Factitious Munchausen's syndrome--a confession.
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Biomedical subjects
Publications and source records attributed to M D Feldman.
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Anti-adenosine antibodies were produced in rabbits immunized with N6-carboxymethyladenosine conjugated to methyl albumin. 125I-N6-Aminobenzyladenosine was synthesized and used as a high-specific-activity, high-affinity ligand. A radioimmunoassay (RIA) was developed that can detect 6.25 nM (312.5 fmol) of underivatized adenosine and cross-reacts less than 0.02% with adenine nucleotides and guanosine and not at all with 1 mM inosine. The sensitivity of the RIA can be increased to a detection limit of 0.125 nM (6.25 fmol) by derivitizing samples with benzyl bromide to form N6-benzyladenosine. The assay was adapted to an automated RIA procedure. Assay precision was increased by: (i) inhibiting slight adenosine deaminase activity present in anti-sera; (ii) treating buffers and albumin used in the RIA with charcoal to remove contaminating adenosine; and (iii) correcting for a small but variable component of immunoreactivity not attributable to adenosine. A second antibody prepared with a 2',3'-disuccinyladenosine-albumin conjugate was also found to detect some non-adenosine-mediated immunoreactivity in plasma samples. Immunointerference in human plasma was eliminated in samples treated with ZnSO4/Ba(OH)2 or partially purified over C18 Sep Paks to remove nucleotides and assayed after sample benzylation or succinylation. Human blood was mixed with a novel "stop" solution that was optimized to inhibit adenosine formation from AMP by greater than 99% and to inhibit adenosine uptake into red cells and degradation by greater than 94%. Human plasma/stop solution was assayed by RIA and HPLC with equivalent results.
Attempts to monitor coronary sinus adenosine as a clinical marker of myocardial ischemia in humans have been disappointing. Accordingly, procedures have been developed for detecting adenosine in blood collected from the human coronary sinus. Collection involves using a double-lumen metabolic catheter, which allows blood to be mixed with a stop solution at the catheter tip, thereby minimizing adenosine formation and degradation. A five-component stop solution almost completely arrests adenosine formation and degradation. Adenosine analysis is improved by using both boronate and C18 Sep-Pak columns to purify and concentrate adenosine in human plasma before HPLC. Plasma adenosine in the coronary sinus of patients with and without coronary artery disease, measured before and during peak atrial pacing, showed a twofold atrial pacing-induced increase in adenosine in the patients with coronary artery disease (n = 9, P less than 0.001) but no change in the patients with normal epicardial coronary arteries (n = 6). These preliminary results indicate that coronary sinus adenosine may provide an index of myocardial ischemia in patients with coronary artery disease.
The influence of contrast media on thrombus formation during percutaneous transluminal coronary angioplasty was assessed in 124 consecutive patients undergoing coronary angioplasty and receiving either ionic (n = 57) (Group I) or nonionic (n = 67) (Group II) contrast medium. The presence of thrombus was assessed by qualitative analysis of angiograms in identical pre- and postangioplasty projections by four observers who had no knowledge of other data. Quantitation of stenosis severity before and after angioplasty and qualitative analysis of lesion eccentricity and complexity and of the presence of dissection were also performed. Although the baseline clinical characteristics of the two groups (including presenting syndromes and procedural and angiographic variables) did not differ, more patients in Group II than Group I developed new thrombus during coronary angioplasty (18% vs. 4%, p less than 0.02). In particular, patients with a presenting syndrome of recent myocardial infarction or rest angina, or both, and patients with an eccentric coronary plaque were more likely to develop new thrombus if they received nonionic than if they received ionic contrast medium (p less than 0.05). Patients with new thrombus formation and patients with thrombus present both before and after angioplasty had a high incidence of acute procedural complications (36% and 23%, respectively). Patients in Groups I and II had a similar incidence of ischemic events during follow-up.
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The central goal of patients with factitious disorders is to receive medical care. Unnecessary diagnostic procedures and recurrent hospitalizations often ensue. We saw a 39-year-old man with a novel variation of this disorder: factitious cyclic hypersomnia, or the simulation of recurrent episodes of excessive sleep. This case highlights the observations that patients whose illnesses are simulated may have diverse symptoms, that no syndrome is immune to factitious imitation, and that attempts at treatment, though exceedingly challenging, are always contingent upon appropriate recognition.
We tested the hypothesis that intracellular Ca++ [( Ca++]i) overload underlies the diastolic dysfunction of patients with hypertrophic cardiomyopathy. Myocardial tissue was obtained at the time of surgery or transplantation from patients with hypertrophic cardiomyopathy and was compared with control myocardium obtained from patients without heart disease. The isometric contractions and electrophysiologic properties of all myocardial specimens were recorded by standard techniques and [Ca++]i was measured with the bioluminescent calcium indicator aequorin. In contrast to the controls, action potentials, Ca++ transients, and isometric contraction and relaxation were markedly prolonged in the hypertrophic myocardium, and the Ca++ transients consisted of two distinct components. At 38 degrees C and 1 Hz pacing frequency, a state of relative Ca++ overload appeared develop, which produced a rise in end-diastolic [Ca++]i, incomplete relaxation, and fusion of twitches with a resultant decrease in active tension development. We also found that drugs with increase [Ca++]i, such as digitalis, exacerbated these abnormalities, whereas drugs that lower [Ca++]i, such as verapamil, or agents that increase cyclic AMP, such as forskolin, prevented them. These results may explain why patients with hypertrophic cardiomyopathy tolerate tachycardia poorly, and may have important implications with regard to the pharmacologic treatment of patients with hypertrophic cardiomyopathy.
We studied post-extrasystolic potentiation (PESP) and frequency potentiation (FP) of human working myocardium isolated from the ventricles of 10 patients with end-stage heart failure (CHF) and 17 non-failing controls (CTL). The contractility index was peak isometric tension developed in vitro by trabeculae carneae (CTL n = 34, CHF n = 31); programmed electrical stimulation was used to initiate as well as alter the timing relationship of the contractile events. While holding constant the total number of contractions per unit of time, we compared the augmentation of contractile performance that occurred upon doubling the stimulation frequency (FP) to that of changing the stimulation pattern (PESP). In the CTL group we found that FP and PESP differed in their ability to augment cardiac contractile performance, PESP being more effective; 105 +/- 13% for PESP vs. 34 +/- 11% (mean +/- S.E.M.) for FP. In the CHF group, the inotropic response to PESP was similar to CTL; in contrast, the relative efficacy of FP (3 +/- 3%) compared to PESP (81 +/- 14%) was markedly diminished. Studies with positive inotropic agents revealed that the percent change in contractility induced by FP and PESP depends upon the relative inotropic state of the heart; however, the contractile response to PESP always equaled or exceeded those produced by clinically relevant concentrations of inotropic agents, particularly in CHF muscles. Agents that increase intracellular levels of adenosine 3',5'-cyclic monophosphate reversed the FP abnormalities seen in the CHF group, suggesting that deficient production of this second messenger in heart failure may cause the abnormal force-frequency relationship in failing myocardium. We conclude that the differential responses of myopathic muscle to PESP and FP may be caused by abnormal restitution processes during diastole. Our results suggest that PESP may be an effective therapeutic modality for patients with severe heart failure who have failed to adequately respond to inotropic drugs, and may serve as a useful indicator of cardiac contractile reserve in these patients.
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A twenty-eight-year-old man presented emergently after ingesting 800 mg of potassium cyanide in a suicide attempt. He survived only with intensive medical and psychiatric intervention, and went on to develop severe parkinsonian symptoms, including profound micrographia and hypersalivation. Bilateral, symmetrical basal ganglial abnormalities were demonstrated with magnetic resonance imaging. Survival following cyanide poisoning is rare; the clinical, radiologic, and neuropathologic sequelae in other documented cases are reviewed.
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Several studies have been performed in patients with a variety of myocardial diseases that have identified a prolongation of tau. However, it is not clear whether prolongation of tau represents abnormal myocardial physiology or the effect of excessive load associated with a particular disease process. Accordingly, we evaluate the effect on tau of an isolated decrease in preload induced by inferior vena cava occlusion before the appearance of reflex changes in six patients designated as normal by catheterization criteria. A computer-based digitization routine identified cardiac contractions in all patients early after inferior vena cava occlusion where left ventricular end-diastolic pressure decreased (18.3 +/- 6.3 to 9.3 +/- 5.8, p less than 0.05) while left ventricular systolic pressure (113.3 +/- 13.8 to 111.8 +/- 14.0, p = NS) and heart rate (66.0 +/- 10.0 to 65.9 +/- 10.3, p = NS) did not change. After this alteration in preload, no change in tau from baseline, as calculated by the logarithmic (TL), derivative (TD), or method of Mirsky (T1/2), was noted: TL, 47.4 +/- 6.5 to 44.6 +/- 7.6; TD, 39.3 +/- 8.1 to 39.8 +/- 8.4; T1/2, 33.0 +/- 4.0 to 31.8 +/- 4.6; all p = NS. The baseline pressure extrapolated from isovolumetric relaxation did not change in these preload beats compared with baseline (+4.26 +/- 6.20 to -0.80 +/- 4.87, p = NS). Subsequent beats were identified where left ventricular systolic pressure showed a numeric decrease compared with baseline (113.3 +/- 13.8 to 100.8 +/- 14.3, p = NS) despite no change in heart rate (66.0 +/- 10.0 to 66.8 +/- 10.5, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
Intramuscular hemangiomas make up less than 1% of all hemangiomas [1]. These invasive and aggressive lesions appear to have a predilection for large muscle masses. They can be strikingly aggressive in the head and neck, and persistence despite radical treatment is common. Spontaneous resolution in adults to our knowledge has not been reported in the literature. We present a case report of an invasive intramuscular hemangioma involving the parotid gland, the masseter and pterygoid muscles, and the infratemporal fossa after local resection of an apparently isolated lesion of the lip and the submandibular triangle. We describe a detailed course of treatment and review the literature.
A safe, effective method for securing autologous and alloplastic implants would benefit modern surgery substantially. We studied the effects of a new autologous fibrin tissue adhesive with various alloplastic implants and ear cartilage. Twelve rabbits had Proplast (a woven combination of Teflon and organic fibers), Silastic, Supramid polyfilament surgical sheeting, and ear cartilage implanted. One side of each animal had implants secured with tissue adhesive. The other, control side had identical implants placed in "subcutaneous tunnels." The tissue adhesive was biodegradable and produced no apparent toxic reaction, infection, or foreign-body reaction. It did not adhere to Silastic, but bound to the other implants. Glued implants had no more clinical or histologic evidence of inflammation than controls. Autologous fibrin tissue adhesive seems to be promising as a safe, biologic bonding material for securing certain alloplastic and autologous implants.