Biomedical subjects
Publications and source records attributed to R O Hickman.
A severe generalized multisystem allergic reaction occurred in a 16-month-old infant following the use of trimethoprim-sulfamethoxazole. Acute interstitial nephritis developed three weeks following the onset of this reaction and resolved after three months. This is the first description of this renal toxicity with TMP-SMX in a child.
To define factors related to renal prognosis in children with vesicoureteral reflux and renal insufficiency, we reviewed 908 children with vesicoureteral reflux. Twenty-five patients were found who had initial creatinine clearances of less than 60 mL/min/sq m and had five-year follow-up examinations. All had severely dilated ureters. Renal function improved in eight, remained stable in ten, and deteriorated in seven. Probability of deterioration of renal function in these children was related to factors measurable at clinical presentation: (1) a corrected creatinine clearance of less than 25 mL/min/sq m; (2) 2r greater reaction for protein on urinalysis that disclosed no infection; and (3) being in less than the fifth percentile of body length. The total number of the three factors present in each patient was more significantly related to prognosis than any one factor.
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The use of a central venous catheter for long-term intravenous therapy is described. The catheter's history, physical description, and uses are discussed. Also reviewed are complications from use of the catheter, the pharmacist's role in patient teaching, and the procedure for administering medications through the catheter. A listing of drugs administered through the catheter, incompatibility data and patient teaching instructions are also included.
One hundred patients, 54 with acute myelogenous leukemia (AML) and 46 with acute lymphoblastic leukemia (ALL), considered to be in the end stages of their disease, after combination chemotherapy were treated by marrow transplantation. All patients were given a marrow graft from an HLA-identical sibling after receiving 1000-rad total body irradiation (TBI). One group of 43 patients was given cyclophosphamide (CY), 60 mg/kg on each of 2 days, 5 and 4 days before TBI. In a second group of 31 patients, additional chemotherapy was given before CY and TBI. In a third group of 19 patients, BCNU was given before CY and TBI. A fourth group of 7 patients received other chemotherapy regimens before TBI. Six patients died 3-17 days after marrow infusion without evidence of engraftment. Ninety-four patients were engrafted and only one patient rejected the graft. Thirteen patients are alive with a marrow graft, on no maintenance antileukemic therapy, and without recurrent leukemia 1-4 1/2 yr after transplantation. Three have chronic graft-versus-host disease (GVHD). Four patients are alive 1 1/2 - 3 1/2 yr after grafting but have had a relapse of their leukemia. Of 93 evaluable patients, 19 did not develop GVHD and 24 developed very mild GVHD. Fifty patients developed moderate to severe GVHD, and 40 of these were treated with antithymocyte globulin. Interstitial pneumonia occurred in 54 patients and was the primary cause of death in 34. Interstitial pneumonia often occurred in association with GVHD and the most common etiologic agent was cytomegalovirus. A total of 31 patients have had a relapse of leukemia. There was no definite correlation between relapse of leukemia and the presence or absence of GVHD. The relapse rate appeared to be relatively constant over the first 2 yr and was extremely low after that time. Neither survival nor leukemic relapse appeared to be influenced by the type of leukemia nor by the preparative chemotherapy regimen given before TBI. Patients in fair clinical condition at the time of transplantation showed significantly longer survival times than patients in poor condition (p = 0.001). This observation, coupled with the observation that some patients may be cured of their disease, indicates that marrow transplantation should now be undertaken earlier in the management of patients with acute leukemia who have an HLA-matched sibling marrow donor.
18 children with clinical and laboratory findings characteristic of the hemolytic uremic syndrome were retrospectively studied. Thrombocytopenia due to platelet destruction was accompanied by only minimal changes in fibrinogen turnover and fibrinolytic degradation products. The most consistent pathologic feature was severe renal endothelial cell injury, which was postulated to produce both platelet and red cell destruction. Despite initially severe renal damage, 90% of the patients ultimately recovered normal renal function if adequately supported during the acute phase of the disease.
The clinical features and renal histology of twelve chinldren who developed nephrotic syndrome in the first year of life were studied. Six suffered from microcystic disease and six from primary mesangial cell proliferation and/or sclerosis. A consistent family history, premature birth, large placenta pressence of other congenital abnormalities, onset in the first two months of life and lower plasma albumin level all suggested microcyste disease, but the most reliable distinction was histological. All microcystic children died within two years, whereas four with primary mesangial disease survived indefinitely. Corticosterid and immunosuppressive herapy failed to help either group and most deaths were due to sepsis, especialy with E. coli.
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Although the biologically active metabolite of vitamin D, 1,25-dihydroxycholecalciferol, is synthesized exclusively by kidney tissue, severe hypercalcemia developed in an anephric child treated with large doses of vitamin D. Treatment by calcium-free peritoneal dialysis acutely reduced serum calcium from 17.2 to 14.2 mg/100 ml. This decrement was effected by removal of three times the total calcium in extracellular fluid, suggesting enhanced bone resorption. Oral prednisolone for 7 days reduced serum calcium to 13 mg/100 ml, but hypercalcemia recurred rapidly after prednisolone was stopped. Calcitonin, given for only 4 one-half days, produced normocalcemia. Maximum serum 25-hydroxyvitamin D (25-OHD), observed immediately after vitamin D was stopped, was 635 ng/ml (normal range 23-32 ng/ml) and subsequently decreased with an initial half-time of 10 days. Losses in peritoneal dialysate may have contributed to disappearance of serum 25-OHD. Because of the high serum levels of 25-OHD and absence of renal tissue, 25-OHD was the likely metabolite that caused hypercalcemia, probably by stimulation of bone resorption, though contribution to hypercalcemia by another vitamin D metabolite cannot be absolutely excluded.
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