Cases reported "Hypothyroidism"

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1/11. pancytopenia induced by hypothermia.

    hypothermia has been demonstrated to induce pancytopenia in animals, but whether this association exists in humans is unknown. The authors report the case of an 8-year-old girl in whom hypothermia (temperature 33 degrees C-35 degrees C) is the cause of pancytopenia. The patient developed thermoregulatory dysfunction subsequent to surgical resection of a craniopharyngioma. Her recurrent cytopenias could not be explained by any etiology except chronic hypothermia. The pancytopenia improved upon rewarming the patient to a temperature of 36 degrees C. This association between hypothermia and pancytopenia has rarely been reported in humans and may be underdiagnosed especially in cases of transient or milder presentations. The authors recommend careful hematologic monitoring of patients with thermoregulatory dysfunction.
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2/11. Reversible alterations in myocardial gene expression in a young man with dilated cardiomyopathy and hypothyroidism.

    Thyroid hormone effects on myocardial gene expression have been well defined in animal models, but their relationship to the pathogenesis of cardiac dysfunction in hypothyroid humans has been uncertain. We evaluated a profoundly hypothyroid young man with dilated cardiomyopathy. Before and during 9 months of thyroxine therapy, serial assessment of myocardial performance documented substantial improvements in the left ventricular ejection fraction (16-37%), left ventricular end-diastolic diameter (7.8-5.9 cm), and cardiac index (1.4-2.7 liters.min-1.m-2). Steady-state levels of mRNAs encoding selected cardiac proteins were measured in biopsy samples obtained before and after thyroxine replacement. In comparison with myocardium from nonfailing control hearts, this patient's pretreatment alpha-myosin heavy-chain mRNA level was substantially lower, the atrial natriuretic factor mRNA level was markedly elevated, and the phospholamban mRNA level was decreased. All of these derangements were reversed 9 months after restoration of euthyroidism. These observations in an unusual patient with profound myxedema and cardiac dilatation permit correlation between the reversible changes in myocardial function and steady-state mRNA levels in a cardiomyopathy. They suggest that alterations in gene expression in the dilated myopathic heart may be correctable when a treatable cause is identified.
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3/11. Suppression of thyrotropin by morphine in a severely stressed patient.

    Opiates suppress TSH in experimental animals but are reported to increase TSH in human subjects. We describe a patient in severe pain treated with morphine, whose previously normal TSH fell to a level usually associated with hyperthyroidism. After returning to a normal concentration, TSH again decreased with morphine administration. This suggests that, in contrast to the stimulation of TSH secretion that has been reported in unstressed experimental subjects, morphine can inhibit TSH secretion during stress in man as it does in experimental animals. This observation is consistent with the known sensitization of opiate receptors by stress. Consideration should be given to the possibility that severe suppression of TSH by opiates in stressed patients may induce clinically significant central hypothyroidism.
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4/11. Pharyngeal fistulas in postoperative hypothyroid patients.

    hypothyroidism is a well-recognized complication of combined treatment for head and neck cancer. We discuss four patients who developed pharyngeal fistulas after total laryngectomy and preoperative (one patient) or postoperative (three patients) radiation therapy. The fistulas were refractory to conservative and surgical repair. Once the existence of hypothyroidism was established, immediate substitution therapy resulted in rapid healing of the fistulas and marked improvement of the patients' general condition. Few clinical reports exist on postoperative hypothyroidism and wound healing complications. Experimental work shows delay and impairment of wound healing in hypothyroid animals as opposed to hyperthyroid ones, in which wound healing was accelerated. Suspicion is warranted in patients after treatment for head and neck cancer when they exhibit even minimal symptoms of hypothyroidism or develop postoperative complications refractory to conservative treatment.
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5/11. Spontaneous ovarian hyperstimulation syndrome associated with hypothyroidism.

    A causal link between hypothyroidism and spontaneously occurring ovarian hyperstimulation syndrome is suggested by analysis of data from a patient with myxedema and review of data from animal research.
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6/11. Factitious elevation of thyrotropin in a new ultrasensitive assay: implications for the use of monoclonal antibodies in "sandwich" immunoassay.

    Three patients who had falsely elevated serum TSH concentrations (initial values, 30.5, 74, and greater than 50 mU/L) in a mouse monoclonal immunoradiometric assay are reported. Two patients were treated for hypothyroidism inappropriately, and one underwent unnecessary diagnostic testing. Immunoaffinity chromatography of serum from one patient indicated that the serum TSH level was truly low. Addition of mouse serum or immunoglobulin g (IgG) or absorption of patient serum with solid phase-bound mouse IgG-1 reduced the TSH content in the serum of the three patients to undetectable levels. Blocking studies revealed that all patients had antibodies directed at mouse IgG-1, the subclass of mouse antibody present in the assay kit. The serum of one patient who had autoimmune disease with elevated serum Igs had much broader species cross-reactivity than that of another patient who had known exposure to rats and mice. We hypothesize that such antimouse antibodies can arise either from endogenous autoimmunity or exogenous animal exposure. serum TSH elevations also were found when the serum samples were tested in other mouse monoclonal immunoassays, underscoring the fact that antibody interference can potentially affect many assays used in endocrinology and other areas of medicine to make major diagnostic and therapeutic decisions. Clinicians must be aware of such interactions; relatively simple laboratory maneuvers can differentiate true from false results in assays of this type.
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7/11. Severe alcoholic hepatitis in a hypothyroid patient.

    A treated hypothyroid patient with chronic alcoholism stopped replacement therapy with the onset of heavy drinking. The resulting hypothyroid state did not protect against an eventually fatal termination of acute alcoholic liver disease. Unlike the controlled trials of anti-thyroid therapy for alcoholic hepatitis, this experience simulates the animal experiments suggesting a hypermetabolic mechanism in alcohol hepatotoxicity. The outcome in this instance, however, is not supportive of this hypothesis.
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8/11. Suppression of cell-mediated immunity in hypothyroidism.

    A 71-year-old man had severe hypothyroidism, chronic autoimmune thyroiditis, and bacteremia due to edwardsiella tarda. review of the literature identified the hypothesis that E tarda infections may occur more frequently in immunocompromised patients. Previous animal studies have shown decreases in lymphocyte function during hypothyroidism, with return of normal lymphocyte function during euthyroid states. Therefore, lymphocyte transformation studies were obtained, demonstrating severe decreases in our patient's lymphocyte function. Except for chronic autoimmune thyroiditis, other immune system abnormalities were excluded. Serial lymphocyte transformation studies showed gradual improvement in lymphocyte function during gradual return to euthyroid state. Possible pathophysiologic mechanisms for these findings will be reviewed.
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9/11. hypothyroidism in head and neck cancer patients: experimental and clinical observations.

    Damage to the thyroid gland may occur in patients undergoing treatment for head and neck neoplasms. This injury may result from damage incurred during surgery, from radiation therapy, or a combination of the two. Development of hypothyroidism is often insidious with potential harmful effects. An experimental study was performed to study the effects of hypothyroidism in pigs whose skin closely approximates that of the human. Wound tensile strength and flap necrosis were studied in the hypothyroid animal treated by surgery, radiation, and a combination of the two. The results of this study indicate that hypothyroidism alone has no significant unfavorable impact on wound tensile strengths or flap survival. When combined with preoperative radiation, however, there are statistically significant deleterious effects on both wound tensile strengths and flap survival. Histologically, collagen fibers within the wound appear shorter and thinner, which probably accounts for decreased wound tensile strengths. A clinical review of 62 head and neck cancer patients was also conducted. Within the study group, 10% of patients developed abnormally low thyroxine measurements, whereas 15% developed high thyroid-stimulating hormone levels as the only evidence of early primary hypothyroidism. hypothyroidism was not statistically related to tumor size, nodal status, clinical staging, or treatment group (surgery alone, radiation alone, or combination surgery and radiation). A previously unreported finding is that patients who develop a second primary tumor are significantly at risk for developing hypothyroidism. All patients diagnosed with a head and neck cancer should undergo baseline thyroid function testing, including measurement of TSH, and have serial repeat testing after treatment. Thyroid function determination should be mandatory in patients undergoing oncologic salvage procedures or treatment of a second primary tumor.
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10/11. Diabetic death bed: post-mortem determination of hypoglycaemia.

    The post-mortem biochemical determination of hypoglycaemia in the practice of forensic medicine is notoriously imprecise and attracts perennial criticisms, particularly from those who may be alien to the peculiarities of medical jurisprudence. There has been re-emphasis recently on the neuropathological pathoclisis ascribed to prolonged hypoglycaemia. Unfortunately, the value perceived is limited by pathognomonic unreliability owing to agonal multifactorial influences and rapidly fatal nocturnal hypoglycaemia. The predicament is oppressive to a consideration of preponderant evidence and an unpopular diagnosis of peri-mortem hypoglycaemia, unless audacious, may be precluded simply because the proof is difficult. This is likely to contribute to diagnostic under-estimation of enigmatic diabetic deaths. A suspected case of lethal nocturnal hypoglycaemia in a young diabetic on 'animal' insulin is presented to restore some perspective to the clinico-pathological deference for an endangered post-mortem diagnosis of hypoglycaemia inferred from minimal evidence.
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