements. Hyperkalemia is observed at the time of renal insufficiency, tissue lesions, vomiting, and diarrhea. When serum potassium level rises, it causes bradycardia, ventricular fibrillation, or cardiac arrest. It is important to diagnostically apprehend the severity of this condition using EKG and determining the serum K1+ level. For emergency treatment injection of calcium gluconate is very effective. Hypokalemia is often manifested by the loss of intestinal fluids due to diarrhea or during administration of diuretic agents. Clinical symptoms include neural paralysis but emergencies occur relatively infrequently. K C1 injections are used in treating this condition. Hypercalcemia is manifested in cancer patients during hyperparathyroidism. Its clinical symptoms include lassitude, tachycardia, nausea, vomiting, and renal dys-function, leading to neural symptoms in severe cases. The main treatment consists of injection of physiological saline solution and administration of calcitonin, mithramycin. Hypocalemia is manifested during renal insufficiency, lack of vitamin D, and hypothyroidism. In classic cases it causes tetanic spasms. Injection of calcium is an effective treatment but since during tetanic spasms alcalosis may easily occur, treatment should only be provided after obtaining a complete understanding of the patient's condition. The pathological conditions described above can not be said to specific to cancer but it should be kept in mind that one of their main causative factors is the involvement of mechanism which produces ectopic hormones from cancerous tissues.
 ...
PMID:[Electrolyte metabolism and emergency]. 688 72

This is a report on a patient 57 years old, hospitalized because of expressed fatigue, nausea, vomiting and epigastrium pain. Hyperpigmentation of skin and mucous and hypotension were present; and hypocorticism was suspected while ex iuvantibus substitutional therapy of corticosteroides was introduced. By testing thyroid gland function, hypothyroidism was established, so we suspected the presence of united pluriglandular insufficiency--Schmidt Syndrome. The patient reacted well to the substitutional therapy of hydrocortisone and levothyroxine. The diagnosis has been confirmed at the Clinic for Endocrinology in Novi Sad and today the patient has regular checks at the outpatients clinic for endocrinology in Sombor. The discussion contains important diagnostic and therapeutic problems.
 ...
PMID:[Addison's disease]. 773 45

Current diagnostic studies [radioiodine uptake and serum thyroglobulin (Tg) levels] for residual or metastatic thyroid tissue in patients with differentiated thyroid carcinoma require a hypothyroid status necessary for adequate endogenous TSH stimulation. However, almost all patients have symptoms of clinical hypothyroidism during this period. As shown in the present study, recombinant human TSH (rhTSH) allows stimulation of 131I uptake and Tg release from residual thyroid tissue in euthyroid patients. To assess safety, dosage, and preliminary efficacy, comparison was made of the stimulation of 131I uptake and Tg release after rhTSH administration and after T3 withdrawal in 19 patients after a recent thyroidectomy for differentiated thyroid carcinoma. Various doses (10-40 U) of rhTSH were injected im for 1-3 days in patients receiving suppressive doses of T3. Twenty-four hours after the last dose of rhTSH, 1-2 mCi 131I were administered, followed by a neck and whole body scan 48 h later. After discontinuing T3 for a median period of 19 days (range, 15-28), endogenous serum TSH levels were markedly elevated, and the patients were given a second dose of 131I and rescanned 48 h later. The injections of rhTSH were tolerated well. No major adverse effects were reported; nausea was reported in 3 (16%) and vomiting in 1 of the patients treated with high doses. The quality of life, as measured by two psychometric scales, was far better during rhTSH treatment than after T3 withdrawal. The peak levels of serum TSH (mean +/- SD) after a single dose of 10, 20, or 30 U were 127 +/- 19, 309 +/- 156, and 510 +/- 156 mU/L, respectively, and occurred 2-8 h after injection. Twenty-four hours after the injection, TSH levels decreased to 83 +/- 31, 173 +/- 73, and 463 +/- 148 mU/L in these treatment groups, respectively. The quality of the thyroid scans and the number of sites of abnormal 131I uptake were similar after rhTSH treatment and in the hypothyroid scans in 12 (63%) patients. Two additional sites of uptake in the chest and one in the thyroid bed, not visible on the hypothyroid scans, were identified in 3 (16%) patients after rhTSH. In 1 patient a focus of uptake was better visualized after rhTSH than after withdrawal. In 3 (16%) other patients, 1 lesion in the chest and 2 in the neck were seen only after T3 withdrawal.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Diagnostic use of recombinant human thyrotropin in patients with thyroid carcinoma (phase I/II study). 828 3

Acute adrenal insufficiency is a rare disorder associated with high morbidity and mortality if allowed to progress unrecognized. A constellation of nonspecific symptoms including weakness, easy fatigue, nausea, anorexia, and weight loss are typical features of adrenal insufficiency. The index of suspicion should be particularly high if the patient has hyperpigmentation; hyponatremia and/or hyperkalemia; a history of autoimmune disease (hypothyroidism, diabetes) or recent prior use of exogenous steroids or if the patient is on anticoagulant therapy. Any decline in clinical status (hypotension, fever, decreasing mental status), especially in the setting of an acute intercurrent illness, should be treated aggressively, even before laboratory confirmation of the diagnosis. Diagnostic testing is fairly straightforward and readily available. The development of purified synthetic corticosteroid preparations has provided a safe and effective means of replacement. Early awareness, recognition, and intervention remain significant steps in altering the course of acute adrenal insufficiency.
 ...
PMID:Acute adrenal insufficiency. 832 89


1 2 3 4 5 6 7 8 Next >>