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Biomedical subjects

D A Hoffman

Publications and source records attributed to D A Hoffman.

36 records · Page 2Linked to original sources
PubMed1984

Relationship of thyroid disease and use of thyroid supplements to breast cancer risk.

An interview study of 1362 breast cancer cases and 1250 controls identified through a multi-center screening program allowed evaluation of effects of thyroid disease and supplementation on breast cancer risk. A previous diagnosis of treated thyroid disease was not associated with an excess risk (RR = 1.0), nor were any specific diagnoses, including hypothyroidism, hyperthyroidism, or goiter. Although based on limited numbers, women with untreated hypothyroidism or goiter had a significantly reduced risk of breast cancer (RR = 0.3, 95% CI 0.1-0.7). Thyroid supplementation for non-disease reasons (primarily weight loss and fertility problems) was associated with a slight elevation in breast cancer risk (RR = 1.2, 95% CI 0.9-1.7), but patterns of risk by duration and latency generally failed to provide evidence of causality. Elevated risks were noted among women who received thyroid medications for fertility problems (RR = 4.2) and among those with a family history of breast cancer (RR = 2.6) or a late age at first childbirth (RR = 2.4), possibly indicating an hormonal interaction.

Adult↗
PubMed1984

Multiple primary breast and thyroid cancer.

The occurrence of breast and thyroid multiple primary cancers was evaluated using data from the Connecticut Tumor Registry. The study population consisted of 1618 women with primary thyroid cancer and 39,194 women with primary breast cancer diagnosed between 1935 and 1978. Thirty-four thyroid cancer patients subsequently developed breast cancer and 24 breast cancer patients later had thyroid cancer. A significantly elevated risk of thyroid cancer following breast cancer (SIR = 1.68) and breast cancer following thyroid cancer (SIR = 1.89) was demonstrated. The finding was even more notable when compared with the risks obtained for other sites. The elevated risk was particularly evident in women under 40 years of age at time of diagnosis of the first cancer. Analysis by histologic type revealed that the highest risk of second primary breast cancer was found among patients with follicular or mixed papillary-follicular thyroid cancer. Women under age 40 with follicular carcinoma had a 10-fold risk of developing breast cancer (4 observed, 0.4 expected). An enhanced risk of second primary tumours was evident for the entire period after treatment of the first primary, although it was highest within one year after diagnosis of the first primary. This may be due to the close medical surveillance of cancer patients which would increase early diagnosis of second tumours. Our findings suggest that breast and thyroid cancer may share common aetiologic features.

Adult↗
PubMed1983

Profound hyperglycemia and metabolic acidosis after verapamil overdose.

Verapamil, a potent calcium antagonist, possesses varied systemic effects, including smooth muscle relaxation leading to both peripheral and coronary artery vasodilation, slowed atrioventricular nodal conduction and decreased insulin release from the pancreatic B cells. Reports concerning the effects of acute intoxication with verapamil are scarce. A case is presented of a 22 year old woman who developed profound hyperglycemia and metabolic acidosis after the inadvertent overdose of thirty 80 mg tablets (2,400 mg) of verapamil. This case illustrates the need for physicians to be aware of verapamil's inhibitory effects on insulin release and to exercise special care when prescribing verapamil in patients with preexisting diabetes mellitus.

Acidosis↗
PubMed1983

Second primary malignancies following salivary gland cancers.

Four hundred and fifteen males and 367 females who had invasive malignant tumours of the salivary glands as their first cancer diagnosed in Connecticut between 1935 and 1978 were identified and followed 2342 and 2868 person-years respectively. Overall a slight excess of second primary cancers (relative risk 1.35) was observed. Significant excesses were noted for respiratory cancers in males (relative risk 2.8) and for ovarian cancer (relative risk 5.3) but not breast cancer (relative risk 1.3) in women. Possible reasons for excesses at these sites are discussed, but it seems most likely they are related to small number variation.

Adenocarcinoma↗
PubMed1983

Breast cancer following iodine-131 therapy for hyperthyroidism.

A retrospective cohort study of women treated for hyperthyroidism at the Mayo Clinic between 1946 and 1964 was conducted to determine if 1,005 women treated with iodine-131 (131I) were at increased risk of breast cancer compared with 2,141 women traced, and a response (death certificate or questionnaire) was received for 99% of the traced women. The average duration of follow-up was 15 years for the 131I-treated women and 21 years for women treated surgically. No increased risk of breast cancer was observed in the 131I-treated women (adjusted relative risk = 0.8). No patterns were found of increased breast cancer risk by age at first treatment, by time since treatment, or by total exposure to 131I. Failure to detect an increased risk of breast cancer in the 131I-treated women was attributed to the moderately low doses from 131I therapy and the relatively small number of exposed women. The study also failed to find any increased risk of breast cancer associated with hyperthyroidism.

Adult↗
PubMed1982

Cancer incidence following treatment of hyperthyroidism.

A retrospective cohort study of women treated for hyperthyroidism at the Mayo Clinic was conducted to evaluate the risk of cancer according to type of therapy. One or more years after the start of treatment, there were 105 cases of cancer observed among 1005 women treated with radioiodine (131I) and 247 cases among 2141 women treated with surgery. No difference was observed between the two study groups for total cancer incidence (RR = 1.0), breast cancer (RR = 0.8), or leukaemia (RR = 0.6). Although based on small numbers of cases, an elevated risk of cancer was observed in organs that concentrate 131I (salivary glands, digestive tract, kidney and bladder) (RR = 1.8). While the findings are suggestive, they indicate the need for larger surveys to evaluate the carcinogenic potential of 131I.

Age Factors↗
PubMed1982

Mortality in women treated for hyperthyroidism.

To evaluate the late effects of exposure to radioiodine (131I), a retrospective cohort study was conducted of women treated for hyperthyroidism at the Mayo Clinic, Rochester, Minnesota, from 1946 through 1964. Cause of death was determined in 1005 women treated with 131I and in 2141 women surgically treated. No increased risk of total mortality was observed for the 131I-treated women (relative risk = 1.0). There were no increased risks for the major causes of mortality (cancer, cardiovascular-renal disease or cerebrovascular lesions) in the 131I-treated women; in addition, there were no increased risks for site-specific cancer mortality. Several hypotheses are presented to suggest reasons for the lack of an association between 131I exposure and increased cancer mortality.

Adult↗
PubMedDate not supplied

Cancer mortality following treatment for adult hyperthyroidism. Cooperative Thyrotoxicosis Therapy Follow-up Study Group.

CONTEXT: High-dose iodine 131 is the treatment of choice in the United States for most adults with hyperthyroid disease. Although there is little evidence to link therapeutic (131)I to the development of cancer, its extensive medical use indicates the need for additional evaluation. OBJECTIVE: To evaluate cancer mortality among hyperthyroid patients, particularly after (131)I treatment. DESIGN: A retrospective cohort study. SETTING: Twenty-five clinics in the United States and 1 clinic in England. PATIENTS: A total of 35 593 hyperthyroid patients treated between 1946 and 1964 in the original Cooperative Thyrotoxicosis Therapy Follow-up Study; 91 % had Graves disease, 79% were female, and 65% were treated with (131)I. MAIN OUTCOME MEASURE: Standardized cancer mortality ratios (SMRs) after 3 treatment modalities for hyperthyroidism. RESULTS: Of the study cohort, 50.5% had died by the end of follow-up in December 1990. The total number of cancer deaths was close to that expected based on mortality rates in the general population (2950 vs 2857.6), but there was a small excess of mortality from cancers of the lung, breast, kidney, and thyroid, and a deficit of deaths from cancers of the uterus and the prostate gland. Patients with toxic nodular goiter had an SMR of 1.16 (95% confidence interval [CI], 1.03-1.30). More than 1 year after treatment, an increased risk of cancer mortality was seen among patients treated exclusively with antithyroid drugs (SMR, 1.31; 95% CI, 1.06-1.60). Radioactive iodine was not linked to total cancer deaths (SMR, 1.02; 95% CI, 0.98-1.07) or to any specific cancer with the exception of thyroid cancer (SMR, 3.94; 95% CI, 2.52-5.86). CONCLUSIONS: Neither hyperthyroidism nor (131)I treatment resulted in a significantly increased risk of total cancer mortality. While there was an elevated risk of thyroid cancer mortality following (131)I treatment, in absolute terms the excess number of deaths was small, and the underlying thyroid disease appeared to play a role. Overall, (131)I appears to be a safe therapy for hyperthyroidism.

Adult↗
PubMedDate not supplied

Role of an A-type K+ conductance in the back-propagation of action potentials in the dendrites of hippocampal pyramidal neurons.

Action potentials elicited in the axon actively back-propagate into the dendritic tree. During this process their amplitudes can be modulated by internal and external factors. We used a compartmental model of a hippocampal CA1 pyramidal neuron to illustrate how this modulation could depend on (1) the properties of an A-type K+ conductance that is expressed at high density in hippocampal dendrites and (2) the relative timing of synaptic activation. The simulations suggest that the time relationship between pre- and postsynaptic activity could help regulate the amplitude of back-propagating action potentials, especially in the distal portion of the dendritic tree.

Action Potentials↗
PubMedDate not supplied

Effect of low-level body burdens of lead on the mental development of children: limitations of meta-analysis in a review of longitudinal data.

The effect of low-level body burdens of lead on the intelligence of children, as measured by intelligence quotient (IQ), was assessed. We reviewed 35 reports from five longitudinal studies conducted in the United States and Australia. In each of these studies, infants were followed for 58 mo or less. The study populations consisted of low- and middle-socioeconomic-class infants who had low-level exposure to environmental lead. Blood-lead levels were measured in a standard fashion at various times, beginning in the prenatal period, and intelligence was first measured at 6 mo of age and was followed by subsequent assessments. Studies were assessed for quality by a review panel blinded to the identity of the investigators and their affiliations. Efforts were made to pool the data with meta-analytic techniques, but efforts were unsuccessful because the methods used to analyze and report data were inconsistent. Inconsistencies were as follows: (a) there were few instances in which IQ and blood-lead levels were measured at comparable times in different studies; (b) incompatibilities existed among the studies, including differences in independent variables, data transformations, and statistical parameters reported; (c) results conflicted when measurement intervals were comparable (i.e., heterogeneity); (d) patterns of regression and correlation coefficients were inconsistent; and (e) data were insufficient to interconvert the parameters reported. Consequently, definitive conclusions regarding the effect of low-level body burdens of lead on IQ could not be determined from the longitudinal data. Examination of the weight of the evidence from this and other studies, however, suggests an adverse relationship of lead on the intelligence of children.

Bias↗