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)

A 25-year-old white man with gout and nephropathy and with a previous reaction to allopurinol was given a trial dose of oxypurinol. He developed malaise, a generalized erythematous reaction with edema, pruritus, and emesis; this was clinically identical to the reaction he experienced with allopurinol. When the patient's lymphocytes were exposed in vitro to oxypurinol and allopurinol, increased DNA synthesis was observed, suggesting an immunologic basis for the reaction. This patient indicates that clinical cross reactivity to allopurinol and oxypurinol does occur and may be of an immunologic basis. There is a need for additional xanthine oxidase inhibitors for such patients.
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PMID:Allergic reaction to allopurinol with cross-reactivity to oxypurinol. 13 55

Electrolyte disturbances in leukemia can be the result of the disease process or drug therapy. One group of electrolyte abnormalities is related to the stage of the leukemic process. Included in this group are newly diagnosed patients who may show elevated serum potassium, phosphorus, and magnesium--a result of their release from malignant cells after cytotoxic therapy or their accumulation due to urate nephropathy. Patients in remission usually have normal serum electrolyte concentrations, but acute leukemia patients during relapse may have hypokalemia, hypophosphatemia, and hypomagnesemia. This imbalance may be related to cellular uptake of these electrolytes in the presence of inadequate dietary intake. Other factors contributing to electrolyte derangements, and related to the leukemic process, include hyponatremia and hypochloremia secondary to the SIADH, hypokalemia in acute monocytic or acute myelomonocytic leukemia due to lysozyme-induced tubular damage, hypercalcemia possibly secondary to leukemic infiltration of bone or parathyroid glands (with PTH release), or production of a PTH-like substance by leukemic cells. Nonspecific factors related to the disease process which may aggravate the electrolyte imbalance include gastrointestinal loss through nausea, vomiting, and malnutrition. The drug-related electrolyte abnormalities include cyclophosphamide- and vincristine-induced SIADH; decreased serum sodium, chloride, potassium, and calcium concentrations as a result of polymyxin B nephrotoxicity; hypokalemia and hypomagnesemia secondary to amphotericin B; hypocalcemia, hypophosphatemia, and hyperphosphaturia due to L-asparaginase-induced hypoparathyroidism; hypokalemia due to a nonreabsorbable anion effect of antibiotics in the distal tubule or changes in membrane ionic transport of all cells by large doses of antibiotics. Electrolyte disturbance in leukemia thus have a multifactorial pathogenesis which can best be delineated according to the stage of the leukemic process and the drugs being used. Recognition of the cause or causes in a particular patient is essential for an effective approach to management. This review emphasizes the need for routine measurement of serum electrolytes during all phases of the leukemic process.
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PMID:Electrolyte and acid-base disturbances in the management of leukemia. 26 90

After an inability to work lasting 15 months with 9 treatments in an inpatient department in several institutions in a 33-year-old patient the relapsing metabolic alkalosis in hypopotassiaemia and relapsing increase of the creatinine level could causally be clarified by establishment of a pylorus stenosis in chronic duodenal ulcer. Due to the Billroth II operation a complete clinical and objective improvement developed. In this case the transient retention of substances normally contained in the urine was conditioned by a hypokalaemic nephropathy. The cause of the hypokalaemia was the vomiting by pylorus stenosis. The histologically ascertained glomerulonephritis had no causal significance for the pathological process.
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PMID:[Recurrent metabolic alkalosis due to pyloric stenosis]. 59 99

Twenty patients with end-stage renal disease and a creatinine clearance of less than 5 ml/min were tre ated with oral gastrointestinal (GI) dialysis. The dialyzate contained an electrolyte solution with 180-220mmoles/l of mannitol. In fasting state in the morning the self-prepared 7 liters of dialyzate was drunk at a rate of one glass every 5 minutes for about 3 hours. Intermittent diarrhea with passage of watery fluid occurred during the whole period. After each treatment the average drop in BUN in individual patients was 11--22%, but no significant decrease in serum creatinine. With twice to thrice weekly GI dialysis uremic symptoms such as anorexia, nauseal and vomiting were usually improved with slight prolongation of life. However, treatment is usually difficult when the patient becomes oliguric or anuric, so its value in long-term management of chronic uremia is limited. Most of our patients either died or shifted to hemodialysis within a few months of institution of the therapy.
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PMID:Home treatment of uremia with gastrointestinal dialysis. 69 95

A case of Turner's syndrome is presented; many congenital defects were detected. Predominant clinical findings were cheilognatoschisis, respiratory distress, caused by congenital bronchiektasis and chronic hypokalemia with paroxysmal attacks of paralysis and tetania. Hypokalemia was mainly due to gastrointestinal losses as a consequence of permanent vomiting in the presence of stomach atonia and hiatus insufficiency or because of "third space losses", while a subileus persisted chronically. Furthermore also a renal loss of serum potassium was evident in the patient's predialytic time. Basic renal diseases were pyelonephritis, renal damage from phenacetine abuse, or probably even a nephropathy due to potassium depletion. Uraemia was controlled by dialysis treatment and by a dialysate consisting of 7 and 6 mmol/l potassium respectively. The result of this intense therapy was physical rehabilitation and the patient finally could resume her professional work again.
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PMID:[Intractable renal and enteral loss of potassium in a case of Turner's syndrome (author's transl)]. 72 52

Hypertensive emergencies of 10 children with renal hypertension were analysed. Cause of renal disease are chronic renal failure in three, acute renal failure in three, hemolytic uremic syndrome in two, acute post streptococcal glomerulonephritis in one, and renal arterial stenosis in a further patient. Therapy should be started early in the course of the hypertensive emergency, first symptoms are headache and vomiting. Drug of first choice is diazoxide (3-5-(8)mg/kg i.v.). Three patients developed transitory hyperglycemia after repeated injections of diazoxide.
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PMID:[Hypertensive emergencies in children with renal hypertension (author's transl)]. 76 42

Preliminary results of this retrospective-prospective analysis of renal hypertension in 110 children indicate that hypertension may be secondary to a wide variety of acute progresive, and chronic renal diseases which may be either congenital or acquired. Affected children may be detected at any time from infancy through adolescence. Symptoms usually associated with acute glomerulonephritis (i.e., headache, swelling, nausea, vomiting, anorexia, fatigue, dizziness, and fever) occur in both acute and chronic renal diseases associated with hypertension. Headache and swelling are the most common symptoms in this series. Peripheral edema, rales, and increased heart size were found in between 10 and 25% of these children. Differential diagnosis may be approached by a consideration of causes of acute and chronic hypertension. The child with chronic renal disease usually presents with a long history of fatigability, poor growth, and pallor, and laboratory tests reveal elevation of the creatinine and BUN along with anemia, hypocalcemia, and hyperphosphatemia. In contrast, the child with acute renal disease and hypertension presents with a history of prior good health followed by the abrupt onset of signs and symptoms of renal disease; laboratory tests usually reveal modest elevations of creatinine and BUN, anemia is unusual, an abnormal urinalysis is common, and serum calcium and phosphorous levels are usually normal. Renovascular and asymmetric renal parenchymal disease represent uncommon but important conditions because surgery may be curative. Treatment may be surgical, medical, or combined. Surgical conditions include renal trauma, hydronephrosis, asymmetric renal disease, and renal arterial disease. Adequate blood pressure control without medication can be expected following surgery in instances of unilateral involvement with a normal contralateral kidney. Meticulous assessment of the contralateral kidney is needed to determine that it is normal. If surgery is unsuccessful or is not indicated, pharmacologic therapy is initiated with a stepwise regimen starting with the mildest agent (e.g., thiazides) and then adding additional antihypertensive drugs when adequate blood pressure control has not yet been achieved. The goal of therapy is the lowest, safest, tolerated blood pressure levels. Long-term, carefully designed studies of antihypertensive agents for children with renal hypertension are not available. The need for collection and critical analysis of data concerning the clinical course of children with renal hypertension is evident from a review of the literature and from the preliminary data presented in this series. The presentation of such information and a critique of outcome variables will provide a basis for program planning for affected children and improvement in patient care where indicated.
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PMID:Renal hypertension in children. 99 44

Shi-Quan-Da-Bu-Tang (Ten Significant Tonic Decoction), or SQT (Juzentaihoto, TJ-48) was formulated by Taiping Hui-Min Ju (Public Welfare Pharmacy Bureau) in Chinese Song Dynasty in AD 1200. It is prepared by extracting a mixture of ten medical herbs (Rehmannia glutinosa, Paeonia lactiflora, Liqusticum wallichii, Angelica sinesis, Glycyrrhiza uralensis, Poria cocos, Atractylodes macrocephala, Panax ginseng. Astragalus membranaceus and Cinnamomum cassia) that tone the blood and vital energy, and strengthen health and immunity. This potent and popular prescription has traditionally been used against anemia, anorexia, extreme exhaustion, fatigue, kidney and spleen insufficiency and general weakness, particularly after illness. In order to restore immunity in cancer patients, potentiate the therapeutic effect and ameliorate adverse toxicity of anticancer agents, 116 Chinese herbal formularies (Kampo) have been screened and evaluated. Fifteen compounds were found to have such actions. Among these, SQT was selected as the most effective as a potent biological response modifier. During the last eight years, animal models and clinical studies have revealed that SQT demonstrates extremely low toxicity (LD50 > 15 g/kg op murine), self-regulatory and synergistic actions of its components in immunomodulatory and immunopotentiating effects (by stimulating hemopoietic factors and interleukins production in association with NK cells, etc.), potentiates therapeutic activity in chemotherapy (mitomycin, cisplatin, cyclophosphamide and fluorouracil) and radiotherapy, inhibits the recurrence of malignancies, prolongs survival, as well as ameliorate and/or prevents adverse toxicities (GI disturbances such as anorexia, nausea, vomiting, hematotoxicity, immunosuppression, leukopenia, thrombocytopenia, anemia and nephropathy, etc.) of many anticancer drugs. The application and mechanistic studies of SQT in future development have potential importance in basic and clinical research of the traditional Chinese therapeutic approach of "toning the blood and strengthening Qi (vital energy)" in cancer immunotherapy.
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PMID:Shi-quan-da-bu-tang (ten significant tonic decoction), SQT. A potent Chinese biological response modifier in cancer immunotherapy, potentiation and detoxification of anticancer drugs. 129 61

Salt losing nephropathy, occurring predominantly in male infants, has been reported in association with a spectrum of urologic diseases including obstructive uropathy and massive, infected vesicoureteral reflux (VUR). This has been called pseudo-hypoaldosteronism (PHA) or alternatively, pseudo salt-losing congenital adrenal hyperplasia (CAH), and is thought to reflect a tubular unresponsiveness to aldosterone. We report our experience with six cases, discuss one case in detail and review the 39 cases previously reported. A one month old male infant presented with a left upper quadrant mass. Signs and symptoms included vomiting, dehydration, hyponatremia and hyperkalemia. This suggested the diagnosis of CAH for which therapy was instituted. Ultrasonographic examination subsequently revealed the mass to be a urinoma in an infant with posterior urethral valve (PUV) and obstructive hydronephrosis.
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PMID:Salt losing nephropathy simulating congenital adrenal hyperplasia in infants with obstructive uropathy and/or vesicoureteral reflux--value of ultrasonography in diagnosis. 174 73

A patient with end-stage renal disease (ESRD) developed metabolic alkalosis and alkalemia from protracted vomiting. As a result of the absence of the alkali excretory capacity in this patient with ESRD, the alkaline load accumulated rapidly. Once the amount of acid lost from vomiting exceeded the amount of acid gained from metabolism, alkalemia supervened. The initial arterial blood gas on room air revealed hypercarbia, hypoxia and alkalemia. Her serum bicarbonate was greater than 50 mEq/l. Compensatory hypoventilation occurred. In this report, the extent of compensatory hypoventilation in the setting of metabolic alkalosis in patients treated for ESRD and therapeutic approaches to this problem will be discussed. Treatment was aimed at correcting the primary disorder, namely metabolic alkalosis. Conventional bicarbonate dialysis was shown to be effective in improving acid-base homeostasis in this patient.
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PMID:Hypoventilation in a dialysis patient with severe metabolic alkalosis: treatment by hemodialysis. 176 Jan 42


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