Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sodium chloride deficiency (SCD) was observed within the 1st year of life in 12 of 46 cystic fibrosis (CF) patients between July 1989 and September 1992. All patients showed sweating, loss of appetite, fever, vomiting, irritation, dehydration, weakness, and cyanosis during an attack. Mean plasma sodium, potassium and chloride levels were 122.9 (range 106-135), 2.5 (range 1.6-3.5), and 73.3 (range 60-90) mEq/l respectively. Alkalosis and elevated plasma renin activity were detected in all patients. Of the patients, 50% showed microscopic haematuria, and hypercalciuria was detected in two out of four patients. Low urinary sodium and high urinary potassium were observed in the four examined patients. Increased creatinine, BUN and uric acid values returned to normal with treatment. All the patients were treated initially with intravenous fluids and electrolyte solutions. All patients were less than 7 months of age during the first attack, five received only breast milk and the others breast milk with formula milk. Their oral salt supplement was 2-4 mEq/kg per day, which is recommended for CF patients, but could be deficient in excessively sweating infants. The genotype of these patients might be cause of high salt losses. F508 is the most common mutation with the frequency of 38% in our CF patients with SCD, but the frequency of unknown mutations is high (54%).
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PMID:Sodium chloride deficiency in cystic fibrosis patients. 784 98

Review of 20 patients with glucocorticoid deficiency (three cases also with salt loss) associated with absent tear secretion (19 cases) and achalasia of the cardia (15 cases) revealed neurological abnormalities in 17 including hyper-reflexia, muscle weakness, dysarthria, and ataxia together with impaired intelligence and abnormal autonomic function, particularly postural hypotension. These findings indicate that significant neurological problems are common in this multisystem disorder.
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PMID:Neurological and adrenal dysfunction in the adrenal insufficiency/alacrima/achalasia (3A) syndrome. 833 72

Contrary to previously accepted observations, the quokka (Setonix brachyurus), a small macropodid marsupial, survival bilateral adrenalectomy indefinitely if injected with appropriate doses of cortisol and aldosterone, either singly or combined. Normal behavior and plasma solute concentrations could be maintained indefinitely by daily i.m. injection of 0.2 mg cortisol acetate and 0.01 mg aldosterone/kg. Plasma glucose concentration was maintained at the control value when the supplement contained cortisol but was significantly reduced with only a mineralocorticoid. Cortisol also caused a dose-related enhancement of food intake. There was no significant effect of supplementation on plasma urea concentration. Deoxycorticosterone, with or without cortisol, caused Na+ retention but aldosterone had this effect only when combined with cortisol. Urinary K+ excretion was not significantly affected by any of these corticosteroids. Withdrawal of hormone supplements caused muscular weakness and cessation of food intake within 3-6 days, accompanied by a moderate fall in Na+ and rise in K+ concentration of blood plasma as well as instability of plasma glucose concentration with hypoglycemic episodes. Renal excretion of both Na+ and K+ exceeded intake only when food intake had declined to negligible levels. Glomerular filtration rate (GFR) and renal plasma flow (RPF) fell when corticoids were withheld, without change in inulin space. However, p-aminohippurate (PAH) space fell, as did the intercompartmental exchange parameters of both inulin and PAH. Cortisol and aldosterone or aldosterone alone restored GFR, but not RPF, to the normal range. The fractional reabsorption of K+, but not Na+, was reduced in the absence of corticoids. It is suggested that, in this species, the circulatory effects of corticoids are essential for normal tissue perfusion and their influence on renal circulation is important in the control of salt and water balance. Metabolic effects are probably mainly permissive, as in other macropodid marsupials.
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PMID:Adrenalectomy and steroid replacement in a small macropodid marsupial, the quokka (Setonix brachyurus): metabolic and renal effects. 850 24

Acute mountain sickness (AMS) affects, to varying degrees, all travelers to high altitudes (elevations greater than 5280 feet). In a small percentage of patients, AMS can lead to high-altitude pulmonary edema (HAPE) or high-altitude cerebral edema (HACE). Symptoms of AMS range from a combination of headache, insomnia, anorexia, nausea, and dizziness, to more serious manifestations, such as vomiting, dyspnea, muscle weakness, oliguria, peripheral edema, and retinal hemorrhage. Although the primary cause of these symptoms is related to the reduced oxygen content and humidity of the ambient air at high altitudes, the physiologic pathway relating hypoxemia to AMS and its sequelae remains unclear. Tips on self-diagnosis and symptom recognition are critical elements to be included in educating patients who are contemplating a trip to high altitudes. Preventive strategies include allowing 2 days of acclimatization before engaging in strenuous exercise at high altitudes, avoiding alcohol, and increasing fluid intake. Conditioning exercise for patients older than 35 years is also recommended before departure. A high-carbohydrate, low-fat, low-salt diet can also aid in preventing the onset of AMS. Acetazolamide (125 mg two or three times daily, or once at bedtime) has also been shown to reduce susceptibility to AMS and the incidence of HAPE and HACE. Although effective in treating cerebral symptoms of AMS, dexamethasone is not routinely recommended as a prophylactic agent for AMS.
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PMID:A trek to the top: a review of acute mountain sickness. 855 56

Twenty-three children from 8-60 months (mean age 21.13 months) admitted with neuromuscular manifestations of diarrhea related hypokalemia were studied. Forty four per cent cases were suffering from diarrhea at the time of admission but in majority of cases (56%), the diarrheal episode had already terminated. Mild hypokalemia was seen in 17.4%, moderate in 43.5% and severe in 39.1%. Neck flop was the commonest (100%) neuromuscular manifestations followed by diminished bowel sounds (82.6%), truncal weakness (52.2%), weakness of limbs (52.2%), lethargy (43. 5%), abdominal distension (43.5%), respiratory involvement (4.3%) and phantom hernia (4.3%). Two cases (8.7%) had flaccid paralysis of both the lower limbs. Severe hypokalemia was more frequently observed in children below 24 months of age and those who had received i.v. fluids or salt sugar solution before reporting in the hospital. A significant correlation was noticed between severity of hypokalemia and frequency of stools (p < 0.05), degree of dehydration (p < 0.01), severity of nutrition (p < 0.01) and extent of neuromuscular involvement (p < 0.01). Our results highlights the importance of diarrhea related hypokalemia particularly in young malnourished children who are rehydrated with solutions inadequate in potassium. Early diagnosis and appropriate treatment can promptly reverse these manifestations within 48-72 hours.
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PMID:Neuromuscular manifestations of diarrhea related hypokalemia. 863 3

We present a 72-year-old man who had episodes of severe, acute renal failure during severe attacks of diarrhea caused by Vibrio cholerae. Patterns of acute tubular necrosis and tubulointerstitial nephritis developed following hypotension and decrease in renal blood flow, causing secondary renal ischemia. There was severe dehydration with profound hypovolemia and infection. The clinical picture included fever, weakness, arthralgia, pedal edema, mild bilateral pleural effusions, anemia, leukocytosis, azotemia with a maximum of 330 mg/dl of urea, creatine to a maximum of 9.8 mg/dl, hypoproteinemia, severe metabolic acidosis, marked increase in lactate dehydrogenase (LDH) and creatine phosphokinase (CPK), microscopic hematuria, sterile leukocyturia, normoglycemic glucosuria and phosphaturia with diminished tubular reabsorption of phosphorus. A short oliguric phase was followed by a polyuric phase lasting about 10 days, and glomerular and tubular function became normal after about 3 weeks. Treatment was by intensive infusions of fluids, electrolytes, sodium bicarbonate, salt-free albumin and antibiotics. To the best of our knowledge, this renal complication of cholera has not yet been described in Israel.
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PMID:[Acute renal failure as a complication of cholera]. 868 55

A 77-year-old woman with severe valvular heart disease and chronic renal failure was admitted to hospital for control of her heart condition and to improve her ability to perform activities of daily living. In the past 2 years, she had been admitted to hospital four times due to severe congestive heart failure, and she was bedridden because of muscle weakness. A multidisciplinary approach was taken. A cardiologist reassessed her medications and determined an exercise level in co-operation with a physical therapist. After 40 days of rehabilitation, the patient was able to walk 200 m without the help of a cane. With an increase in the exercise level, her cardiothoracic ratio increased from 68 to 74%. The furosemid was then increased from 40 to 60 mg per day and 20 mg of denopamine was added, which resulted in a decrease of the cardiothoracic ratio to 66%. Dietary assessment revealed her usual salt intake was more than 10 g per day, and the dietitian advised the patient that her daily salt intake should be lower than 7 g and water intake less than 800 ml per day. Consultations with social-service personnel made revealed problems in her family and living environment, and she was advised of available social services. For good compliance, the patient had her medication explained by a pharmacist. Assessment of activities of her daily living and intensive education about congestive heart failure were performed by the nurse in charge. After discharge, a nurse team visited her home every two weeks and watched for signs of heart failure. This comprehensive intervention prevented an exacerbation of heart failure and readmission for nine months.
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PMID:[Multidisciplinary approach to an elderly patient with severe congestive heart failure]. 949 70

Primary adrenocortical insufficiency (Addison's disease) is characterised by weakness, tiredness, fatigue, weight loss, hypotension, hyperpigmentation and a craving for salt. Without treatment lethality is 100%; correctly treated, life expectancy is normal. Addison's disease may appear isolated or as part of a polyendocrine syndrome. Because several of the symptoms are unspecific and develop over the course of several years, many patients are not diagnosed before a life-threatening adrenal crisis develops. Autoimmune destruction of the adrenal cortex is the main cause of adrenocortical failure in the industrialised world. This condition is characterised by circulating autoantibodies against the steroidogenic enzyme 21-hydroxylase. These autoantibodies can now easily be quantified. More unusual causes of adrenocortical failure are tuberculosis, bleeding, metastasis and adrenoleukodystrophy. Using three cases we highlight the clinical, diagnostic and therapeutic aspects of adrenocortical failure.
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PMID:[Primary adrenal cortex insufficiency--a diagnostic challenge]. 952 May 81

We describe a patient who had metastatic carcinoma of the stomach and severe headaches, weakness, and diplopia. The patient had meningeal carcinomatosis that was confirmed by examination of the cerebrospinal fluid after computed tomography of the brain was normal. Weakness was explained by the finding of hyponatremia due to the syndrome of inappropriate antidiuretic hormone (SIADH). We believe this is the first reported case of meningeal carcinomatosis in which stomach carcinoma caused SIADH. The differentiation between SIADH and cerebral salt wasting due to malignant tumors is emphasized.
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PMID:Meningeal carcinomatosis and syndrome of inappropriate antidiuretic hormone in a patient with metastatic carcinoma of the stomach. 982 97

Patients with acute viral hepatitis B, A and mixed hepatitis B + C were treated in two independent clinics with phosphogliv--a new hepatoprotective drug based on polyunsaturated phosphatidylcholine and glycyrrhizic acid salt. Phosphogliv removed some symptoms of intoxication (nausea, weakness, jaundice, etc.) quicker than basic therapy. Among biochemical hepatitis markers, serum bilirubin level was most responsive to phosphogliv. Standard therapy decreases bilirubin by 30% on the average for 5 days, phosphogliv reduces bilirubin for one more week to half those values observed in control patients. At that point low aminotransferase activities were seen in phosphogliv treated patients. No side effects were seen. The new hepatoprotector phosphogliv which repairs biomembranes represents drugs of new generation compared to phospholipid drug essential.
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PMID:[New domestic phospholipid preparation "Fosfogliv" as an effective treatment for patients with acute viral hepatitis]. 1088 9


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