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Biomedical subjects

J H Patterson

Publications and source records attributed to J H Patterson.

At least 73 records · Page 4Linked to original sources
PubMed1972

Metabolic effects of human growth hormone and of estrogens in boys with Duchenne muscular dystrophy.

Metabolic balance studies were conducted in seven boys with Duchenne-type muscular dystrophy, and in six normal boys of similar age, during a 12 day control period and during a 12 day period of treatment with human growth hormone (HGH) at the following doses: 0.0168, 0.0532, and 0.168 U/kg body weight (BW)((3/4)) per day (doses A, B, and C, respectively). In five of the six normals, dose C caused positive balances in N, P, Na, and K; doses B and A had anabolic effects in two and one normal subjects, respectively. In six of the seven Duchenne cases, dose C caused negative balances of N and K, and sometimes of P. Negative balances were produced in three of the Duchenne subjects by dose B, and in one by dose A. None of the dystrophy cases exhibited an anabolic response to any dosage of HGH tested. The release of endogenous HGH in response to insulin, after 2 days' pretreatment with diethylstilbestrol, was similar in both groups of subjects. In the course of these tests, a marked anabolic effect of diethylstilbestrol in the Duchenne patients was apparent. Therefore metabolic balance studies were repeated, in both Duchenne and normal cases, during a 12 day control period and during 12 days of treatment with diethylstilbestrol (0.106 mg/kg BW((3/4)) per day). In three of the normal children, diethylstilbestrol had no effect on the elemental balances; in two cases, a retention of Na was observed. In all seven Duchenne cases, diethylstilbestrol caused positive balances in N, P, Na, and K. Ethinyl estradiol (0.0106 mg/kg BW((3/4)) per day) produced positive N, P, Na, and K balances in all three Duchenne cases tested with this agent. The data show that exogenous HGH causes a catabolic effect in boys with Duchenne dystrophy. These patients are hyperresponsive to the anabolic effect of diethylstilbestrol. The latter phenomenon may reflect the inhibitory effect of estrogen upon the peripheral actions of these boys' endogenous HGH.

Adolescent↗
PubMed1971

The potential use of xylitol in glucose-6-phosphate dehydrogenase deficiency anemia.

NADP-linked xylitol dehydrogenase has been found to be present in human red blood cells. This enzyme activity is normal in most glucose-6-phosphate dehydrogenase (G6PD)-deficient red cells. Xylitol was explored as a potential agent for treatment of hemolysis in patients with G6PD-deficiency. Intracellular GSH (glutathione, reduced) was first converted to its oxidized form by incubation of the erythrocytes with acetylphenylhydrazine or by pretreatment with methyl phenyldiazenecarboxylate. The addition of 0.15 M xylitol was shown to be more effective than 0.15 M glucose in maintaining the levels of GSH in G6PD-deficient red cells during such oxidative challenge. Rabbit erythrocytes contain less activity of G6PD and glutathione reductase compared with the normal human adult values, but have an active xylitol dehydrogenase. The rabbit erythrocyte is sensitive to acetylphenylhydrazine and primaquine phosphate. In both in vivo and in vitro experiments, xylitol was found to partially prevent acetylphenylhydrazine induced acute hemolysis of the rabbit red cell and GSH content was found to be preserved. The intravenous injection of xylitol (0.5 g/kg body weight per 6 hr) for 6 days, seemed to be nontoxic to the animal. The results suggest that xylitol should be further investigated as an agent for the treatment of G6PD-deficient patients during acute hemolytic episodes.

Alcohol Oxidoreductases↗
PubMed1971

Observations on the responsiveness of human subjects to human growth hormone. Effects of endogenous growth hormone deficiency and myotinic dystrophy.

The effect of human growth hormone (HGH) on the N, P, Na, and K balance, and on the body weight (BW) of three groups of subjects was measured. In group I were nine cases (age 6-69) with HGH deficiency; in group II, eight cases (age 9-79) with normal endogenous HGH; in group III, four cases with myotonic dystrophy (age 45-51). After a 7 day control period, the hormone was administered for 7 days. Each subject was tested with three doses of HGH: dose A, 0.0168 U/kg BW(3/4) per day; dose B, 0.0532 U/kg BW(3/4) per day; dose C, 0.168 U/kg BW(3/4) per day. In group I, the responsiveness to HGH declined with age. Two subjects aged 6 yr responded to all three doses of HGH with positive balances in N, P, Na, and K and increases in BW. At ages 15-17, responses were obtained only to doses B and C in three cases, and only to dose C in two cases. Two subjects, aged 42 and 69, responded only to dose C. Not only did the threshold dose increase with age in group I, but the magnitude of the responses declined with age as well.Patients of group II were less responsive to all doses of HGH than were patients of group I at comparable age. None responded to dose A or dose B. All responded to dose C, but the increments in balances and in BW stimulated by this dose were only one-third to one-half as great as in HGH-deficient subjects of similar age. Three patients of group III responded to all three doses of HGH, and one responded to doses B and C. The responses were similar in magnitude to those in the 6-yr old HGH-deficient children, and greater than those in all other subjects studied. These data show that responsiveness to exogenous HGH rises with deficiency of endogenous HGH, and that individuals with myotonic dystrophy are hyperresponsive to exogenous HGH.

Adolescent↗
PubMed1970

Renal and intestinal hexose transport in familial glucose-galactose malabsorption.

Glucose transport by jejunal mucosa in vitro and kidney in vivo was investigated in a 3 yr old patient with congenital glucose-galactose malabsorption, her family, and 16 normal volunteers. Glucose transport by normal human jejunal mucosa was concentrative, saturable, sodium and energy dependent, and exhibited competitive inhibition. Biopsy specimens from six normal controls and an asymptomatic 5 yr old brother of the proband accumulated glucose to concentrations 16 times that in the incubation medium. The proband's mucosa was unable to concentrate glucose throughout a 60 min incubation period. Both of her parents and a half sister demonstrated impaired glucose transport. Their values fell between normal and those of the proband. Influx of glucose was impaired but efflux of glucose from the mucosa of these three heterozygotes was identical with that in three normal controls. A kinetic analysis indicated a reduced capacity (V(max)), but a normal affinity (K(m)) for glucose transport by their intestinal mucosa. All subjects accumulated fructose similarly.Renal glucose transport was investigated using renal glucose titration techniques. A partial defect in renal glucose reabsorption was found in the proband. Her brother's titration curve was similar to that of seven normal volunteers. We conclude that familial glucose-galactose malabsorption is inherited as an autosomal recessive trait, that heterozygotes for this disorder are detectable and demonstrate a reduced capacity for glucose transport, and that absent intestinal glucose transport is accompanied by partial impairment of renal glucose transport.

Adolescent↗
PubMedDate not supplied

Digoxin toxicity: an evaluation in current clinical practice.

BACKGROUND: Serum digoxin concentrations (SDCs) are frequently sampled before completion of drug distribution. If elevated, these concentrations may be misinterpreted, potentially leading to a misdiagnosis of digoxin toxicity. OBJECTIVES: To determine the frequency of elevated SDCs (>2.6 nmol/L [>2.0 ng/mL]) obtained at appropriate postdosing intervals and to evaluate the frequency of clinically defined digoxin toxicity in patients with elevated SDCs. METHODS: The medical records of adult patients with SDCs assayed at 5 general hospitals in North Carolina during a 3-month period (May 1 through July 31, 1996) were prospectively evaluated. Data on SDC, inpatient or outpatient status, and medical or surgical service were collected for all patients. Data on patient demographics, serum chemistry values, indication for digoxin treatment, clinical evidence of digoxin toxicity, and timing of the blood sample relative to administration of the last dose of digoxin were collected for patients with SDCs higher than 2.6 nmol/L (>2.0 ng/mL). RESULTS: Of 3434 SDCs assayed in 2009 patients, 320 (9.3%) were higher than 2.6 nmol/L (>2.0 ng/mL). Fifty-one (15.9%) of the 320 SDCs were drawn at 6 hours or less following a digoxin dose. Sampling time relative to the digoxin dose could not be determined in 70 (21.9%) of the 320 elevated SDCs, leaving 199 (62.2%) of 320 SDCs in 138 patients evaluable for digoxin toxicity. Eighty-three of the 138 patients had clinical evidence of digoxin toxicity for an overall incidence of 4.1%. CONCLUSIONS: Digoxin toxicity occurs less frequently than historically reported. Continued emphasis needs to be placed on obtaining appropriately timed SDCs.

Adult↗