Biomedical subjects
P Atkins
Publications and source records attributed to P Atkins.
Drug therapy for hyperthyroidism in pregnancy: safety issues for mother and fetus.
Hyperthyroidism (thyrotoxicosis) in pregnancy and the child bearing years is usually attributable to Graves' disease. This is an autoimmune condition in which thyroid-stimulating immunoglobulins (TSI) cause hyperthyroidism. As a rule, pregnancy complicates the management of hyperthyroidism, rather than vice versa. However, patients who remain thyrotoxic during pregnancy are at increased risk of maternal and fetal complications, particularly miscarriage and stillbirth. Therefore, bodyweight loss, eye signs and a bruit over the thyroid gland in a pregnant woman warrant thyroid investigation. Investigations should include measurement of serum free thyroid hormone levels [free thyroxine (T4) and free triiodothyronine (T3)] rather than total T4 and T3 levels, because total T4 and T3 levels may be raised in euthyroid pregnancies due to the presence of increased levels of thyroxine binding globulin (TBG). By 20 weeks' gestational age, the fetal thyroid is fully responsive to TSI and to antithyroid drugs. Maternal T4 and T3 and thyrotropin pass across the placenta in small and decreasing amounts as gestation progresses, but thyrotropin releasing hormone, TSI, antithyroid drugs, iodides and beta-blockers are readily transferred to the fetus from the mother. Hyperthyroidism is usually treated throughout pregnancy with an antithyroid drug, preferably propylthiouracil. The smallest dose which controls the disease is given with careful monitoring of free T4 and T3 levels to minimise the risk of fetal hypothyroidism and goitre. Bilateral subtotal thyroidectomy may be an option for a small number of patients with hyperthyroidism in pregnancy.
Science and religion: rack or featherbed--the uncomfortable supremacy of science
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Chlorofluorocarbon to hydrofluoroalkane formulations: an industry perspective.
The medications prescribed to treat asthma are provided in a range of delivery systems, designed to give patients a choice in how they take their inhaled medication. These include the mainstay of asthma therapy, the metered dose inhaler (MDI), and the breath-operated inhalers. One of the major challenges that all the leading companies in the respiratory area have faced in recent years is the environmental effects of chlorofluorocarbons. The pharmaceutical industry recognized the need to reformulate MDI products containing chlorofluorocarbons, and a number of companies began to develop alternatives in the late 1980s. To help facilitate this change in products, an industry consortium was formed (International Pharmaceutical Aerosol Consortium), and this has managed many of the overarching issues. After an extensive search was conducted, the most suitable alternatives were the hydrofluoroalkanes, which do not contain chlorine, are ozone friendly, and have lower global-warming potentials than the chlorofluorocarbons that they are replacing. To date it is estimated that the industry has invested over $1.0 billion ($US) on global research and development efforts. The first countries to launch the nonchlorofluorocarbon MDIs have been in Europe, and now salbutamol and 2 inhaled steroids are widely available across Europe in their nonchlorofluorocarbon form. Clinical testing has been extensive, and patient acceptance of the new products has proved to be high. Maintaining the smooth progress of the global transition is important, and continued dialogue between all key stakeholders should ensure success in this area.
Lateralization of parathyroid adenomas by intra-operative parathormone estimation.
A simple method for intra-operative lateralization of parathyroid adenomas by venous sampling for intact parathormone (PTH [1-84] is described. After induction of anaesthesia, percutaneous right and left internal jugular and arm vein PTH [1-84] was estimated within 30 minutes by a modification of the Allegro PTH [1-84] assay. Twenty-three patients with primary hyperparathyroidism due to adenoma were explored, 21 with one adenoma and two with two adenomas. Intraoperative jugular PTH [1-84] correctly lateralized 16 (76%) of the single adenomas (P < 0.006), and the side of the neck with the greater weight of parathyroid adenoma in 18 (78%) patients (P < 0.004). Two patients with previous failed neck explorations were correctly lateralized. Thallium/technetium scanning lateralized 41%, significantly less then jugular PTH [1-84] (P < 0.02). Adenomas of 1 g or less were more likely to be lateralized by PTH [1-84] than thallium/technetium scanning (P < 0.05). Intraoperative jugular PTH [1-84] was superior to thallium/technetium scanning for parathyroid adenoma lateralization.
Drug delivery to the respiratory tract and drug dosimetry.
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Comparison of cytosolic calcium shifts, superoxide generation, and lactoferrin secretion in the neutrophils of atopics and nonatopics.
We previously found that platelet-activating factor (PAF) stimulated greater lactoferrin secretion by neutrophils of atopics than nonatopics. To help understand underlying mechanisms, we compared agonist-stimulated lactoferrin secretion with another response, superoxide generation, to determine whether there is a global alteration in the reactivity of atopic neutrophils to these stimuli. We also determined Ca2+ mobilization in such neutrophils because such mobilization is a signaling pathway for both superoxide generation and granule content exocytosis. Although PAF again stimulated greater lactoferrin secretion in atopic than in nonatopic neutrophils, the peak superoxide secretion and cytosolic Ca2+ mobilization were not significantly different in atopics and nonatopics. Leukotriene B4-induced superoxide secretion and cytosolic Ca2+ shifts were also similar in atopics and nonatopics. These findings suggest that (1) the enhanced PAF-induced lactoferrin secretion in atopic neutrophils is not a reflection of greater PAF binding or broad-based cell hyperreactivity and (2) a selective signaling pathway in atopic neutrophils may be responsible for the enhanced lactoferrin secretion. These findings may be relevant to in vivo events because we have found increased PAF and lactoferrin release in skin chambers overlying immunoglobulin E-mediated human skin reactions.
Iodine therapy for thyroidectomy patients exhibiting high thyroid-stimulating hormone values: a randomised study.
After thyroidectomy there is an appreciable incidence of hypothyroidism as judged by FT4I estimates. Pharmacological doses of iodine (10-300 mg/day) usually suppress, whereas physiological doses of iodine (< 5 mg/day) have been reported to both decrease and increase thyroid function. The value of iodine supplementation in preventing post-thyroidectomy hypothyroidism was assessed in a prospective randomised trial. A series of 55 patients with a TSH > 6 mU/l 1 month after bilateral subtotal thyroidectomy or unilateral lobectomy for benign disease were randomised to receive either chloroform water 5 ml/day (placebo) or chloroform water 5 ml/day with 1 mg of iodine to be taken for 20 weeks. With placebo, 62% of bilateral subtotal thyroidectomies were euthyroid at 6 months on no thyroid replacement, while with iodine all were hypothyroid as judged by FT4I. After bilateral subtotal thyroidectomy, the recovery of remnant function is delayed by an iodine supplement of 1 mg/day.
The kallikrein-kinin system in inflammation.
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Pathways of kinin formation and role in allergic diseases.
We have developed new assays for the assessment of the plasma kinin forming system which have increased sensitivity and specificity. We utilize double-antibody ELISA assays for quantitation of complexes of activated Hageman factor-C1 inhibitor, kallikrein-C1 inhibitor, and kallikrein-alpha 2-macroglobulin which reflect activation of each enzyme. The fraction of cleaved high-molecular-weight kininogen is determined by immunoblotting using a monoclonal antibody to the light chain, and bradykinin is determined by radioimmunoassay. Activation of the Hageman factor-dependent pathway of kinin formation can occur when plasma is in contact with initiating surfaces or when C1 inhibitor function is diminished. The latter mechanism can occur in hereditary angioedema, in which the protein is absent or dysfunctional, or when plasma is diluted so that the effect of inhibitors is diminished and Hageman factor autoactivation is facilitated. Thus apparent "spontaneous" generation of bradykinin is seen upon incubation of plasma of hereditary angioedema patients under conditions in which normal plasma is unaffected. Studies of late-phase reactions have used a cutaneous model in which induced blisters are unroofed and challenged with antigen or buffer control using chambers which can be changed hourly. A time course of mediator release is obtained by assay of the blister fluids. Whereas most histamine is released during the first half hour, significantly elevated levels of activated Hageman factor and kallikrein complexes with C1 inactivator are seen in antigen-challenged sites between 4 and 6 hr. The presence of such complexes correlated with the presence of late-phase reactions rather than the histamine values or the magnitude of the immediate reaction. Although late-phase reactions are characterized by cellular infiltration, release of a variety of inflammatory low-molecular-weight mediators, and deposition of fibrin, activation of the Hageman factor-dependent pathway of kinin formation is also likely to be contributory.
Respite care: a partnership between a Veterans Administration nursing home and families to care for frail elders at home.
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Psychiatric patients who marry each other.
Health care workers often advise patients with chronic psychiatric disability against marrying each other. A survey of a group of such marriages revealed no evidence of the predicted ill-effects, but rather a trend towards improvement after the marriage. There is a discrepancy between professional expectations and actual outcome of these marriages.
Identity formation: pregnant and non-pregnant adolescents.
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The value of phenformin and ethyloestrenol in the prevention of deep venous thrombosis in patients undergoing surgery.
The effect of phenformin and ethyloestrenol on the incidence of post-operative deep venous thrombosis was studied in 314 surgical patients in a double-blind randomised trial. Although the laboratory tests suggested that the regime produced an increase in activators of the fibrinolytic system, the drugs used did not lower the incidence of post-operative deep venous thrombosis. Possible explanations of this paradox are advanced.
Respiratory nursing: a community approach.
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Motility of gastric tubes.
In gastric tubes interposed between small bowel a clear wave pattern was found, differing markedly from the bowl above and below. The gastric tube appears to be not an inert conduit since it continues to exhibit automatic rhythmic contraction. The possibility of slowing intestinal transit by the interposition of an antiperistaltic gastric tube seems to be supported by the demonstration of regular contraction.
Acquired angioedema with lymphoproliferative disorder: association of C1 inhibitor deficiency with cellular abnormality.
A patient with a lymphoproliferative disorder, angioedema, and an acquired deficiency of the inhibitor of the activated first component of complement was studied. The patient's complement profile revealed depletion of the first component of complement, which has not been seen in angioedema of the hereditary type. There was no evidence for C1-depleting activity in the patient's plasma. The majority of the patient's peripheral blood mononuclear cells resembled B cells in their memebrane receptor properties and in that they carried easily detectable immunoglobulin, predominantly IgM. However, these cells were unusual in that they phagocytosed both latex particles and C3-coated erythrocytes. Morphological study of the cells infiltrating the patient's lung revealed immature, atypical, and plasmacytoid lymphocytes and immunoblasts. Both the patient's peripheral blood mononuclear cells and a suspension of cells from the pulmonary infiltrate were capable of depleting the first component of complement and its inhibitor from homologous plasma. Normal ABO-compatible cells did not possess this property. The data suggested that the patient's abnormal lymphoid cells may have interacted with the complement system to produce a biochemical defect and a clinical syndrome closely resembling angioedema of the hereditary type.
Letter: Diagnostic criteria in the 125i-fibrinogen test.
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