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Biomedical subjects

E Lieberman

Publications and source records attributed to E Lieberman.

At least 127 records · Page 7Linked to original sources
PubMed1977

Diagnostic evaluation of hypertensive children.

The approach to the diagnosis of established hypertension in childhood can be systematized and focused. The investigation of affected children evolves in an orderly fashion based on data collected from a thorough history and physical examination. Laboratory tests, in the majority of children, can then be selected on the basis of the highest index of suspicion. The cause is often not obscure, and the need to order tests related to several organ systems is avoidable. In a small percentage of patients, however, usually younger children, the cause of hypertension remains obscure until detailed investigations have been performed.

Adolescent↗
PubMed1976

Awareness of pediatric hypertension. Measuring blood pressure.

Surveys of patients at three pediatric teaching hospitals showed a low percentage of blood pressure recordings by the examining physician in the walk-in or emergency clinics. The frequency of blood pressure measurement was higher among inpatients, especially on medical services. A recommendation for obtaining blood pressure measurements is made on three bases: 1. many patients use these ambulatory services as their major source of care, 2. many conditions for which care is sought and many therapeutic agents are associated with hypertension, and 3. unless measurements of blood pressure become customary during training, it is likely that blood pressure recording may not be included as part of routine physical examinations.

Adolescent↗
PubMed1976

Renal hypertension in children.

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.

Adolescent↗
PubMed1976

Cystic diseases of the kidney in children.

Many genetically determined cystic kidney disorders occur in children. Presenting manifestations related to the kidney include failure to thrive, abdominal enlargement or flank masses, progressive renal failure, or urinary tract infection. Radiological techniques often yield information helpful in establishing the type and extent of renal lesions. Cataloging the cystic renal disease in terms of genetic patterns, the involvement of liver or another organs, and the nature of the disorder of renal architecture is helpful in establishing the proper handling of affected children, and in genetic counseling.

Abnormalities, Multiple↗
PubMed1976

Cyclophosphamide in the treatment of idiopathic nephrotic syndrome.

Fifty-three patients 3 1/2 to 20 years of age with steroid-dependent idiopathic nephrotic syndrome (INS) were treated with cyclophosphamide and prednisone. Two dosage schedules were used: a short course (SC) at 3 to 5 mg/kg/day for six to eight weeks and a longer course (LC) at 3 to 5 mg/kg/day for eight weeks followed by 1.5 to 2.5 mg/kg for an additional four weeks. Prednisone was administered concurrently at 50 to 75 mg/sq M every other day. Twenty-nine patients were in the SC group and 24 in the LC group. The two groups did not differ significantly as to age at onset of idiopathic nephrosis nor as to the duration of the INS prior to cyclophosphamide therapy. All patients were followed for a minimum of 42 months after cyclophosphamide therapy. The SC was associated with a higher relapse rate during the first year than the LC (42% and 8% respectively, .01 larger than P less than .025). At 42 months 63% of the LC group were in remission compared with 21% in the SC group.

Adolescent↗
PubMed1975

Gonadal function in children with nephrosis treated with cyclophosphamide.

Conadal function was evaluated in 23 boys and 11 girls treated with cyclophosphamide, 2 to 5 mg/kg/day for periods of 1.5 to 6 months. Serum follicle stimulating hormone (FSH), luteinizing hormone (LH), and testosterone levels were determined by radioimmunoassay. All 16 boys treated when prepubertal or during early puberty had normal, FSH, LH, and testosterone levels. Testicular biopsy was performed in five of the 16, and was abnormal in four and normal in one. Sperm count was normal in two other patients. The remaining seven boys were treated when pubertal; all have decreased spermatogenesis, and five of them have increased FSH levELS. The LH and testosterone levels were normal. No evidence of gonadal dysfunction was detected in any of the girls. Of four patients treated when postpubertal, three have become pregnant.

Adolescent↗
PubMed1975

Polycystic disease and hepatic fibrosis in children. Renal function studies.

Renal function studies were done in five children with infantile polycystic disease (IPCD)of kidneys and liver and in four with congenital hepatic fibrosis (CHF). Glomerular filtration rate was reduced in all IPCD patients and in two of four CHF patients. Urinary concentrating ability following water deprivation and vasopressin administration was impaired in all IPCD patients and in three of four CHF patients. During control period, all patients had asymptomatic metabolic acidosis with total carbon dioxide content less than or equal to 20.5 millimols/liter, and net acid excretion (NAE) was reduced in all but one. Ammonium chloride was administered to seven patients; NAE increased in all, but the increments were subnormal in four. The inability to excrete maximally concentrated urine and an adequate amount of net acid may best be explained by abnormal tubular structure or alterations in medullary architecture secondary to progressive scarring, or both.

Acidosis, Renal Tubular↗