Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019079 (hemoptysis)
 6,129 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Heart failure is not a common manifestation of hypothyroidism if there is no underlying heart disease. We report a case of familial primary hypothyroidism in a young male, that clinically onset with dyspnea, hemoptysis and serum CPK elevation, and in which further explorations revealed a dilated cardiomyopathy due to hypothyroidism. Because of its bad prognosis, we underline the need to identify those cases of dilated cardiomyopathy that can be treated with the appropriate therapy.
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PMID:[Heart insufficiency as first manifestation of familial primary hypothyroidism]. 938 Sep 39

We describe a case of lingual thyroid (LT) with primary hypothyroidism, presenting during pregnancy and continuing beyond it with oropharyngeal obstructive symptoms and sleep apnoea syndrome (SAS) of mixed type. Although SAS of a combined obstructive and central type should not be too surprising in a case of LT with hypothyroidism, we were unable to find such a documentation previously. Only four weeks of L-thyroxin treatment resulted in a dramatic improvement in dysphagia, disturbed phonation, haemoptysis, arterial desaturation, sleep apnoea and overall sleep efficiency, in conjunction with a regression in the size of the lingual mass. This case highlights the vagaries confronted in the management of such a case and focuses on efforts towards accurate diagnosis and treatment.
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PMID:An unusual cause of obstructive sleep apnoea presenting during pregnancy. 1020 20

PURPOSE This phase II/III double-blind study assessed efficacy and safety of cediranib with standard chemotherapy as initial therapy for advanced non-small-cell lung cancer (NSCLC). PATIENTS AND METHODS Paclitaxel (200 mg/m(2)) and carboplatin (area under the serum concentration-time curve 6) were given every 3 weeks, with daily oral cediranib or placebo at 30 mg (first 45 patients received 45 mg). Progression-free survival (PFS) was the primary outcome of the phase II interim analysis; phase III would proceed if the hazard ratio (HR) for PFS < or = 0.77 and toxicity were acceptable. Results A total of 296 patients were enrolled, 251 to the 30-mg cohort. The phase II interim analysis demonstrated a significantly higher response rate (RR) for cediranib than for placebo, HR of 0.77 for PFS, no excess hemoptysis, and a similar number of deaths in each arm. The study was halted to review imbalances in assigned causes of death. In the primary phase II analysis (30-mg cohort), the adjusted HR for PFS was 0.77 (95% CI, 0.56 to 1.08) with a higher RR for cediranib than for placebo (38% v 16%; P < .0001). Cediranib patients had more hypertension, hypothyroidism, hand-foot syndrome, and GI toxicity. Hypoalbuminemia, age > or = 65 years, and female sex predicted increased toxicity. Survival update (N = 296) 10 months after study unblinding favored cediranib over placebo (median of 10.5 months v 10.1 months; HR, 0.78; 95% CI, 0.57 to 1.06; P = .11). Causes of death in the cediranib 30-mg cohort were NSCLC (81%), protocol toxicity +/- NSCLC (13%), and other (6%); for the placebo group, they were 98%, 0%, and 2%, respectively. CONCLUSION The addition of cediranib to carboplatin/paclitaxel results in improved response and PFS, but does not appear tolerable at a 30-mg dose. Consequently, the National Cancer Institute of Canada Clinical Trials Group and the Australasian Lung Cancer Trials Group initiated a randomized, double-blind, placebo-controlled trial of cediranib 20 mg with carboplatin and paclitaxel in advanced NSCLC.
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PMID:Randomized, double-blind trial of carboplatin and paclitaxel with either daily oral cediranib or placebo in advanced non-small-cell lung cancer: NCIC clinical trials group BR24 study. 1991 41

A 66-year-old man, chronic smoker, presented with episodes of syncope, hypotension and constitutional symptoms. Initial evaluation revealed pre-renal azotaemia and acute secondary adrenal insufficiency.MRI performed was interpreted as a pituitary macroadenoma with enlargement of the infundibulum (stalk). Further endocrinological tests performed suggested central hypothyroidism and hypogonadism. Subsequent development of haemoptysis, headache and diplopia warranted further investigations, which revealed stage IV small-cell lung carcinoma with adrenal metastases. Subsequent brain imaging showed lesions in the brain parenchyma, pituitary and stalk, characteristic of metastases. Thus, we present a very atypical case of pituitary metastases presenting with acute secondary adrenal insufficiency.
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PMID:Acute secondary adrenal insufficiency as the presenting manifestation of small-cell lung carcinoma. 2453 38

Ectopic lingual thyroid is a rare developmental anomaly. It is caused by aberrant embryogenesis during the thyroid descent to the neck. It may remain asymptomatic or present with dysphagia, hemoptysis, dyspnoea or dysphonia. Clinically, it presents as a mass lesion on the base of the tongue. The most important diagnostic tool for an ectopic lingual thyroid is the 99mTc radionuclide scan, but imaging modalities such as computed tomography scan and magnetic resonance imaging may also help to assess its location and extent and to rule out the presence of normal thyroid tissue in the thyroid bed. The management of an ectopic thyroid remains controversial. No treatment is required for asymptomatic patients in the euthyroid state. Patients with hypothyroidism should be treated with thyroid hormone substitution therapy. Malignant transformation is an indication for complete surgical resection. Ablative radioiodine therapy can be considered for older patients and those who are unfit for surgery. In complicated cases, surgical resection is recommended through the transoral, transhyoid or lateral pharyngectomy approach. We report a case of ectopic lingual thyroid in a 35-year-old man who presented with nasal twang and hemoptysis.
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PMID:Ectopic lingual thyroid presenting with nasal twang and hemoptysis. 2602