Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe an epidemic of self-limited (6 weeks) thyrotoxicosis which affected 12 index cases, 5 household contacts, and 6 retrospectively identified cases in July, August, and September, 1987 in the town of Winterswijk (28,011 inhabitants), The Netherlands. A small goiter was present in 9 of the 12 index patients, tender upon palpation in only 2. Signs and symptoms of thyrotoxicosis were accompanied by a low grade fever in combination with fatigue, headache, myalgia, and a fine desquamation of the palms and soles. The apparent incubation time between family members was 6 days. Thyroid technetium uptake was decreased in 10 of 11 tested patients. Laboratory findings included elevated sedimentation rates (up to 68 mm/h), increased liver enzymes, lymphopenia in 2 patients, and absence of thyroid autoantibodies. HLA-B35, associated with classical subacute thyroiditis, was found in 1 patient only. An etiological agent was not identified. No evidence was found for thyrotoxicosis factitia. After 10 months, all patients were euthyroid, without a goiter or thyroid autoantibodies. Thus, a new variant of thyroiditis, atypical subacute thyroiditis, was probably the cause of this unusual outbreak. It is unclear at present if this variant of thyroiditis is common in communities and represents a separate disease entity.
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PMID:An outbreak of thyrotoxicosis due to atypical subacute thyroiditis. 229 55

Continuous Holter monitoring of patients with coronary heart disease can show transient ischemic episodes occurring spontaneously with or without angina throughout the day. A controlled double-blind trial was conducted comparing the effects of isosorbide-5-mononitrate (IS-5-MN) and nifedipine in patients with documented transient ischemic episodes. Seventy-five percent of the ischemic episodes were not accompanied by pain. Twenty patients with documented coronary heart disease were included; 15 finished the 4-week study (1 patient had headaches, 1 thyrotoxicosis, 1 hypertensive crisis and 2 unstable angina). On a dual-channel FM-recorded electrocardiogram, ischemic episodes were counted when ST deviation was greater than 1 mm for greater than 1 minute. Patients received IS-5-MN (20 mg 3 times a day or 50 mg in a sustained-release tablet) or nifedipine (20 mg in a sustained-release tablet 3 times a day) in random order over four 1-week periods. At the end of each week, Holter monitoring was repeated and showed reductions of episodes by 67% and 67% after weeks of IS-5-MN therapy and 56% and 58% after weeks of nifedipine therapy (all p less than 0.05). Painful and painless episodes were reduced to a similar extent. Individual responses showed great variability, and in all treatment periods not more than half of the patients were completely free of ischemic episodes. One of the 12 patients did not respond to either way of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nitrates and calcium antagonists for silent myocardial ischemia. 327 43

TSH tumors are associated with both hypothyroid and hyperthyroid states. The proposed mechanism of thyrotroph secretion is illustrated in Figure 8. Pituitary enlargement in hypothyroidism is usually due to reactive hyperplasia and correlates with the degree of TSH elevation. Although this often translates to long-standing hypothyroidism and severe symptoms, this is not always the case. Patients may be asymptomatic or present with other endocrine syndromes. Children may have precocious puberty, and adults may have amenorrhea or decreased libido. One important message to remember is that whenever a patient has evidence of a pituitary tumor, a serum T4 and TSH level must be obtained. The dramatic reduction in pituitary size and resolution of endocrine dysfunction with thyroid hormone is gratifying. Thyrotropinomas producing thyrotoxicosis are autonomous tumors. Given their infrequent occurrence, one could question the cost effectiveness of ordering a serum TSH on all new patients with hyperthyroidism. Features that might favor the possibility of there being a tumor include male sex, headaches, visual impairment, and the absence of ophthalmopathy. Unfortunately, these are not reliable clinical features to suggest the presence of this disorder, and the diagnosis requires a serum TSH determination. Fortunately, the newer assays available are able to provide the sensitivity needed. Therapy should be aimed at the pituitary gland, but currently it is less than optimal. Surgery with or without external irradiation offers the best prognosis and, hopefully, will yield better results when cases are identified earlier. Medical therapy to suppress TSH is still in its infancy. More effective agents will hopefully be discovered in the near future.
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PMID:Thyrotropin-secreting pituitary tumors. 331 2

Although thyrotoxicosis and orbital complications of acute ethmoid or frontal sinusitis are among the most common causes of unilateral exophthalmos, inflammatory pseudotumor is frequently accompanied by progressive acute unilateral proptosis. Because the associated chemosis, scleral erythema, and ophthalmoplegia constitute a spectrum of clinical findings present in numerous inflammatory orbital disorders and systemic diseases, the diagnosis of inflammatory pseudotumor is one of exclusion, often requiring orbital biopsy. Four patients without evidence of sinusitis, endocrinopathy, collagen vascular disease, or Wegener's granulomatosis are described. The diagnosis of orbital pseudotumor was disclosed by computed axial tomography, thus avoiding orbitotomy. The finding of scleral and choroidal thickening with enhancement following intravenous contrast injection represents a select group of patients with orbital pseudotumor and differentiates them from patients with endocrine exophthalmopathy or neoplasms. This noninvasive technique is extremely valuable because early diagnosis is critical for successful treatment. All four patients responded dramatically to high-dose corticosteroid therapy. In the absence of significant clinical response, however, Wegener's granulomatosis, lymphoma, and rhabdomyosarcoma, especially in younger patients, must be carefully excluded. Orbital exploration or decompression or both are used when proptosis, headache, or orbital pain does not resolve promptly, visual acuity deteriorates, or the diagnosis remains unknown.
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PMID:Computerized axial tomography in inflammatory pseudotumor of the orbit. 682 19

Twenty-eight SLE patients (Arabs and Asians) in the UAE were studied in this report. The F:M ratio was markedly high; 27:1 in the group as a whole and 21:1 among Arabs. Local patients (Emirians) developed the disease at an earlier age compared to their expatriate Arab compatriots. Arthropathy occurred in 86% and nephropathy in 43% of cases. Next in frequency were leucopenia, mucocutaneous manifestations and serositis. Apart from lupus headache, the other neuro-psychiatric LE were uncommon or not encountered. Anti-cardiolipin syndrome, Sneddon's syndrome, shrunken lung syndrome, sicca complex, thyrotoxicosis and myasthenia gravis were also present in this small group of patients. Their presence reflects the marked heterogeneity displayed by the disease irrespective of the number of cases involved. An unusually high prevalence of anti ds (DNA) antibodies (92.5%) as compared to ANF (82.5%) was detected (P = NS). Anti-Sm antibody occurred in 30% of cases particularly in those patients with lymphadenopathy and fever. There was a relative paucity in the prevalence of anti RNP, Ro and La antibodies in this group. Differences with and similarities to previous reports concerning other populations are also presented.
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PMID:Characterization of systemic lupus erythematosus in patients in U.A.E. 778 58

Thyrotropin (TSH)-secreting pituitary tumors may be found in two opposite clinical situations: the hyperthyroidism secondary to thyrotroph adenomas, also called central hyperthyroidism, and the long-standing primary hypothyroidism which can be accompanied by a compensatory pituitary enlargement. TSH-secreting pituitary adenomas belong to the syndromes of "inappropriate secretion of TSH" (IST). The adjective "inappropriate" indicates the lack of the expected suppression of TSH secretion when free thyroid hormone levels are actually elevated, as in the other forms of thyrotoxicosis. Moreover, TSH-omas have to be differentiated from the non-neoplastic form of IST which is due to resistance to thyroid hormone. Differently, pituitary hyperplasia, which is reversible on thyroid hormone replacement, is the more frequent cause of a pituitary mass occurring in the context of untreated primary hypothyroidism. Failure or delay in the recognition of the above clinical situations may cause dramatic consequences, such as unnecessary pituitary surgery in hypothyroid patients or improper thyroid ablation in those with central hyperthyroidism. In contrast, early diagnosis and proper treatment of TSH-secreting pituitary tumors prevents the appearance of signs and symptoms of mechanical compression of the adjacent structures by the expanding tumor mass (visual field defects, headache and hypopituitarism).
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PMID:Thyrotropin-secreting pituitary tumors in hyper- and hypothyroidism. 876 13

Considerable uncertainty exists regarding the appropriate use and dose limitations for ergotamine tartrate (ET) and dihydroergotamine (DHE) for the treatment of migraine despite more than 50 years of clinical experience. The Quality Standards Subcommittee (QSS) of the American Academy of Neurology (AAN) appointed an advisory committee from experts in the Headache and Facial Pain Section. As their initial project, the committee elected to review the clinical literature on the appropriate use of these compounds in the treatment of migraine. Subsequently, clinical practice guidelines were formulated and recently published in Neurology. The Headache and Facial Plan Section and the QSS of the AAN were able to reach consensus on the basis of a thorough literature review and formulated practice parameters that describe and define the limits of ergot use, provide information on the oral and parenteral dosing of ET and DHE, and provide physicians with guidance to avoid ET overuse by patients. Because this project was completed prior to the availability of the intranasal (IN) formulation of DHE, intranasal DHE is not included in the practice parameter. Ergotamine tartrate and DHE were found to be safe and effective for the treatment of migraine as long as recommended dosages are not exceeded and high-risk patients such as those with uncontrolled hypertension, coronary or peripheral artery disease, thyrotoxicosis, or sepsis do not receive these compounds. In addition, the committee recommended restricting the use of ET in some instances because the overuse of ET has been associated with physical and psychological dependence resulting in predictable recurrent and/or rebound headaches, and subsequent severe withdrawal symptoms, including nausea, upon discontinuance of ET. None of these symptoms have been reported for DHE. These guidelines should help physicians provide optimal antimigraine therapy with these drugs.
Headache 1997
PMID:Appropriate use of ergotamine tartrate and dihydroergotamine in the treatment of migraine: current perspectives. 900 73

Complete clinical examination covered 37 patients in various stages after acute occupational poisonings with pesticides (8 examinees), with explosive gases (9 subjects), with carbon oxide (3 examinees), with cadmium oxides (1 examinee), with nitrogen compounds (4 ones), with sulfurous gases (2 examinees), with organic solvents (10 subjects) including chlorinated hydrocarbons (2 subjects). Post-intoxication period appeared to include syndromes characteristic for each poison and corresponding to severity of acute state (from cephalgia to parkinsonism and thyrotoxicosis after acute poisoning with carbon oxide, organic neurologic signs and toxic hepatitis after acute poisoning with phosphorus organic compounds, cerebral asthenia after acute exposure to organic solvents, severe encephalopathy and toxic auditory and optic neuropathy after hydrogen sulfide). Inadequate medical rehabilitation and continuous occupational exposure induced deterioration in clinical signs and advanced post-intoxication syndromes.
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PMID:[Diagnostic problems of post-intoxication states]. 1150 30

A 36-yr-old woman began to suffer from headache, anorexia and general fatigue at 35 weeks' gestation. About 2 or 3 months after the delivery, fever, tachycardia and generalized musculoskeletal disorder appeared. Thereafter, they worsened rapidly, accompanied by a disturbance of consciousness and hypercalcemia. Thyrotoxicosis, due to a post-partum thyroiditis, and glucocorticoid deficiency, due to a pituitary failure, probably associated with lymphocytic hypophysitis, were also observed. All the symptoms and hypercalcemia disappeared after the glucocorticoid replacement therapy and the normalization of thyroid hormone levels. Serum and urinary bone resorption markers, such as urine pyridinoline (U-Pyr), urine deoxypyridinoline (U-DPD), urine amino-terminal telopeptide of type I collagen (U-NTx) and serum carboxy-terminal telopeptide of type I collagen (ICTP), were extremely high at the hypercalcemic state. In this case, they were 10 to 20 times higher than the normal upper limits, and then markedly decreased in a normocalcemic state, thereby showing an extreme acceleration of bone resorption in a state of both thyrotoxicosis and glucocorticoid deficiency.
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PMID:Elevated bone resorption markers in a patient with hypercalcemia associated with post-partum thyrotoxicosis and hypoadrenocorticism due to pituitary failure. 1563 35

We report the case of a 28-year-old woman who presented simultaneously with superior sagittal sinus thrombosis and thyroid crisis, and was subsequently found to have protein C deficiency. February 3, 2003, she admitted complaining of abdominal pain. The diagnosis of appendicitis was made, and she was operated on under lumbar anaesthesia. Day 7, she developed acute headache and distal weakness of the left lower limb. On examination she was alert, with a temperature of 38 degrees C, a sinus tachycardia of 124/min and blood pressure 164/84 mmHg. Neurological examination revealed neck stiffness and left hemiparesis, predominantly in her lower limb. Gadlinium-enhanced brain MRI revealed extensive superior sagittal sinus thrombosis. CT scan demonstrated infarction in the right frontal cortex, and subarachnoid hemorrhage adjacent to the right cerebellar tentorium. The patient was treated with a free radical scavenger edarabon, and glycerin. No anticoagulant therapy was instituted. Over the next 24 hours, her condition worsened. She became comatose, as well as developing a generalized tonic-clonic seizure. Day 12, laboratory examinations revealed an undetectable TSH-level CTSH (thyroid stimulating hormone) <0.005 mcIU/ml), with a level of free thyroxin 7.77 ng/dl (0.9-1.7), free triiodothyronin 29.6 pg/ml (2.3-4.3), and positive anti-TSH receptor antibodies determined subsequently. Coagulation factor VIII activity was 155% (normal range 60-150). Protein C deficiency (antigen 59%, activity 49%) was also present, suggesting a congenital type I heterozygous deficiency. A diagnosis of thyroid crisis on the basis of Graves' disease was made. The patient remained comatose and died on Day 16, with renal failure. The patient had protein C deficiency, a well-established risk factor for cerebral venous thrombosis (CVT). However, additional risk factors are required in most cases to precipitate CVT. In our case, this trigger was most likely thyroid crisis, suggesting that thyrotoxicosis, probably through hypercoagulability, may be a predisposing factor for the development of CVT.
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PMID:[Thyroid crisis and protein C deficiency in a case of superior sagittal sinus thrombosis]. 1737 Jun 53


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