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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This report reviews the manifestations in fifteen children of proved adenoviral pneumonia. Patients' ages ranged from 43 days to 4 years and 1 month. Twelve cases were younger than 2 years old. Adenoviral infections were proved by positive viral cultures or a four-fold increase of the complement fixation titer. Prolonged fever and cough were found in all cases. In 13 patients, respiratory distress occurred; 5 needed mechanical ventilation. Injected throats, conjunctivae and ear drums were common. Other clinical pictures included abdominal discomfort, hepatomegaly, skin rash, convulsion and bleeding tendency. Abnormal laboratory findings were mild anemia, leukopenia, thrombocytopenia, elevated erythrocyte sedimentation rate and C-reactive protein, impaired liver function test, and prolonged prothrombin time and partial thromboplastin time. Anemia (11 cases), leukopenia (7 cases) and elevated transaminases levels (7 cases) were more common than previously reported. All patients had para-hilar peribronchial infiltrates in chest roentgenography. Segmental atelectasis and compensated hyper-expansion were found frequently. Pleural effusion were noted in six of our cases. Air leak syndrome occurred in three patients who had received mechanical ventilation. Three of the 15 patients expired: one had a preceding measles infection, all had disseminated intravascular coagulopathy. For patients with antibiotic-resistant pneumonia, adenoviral studies should be done. Extrapulmonary manifestations, and some abnormal laboratory findings, i.e., mild anemia, leukopenia, impaired liver function are clues to adenoviral infections, while bleeding tendency can be regarded as a poor prognostic sign for children with adenoviral pneumonia.
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PMID:Adenoviral pneumonia in children. 132 94

The acute or toxemic form of schistosomiasis mansoni is studied under the anatomic and clinical point of view, according to classification made by Neves, Raso and Bagliolo in 1975. The first phase is characterised by the following facts: cutaneous (immediate and late) manifestations; high fever or in progressive elevation; intense diaphoresis abdominal discomfort; intense aqueous diarrhea; dehydration; loss of weight, dry cough; painful hepatosplenomegaly; discreet lymphadenomegaly, progressive increase of blood leucocytes and eosinophiles; radiological pulmonary alterations; absence of alterations in serum protein and hepatic functional tests; the hepatic function biopsy shows focus of acute hepatitis. The second stage or properly named toxemic period was clinically characterized by the neat aggravation of the previously observed phenomena. At last, the evolutive course of the disease has implication derived not only the worm's presence, but from the intense dissemination of eggs in the tissue. In the pre-laying phase one studied the forms of cercarian dermatitis, prodromic and inapparent. In the post laying phase, the properly named acute toxemic form, with its types: pseudocholeraic, pseudotyphous, pseudodysenteric-bacillary, pseudonephritic, pseudoenterovirotic, the reactivated, the ischemic enterocolitis and others; whenever possible clinical and anatomic correlation will be made.
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PMID:[Acute or toxemic form of schistosomiasis mansoni]. 134 17

Lymphangiomyomatosis was first reported more than forty years ago. Although its incidence is rare, its occurrence is being increasingly recognized and has been the subject of a growing number of cases reports in recent years. This study adds 2 more cases to the file. Both cases involved young women with the characteristic symptoms of dyspnea, cough, abdominal discomfort and swelling, chest pain, and hemoptysis, with abundant formation of refractory chylous, serous ascites. Although the progression of the disease differed in each case, pulmonary function was affected in a similar way by the presence of obstructive and restrictive defects and a decrease in diffusing capacity. Underlying abnormalities were dilated lymphatics, thickened lymphatic walls, and muscular proliferation of leiomyomatous origin, leading to bronchial restriction. The authors point to the subtlety required in arriving at a differentiated diagnosis of lymphangiomyomatosis lymphangioleiomyomatosis and the difference between the two conditions. They also make particular recommendations in respect to the importance of preliminary hormone receptor tests and to the wisdom to be exercised in ligating a main lymphatic duct in the chest to control the formation of ascites. Pneumothorax, a frequent manifestation of lymphangiomyomatosis, is found to be the result of chronic air trapping due to a combination of narrowing of conducting airways and disruption of normal lung parenchyma.
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PMID:Lymphangiomyomatosis--newer concepts in pathogenesis and management--case reports. 224

Thirty-two workers in an electroplating plant accidently drank water contaminated with nickel sulfate and chloride (1.63 g Ni/liter). Twenty workers promptly developed symptoms (e.g., nausea, vomiting, abdominal discomfort, diarrhea, giddiness, lassitude, headache, cough, shortness of breath) that typically lasted a few hours but persisted 1-2 days in 7 cases. The Ni doses in workers with symptoms were estimated to range from 0.5 to 2.5 g. In 15 exposed workers who were tested on day 1 postexposure, serum Ni concentrations ranged from 13 to 1,340 micrograms/liter and urine Ni concentrations ranged from 0.15 to 12 mg/g creatinine. Ten subjects (with initial urine Ni concentrations greater than 0.8 mg/g creatinine) were hospitalized and treated for 3 days with intravenous fluids to induce diuresis, resulting in a mean elimination half-time (T1/2) for serum Ni of 27 hours (SD +/- 7 hour), which was significantly shorter (p less than .001) than the mean T1/2 of 60 hours (SD +/- 11 hours) in 11 subjects who did not receive intravenous fluids. Laboratory tests showed transiently elevated levels of blood reticulocytes (N = 7), urine albumin (N = 3), and serum bilirubin (N = 2). All subjects recovered rapidly, without evident sequellae, and returned to work by the eighth day after exposure.
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PMID:Acute nickel toxicity in electroplating workers who accidently ingested a solution of nickel sulfate and nickel chloride. 318 43

Mercury toxicosis by ingestion was diagnosed in a 3-year-old Quarter Horse mare with a history of anorexia and signs of abdominal discomfort. Ten and 9 days prior to admission, an inorganic mercuric blistering agent has been applied for topical treatment of dorsal metacarpal disease. At referral, signs of depression, dependent edema, pollakiuria, nonproductive cough, and oral ulceration were noticed. Laboratory data were consistent with renal dysfunction. Mercury content of blood and urine was high, confirming the diagnosis. The horse responded to intensive care, consisting primarily of IV fluid treatment, and mercury-chelating agents. However, acute laminitis developed, and the owners elected to euthanatize the horse 18 days after mercury exposure. Necropsy findings included renal tubulonephrosis and ulcerative colitis and enteritis. Mercury concentration was highest in kidney and liver tissues. The potential for mercury toxicosis in horses currently exists, and although the prognosis is grave, some horses may recover with appropriate treatment and long-term supportive medical care.
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PMID:Mercury toxicosis caused by ingestion of a blistering compound in a horse. 775 Dec 24

The patient was 71-year-old male with a history of sinobronchial syndrome since 8 years ago. He has been suffering from cough, sputum and upper abdominal discomfort since January 1994. He was diagnosed as an early gastric cancer by endoscopy, and his chest X-ray film showed an infiltrative shadow in the right upper lung field. A smear of the sputum specimen was positive for acid fast bacilli, which were later identified as Mycobacterium intracellulare. In this case, before the Mycobacterium intracellulare infection, it was confirmed that his mucociliary transport was severely impaired by using aerosol inhalation cine-scintigraphy. This case suggests that an impairment of the local defence mechanisms may play an important role in the pathogenesis of Mycobacterium intracellulare infection.
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PMID:[A case of Mycobacterium intracellulare infection associated with sinobronchial syndrome]. 925 28

To determine adverse events of ribavirin in the treatment of chronic hepatitis C, 41 patients (18 with cirrhosis), treated with ribavirin at an initial dose of 600-1200mg day(-1), were analysed retrospectively (six patients were treated twice because adverse effects during the first treatment necessitated cessation of ribavirin). Indications for ribavirin included a contraindication (n = 15) an intolerance (n = 11) or a non-response (n = 15) to interferon (IFN). Ribavirin was combined with IFN 3 million units (MU) three times weekly for 15 patients and with azathioprine for six patients (five of whom were transplant patients). No cirrhotics and only one patient treated with ribavirin + IFN received azathioprine. The mean duration of treatment was 5 months (range 1-18 months). Sixteen of 47 treatments (34%) with ribavirin were stopped: four because of vomiting (8.5%), two for psychiatric disorder, one for dry cough, one for an unrelated cause, and eight (at 1-2 months) because of a fall in the level of haemoglobin (Hb) of 4.6 g dl(-1) (range 2.7-5.9 g dl[-1]); however, according to the rules of international protocol, we would have expected only four treatments (two in patients receiving azathioprine) with Hb < 8.5 g dl(-1) to be stopped. The decrease in Hb level occurred more slowly in patients treated with IFN plus ribavirin than in patients treated with ribavirin alone and was of lower clinical significance in patients with cirrhosis than in patients without cirrhosis. After exclusion of patients receiving azathioprine, there was no significant difference in the fall of Hb level between cirrhotic and non-cirrhotic patients and between patients treated with IFN plus ribavirin and patients treated with ribavirin alone. Interestingly, the platelet count of patients treated with IFN plus ribavirin fell less than in patients treated with IFN alone. The most important and expected adverse event associated with ribavirin was haemolysis. Anaemia < 8.5 g dl(-1), requiring cessation of ribavirin therapy, was present in 9% of patients and was worsened by azathioprine. Abdominal discomfort and dry cough were other, potentially important, clinical adverse events found in our study.
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PMID:Effects of cirrhosis, interferon and azathioprine on adverse events in patients with chronic hepatitis C treated with ribavirin. 927 22

Familial Mediterranean fever (FMF) is an inherited multisystem disease manifested by painful, febrile attacks affecting the chest, abdomen, joints, and skin. No simple studies confirm the presence of FMF, contributing to the difficulty in diagnosis. A 10-year-old boy initially presented with a diffuse rash and complaints of bilateral joint pain of the hips, knees, and ankles and pain of the right shoulder. The child responded to daily naproxen. One year later, he continued to complain of hip, knee, ankle, and bilateral wrist pain. He also reported mild to moderate recurrent abdominal discomfort. Omeprazole provided intermittent relief. The patient continued to experience episodes of joint and abdominal pain. Two and a half years after he first presented, FMF was considered. In the second case, a 51-year-old man presented to the emergency department with complaints of fever, cough, and abdominal and joint pain. Fever, joint pain, and swelling decreased during the next few days. The patient was maintained on colchicine, with complete resolution of joint pain complaints during the next few days. Colchicine, 1 to 2 mg per day taken continuously during flare and quiescent periods, is the treatment of choice for FMF. Colchicine reduced the severity and frequency of attacks and may also delay or prevent secondary amyloidosis.
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PMID:Familial Mediterranean fever. 1092 6

An 11-year-old crossbred dog was presented with a history of episodic vomiting, diarrhoea, abdominal discomfort and coughing. These signs had been present for several years. Marked peripheral eosinophilia (10.3 x 10(9)/L) was found. No underlying cause of reactive eosinophilia was apparent. Bone marrow aspiration biopsy showed hyperplasia of the eosinophilic cell line, with some increase in immaturity, although all cells were morphologically normal. There were numerous eosinophils in bronchial wash fluid and eosinophilic infiltrates were evident in biopsies of pancreas, liver, small intestine and colon but not stomach. Hypereosinophilic syndrome was diagnosed. The dog responded well to twice daily treatment with hydroxyurea and prednisolone. Clinical signs are well-controlled 16 months later.
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PMID:Successful treatment of hypereosinophilic syndrome in a dog. 1171 8

A rare case of thrombotic microangiopathy in a patient with hemophagocytic syndrome is reported. An 18-year-old girl was admitted following prolonged fever, watery diarrhea, abdominal discomfort, and a 2-week history of rhinorrhea, cough, and painful cervical lymph nodes. Anemia, thrombocytopenia, jaundice, hepatomegaly, and mild azotemia developed within 2 weeks of admission. The diagnosis of a reactive hemophagocytic syndrome, probably secondary to infection, was made based on the findings of bone marrow examination. Extensive investigation failed to identify a causative agent. The disease initially responded rapidly to intravenous steroids and high-dose immunoglobulin therapy but relapsed soon after tapering of the steroids. Although her condition improved again on resumption of treatment with high-dose steroids, nephrotic range proteinuria and microscopic hematuria developed after the steroids were tapered. Fragmented erythrocytes were seen in peripheral blood with elevated serum lactate dehydrogenase and decreased serum haptoglobin concentrations. The results of subsequent renal pathology examination were also compatible with thrombotic microangiopathy. The disease course finally stabilized after a course of pulse methylprednisolone therapy. Immune hyperactivity, particularly hypercytokinemia and monocyte hyperactivity, could have accounted for the development of thrombotic microangiopathy in this case. Only strong immunosuppressive therapy can control such disease activity.
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PMID:Thrombotic microangiopathy in hemophagocytic syndrome: a case report. 1210 56


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