Obesity, estrogen production, and tumor estrogen receptors in women with carcinoma of the breast.

The poor prognosis of obese women with carcinoma of the breast has yet to find a satisfactory explanation. It is suspected that the hormonal milieu of these patients may favor tumor growth. This investigation explored the relationship between obesity, urinary estrogen excretion, and tumor estrogen receptors (ER) in women treated with mastectomy for carcinoma of the breast. The ER levels determined from the primary cancers of 129 women treated with mastectomy were compared with the obesity index (O.I.) of these patients, i.e., weight in pounds/height in inches. In addition, 24-hour total urinary estrogen determinations were performed in 30 postmenopausal women and compared with their O.I. and ER. A weak direct correlation was found between ER and O.I. in postmenopausal women. The urinary estrogens of postmenopausal women were correlated directly with obesity index, but no relationship could be established between urinary estrogens and the ER content of breast cancers. It is concluded that the excess estrogen production of obese women may be responsible for their poor prognosis by promoting tumor growth. The high tumor ER concentrations associated with obesity suggest a high frequency of hormonally sensitive tumors.

Not all bite marks are associated with abuse, sexual activities, or homicides: a case study of a self-inflicted bite mark.

A case of self-inflicted bite mark during an episode of myocardial ischemia is presented. Using current bite mark identification techniques, the bite mark was shown to be self-inflicted. Self-biting may be an emotional response to pain or a type of counterirritation to alleviate pain. The recognition and documentation of this unusual case of a self-inflicted bite mark was due to the cooperation of the forensic pathologist and forensic odontologist.

Death as a result of asthma in Wayne County Medical Examiner cases, 1975-1987.

All deaths ascribed to asthma in the 5-to-40-year age group at the Wayne County Medical Examiners' Office were reviewed from 1975 to 1987 inclusive. Fifty-eight deaths were attributed solely to asthma, and the annual number increased fivefold in the 1980s to a rate of approximately 0.5 per 100,000 per year when extrapolated to the Wayne County population. Blacks were overrepresented to double their proportion in the general population. Almost all cases were known asthmatics, and many had received previous emergency care. Most fatalities occurred at night and did not demonstrate any seasonal variation. The onset of the fatal attack was apparently very rapid in most cases, with many engaged in routine activities and few surviving any length of time in hospital or having sought treatment earlier. Our data reveal a significant increase in sudden death in previously well asthmatics in Wayne County in the 1980s. Similar increases in deaths as a result of asthma have been noted previously in other countries for reasons that remain unclear.

Laboratory investigation of deaths due to anaphylaxis.

To establish a useful laboratory protocol to investigate possible cases of fatal anaphylaxis, we measured mast-cell-derived tryptase levels and allergen-specific immunoglobulin E (IgE) antibody levels in sera obtained prior to or within 24 h after death from 19 anaphylaxis victims. Elevated serum tryptase levels (range = 12 ng/mL to 150 micrograms/mL) were found in nine of nine Hymenoptera sting fatalities, six of eight food-induced fatalities, and two of two reactions to diagnostic therapeutic agents. Tryptase levels were normal (less than 10 ng/mL) in 57 sequential sera obtained postmortem from six control patients. Tryptase could not be measured in pleural or pericardial fluids for technical reasons. Serum IgE antibodies were elevated in five of the nine Hymenoptera sting fatalities and in eight of the eight fatal food reactions; assays were unavailable for the two diagnostic/therapeutic agents. If elevated, the victim's serum IgE antibodies to food could be used to identify allergens in uneaten portions of foods consumed shortly before the anaphylactic event. IgE antibodies were moderately stable during storage in a variety of anticoagulants at room temperature for up to 11 weeks. Elevated mast-cell-derived tryptase levels in postmortem sera reflect antemortem mast cell activation and may be used as a marker for fatal anaphylaxis. If assays are available for IgE antibodies to relevant allergens, such assays provide evidence for antemortem sensitization; these assays may be modified to identify allergens in foods consumed by victims of food-induced anaphylaxis.

Differential calcification of cusps and aortic wall of failed stented porcine bioprosthetic valves.

In this study, we examined separately calcification of cusps (C) and associated aortic wall (AW) of 38 (13 aortic and 25 mitral) porcine bioprosthetic heart valves explanted from 37 patients (ages 25-80 years, mean 59) for structural dysfunction, following 54-210 months (mean 125 months aortic, 119 months mitral). Valves were sectioned into C and corresponding AW components; calcification was assessed by atomic absorption spectroscopy for calcium and histologic examination. Overall, AW calcification was half that of C (33.3 +/- 5.4 vs. 65.9 +/- 6.3 microg/mg, mean +/- standard error of the mean respectively, p = 0.002). Correlation of calcification in individual C/AW pairs was weak (r2 = 0.34). Calcification in C was nodular, largely in the valve fibrosa, but AW calcification predominated in the cells between elastic lamellae; large nodules were sparse. We conclude that since AW calcification in these failed porcine valves was neither prominent nor clinically significant, this process should rarely if ever be a limiting factor in the function of stented porcine valves, and that development of anticalcification therapies directed toward the AW of stented valves should be of low priority. However, in stent-free valves, the AW is not covered by prosthetic material, and the level of calcification could be greater and more likely to cause clinical problems through stiffening, embolism, and/or protrusion into the lumen of calcific masses.

Fatal food-induced anaphylaxis.

Fatal food-induced anaphylaxis is rarely reported. In 16 months, we identified seven such cases involving five males and two females, aged 11 to 43 years. All victims were atopic with multiple prior anaphylactic episodes after ingestion of the incriminated food (peanut, four; pecan, one; crab, one; fish, one). In six cases the allergenic food was ingested away from home. Factors contributing to the severity of individual reactions included denial of symptoms, concomitant intake of alcohol, reliance on oral antihistamines alone to treat symptoms, and adrenal suppression by chronic glucocorticoid therapy for coexisting asthma. In no case was epinephrine administered immediately after onset of symptoms. Premortem or postmortem serum samples were available from six victims; in each case elevated levels of IgE antibodies to the incriminated food were demonstrated. Food-sensitive individuals must self-administer epinephrine promptly at the first sign of systemic reaction. Emergency care providers should be aware of cricothyrotomy as a life-saving procedure.