Muscular temporomandibular disorder (TMD) is a common stress-related condition showing marked comorbidity with depression and fibromyalgia (FM), both of which are associated with dysregulation of cortisol secretion. We measured cortisol levels in 15 women with well-defined TMD and 15 matched controls by sampling blood at 10-minute intervals over 24 hours in a controlled environment. TMD patients showed markedly increased daytime cortisol levels 30% to 50% higher than those of controls (p = 0.0032) and a one-hour phase delay in the timing of maximum cortisol levels (p = 0.048). Increased activation of the stress hormone axis by conscious pain perception is a likely explanation, but the magnitude of the increase could indicate that pain in the facial region acts as a greater stimulus than pain elsewhere in the body.
1. "Thrombotic thrombocytopenic purpura" is the name which we propose for a rare but well-defined disorder which manifests itself clinically as an acute febrile illness and which is characterized by (a) petechiae and ecchymoses, thrombocytopenia, prolonged bleeding time and poor clot retraction, (b) by a severe anemia out of proportion to any observed blood loss, (c) by mild acholuric jaundice, hepato-splenomegaly, (d) by bizarre and intermittent mental and neurologic symptoms and signs, and (e) by a transient leukemoid reaction in the peripheral blood. 2. This clinical picture must be correlated with a remarkable histologic pattern, namely the presence of myriads of platelet thrombi in the small arterioles and capillaries of almost all organs of the body. 3. Eleven such cases have been described in the literature. One case of our own is added. 4. The clinical features of this disease are detailed and the differential diagnosis is discussed. It is emphasized that if the physician is familiar with this syndrome a correct clinical diagnosis may become readily possible.
1. By exposing hemoglobin solutions to an alkaline reagent at a pH of 12.7 it was found that normal pigment is completely denatured within one minute. Thus even small amounts of more resistant hemoglobins, which may also be present in the solution, can be readily detected. Fetal hemoglobin, which is alkali resistant, may remain demonstrable until the end of the second year of life. 2. Alkali resistant hemoglobins were regularly encountered in sickle cell anemia (but not in the trait), in the more fully developed Mediterranean syndromes, and in 1 out of 4 families with hereditary spherocytosis. In addition to these hereditary hemolytic disorders, abnormally denaturing hemoglobin fractions were observed in 3 instances of chronic aregenerative anemia, and, irregularly, in patients with untreated pernicious anemia, acute and chronic leukemia and myelophthisic anemia. All other kinds of anemias were found to have only normally denaturing pigments. 3. Three definite types of hemoglobin are identifiable at present by means of electrophoresis and denaturation. These have been designated as type N (normal adult), type F (fetal), and type S (sickle cell hemoglobin). The hypothesis is advanced that the resistant fraction in the hereditary hemolytic syndromes may represent a continued production of fetal pigment beyond the physiologic age limit and the appearance of the abnormal hemoglobins in the "acquired" disorders may indicate a reactivation of such a mechanism. The implications of such an assumption for the distribution of the various types of hemoglobin in sickling erythrocytes are discussed. 4. The diagnostic significance of the denaturation test and its limitations are outlined.
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