A long–term follow–up of lung function in survivors of paraquat poisoning

2000 ◽  
Vol 19 (2) ◽  
pp. 99-103 ◽  
Author(s):  
M Yamashita ◽  
M Yamashita ◽  
Y Ando

1 Respiratory failure is a frequent cause of death in moderate to severe paraquat poisoning, and a tran- sient fall in the gas transfer factor may be seen in mild poisoning. 2 The objectives of this study were to detect long-term changes in lung function in survivors of paraquat poisoning. 3 We analyzed 12 survivors retrospectively for age, sex, signs and symptoms, laboratory findings, chest X-ray findings, serum paraquat level, and lung function test. The first and the follow-up lung tests were performed at 3.7 + 1.4 weeks and 3.4 + 1.4 years, respectively. 4 Serum paraquat levels were assayed in all patients and 3/12 were above the Proudfoot's predictive line. Liver dysfunction (GOT > 50) and renal dysfunction (BUN > 30) were noted in 5/12 and 8/12, respectively. DL/VA was lower than the normal limit in the first study (3.9 + 0.6 L), but increased significantly and returned to the normal range in the follow-up study (4.5 + 0.6 L).%VC was within the normal range in either examina- tion, but significantly decreased in the follow-up.%TLC was within the normal range in the first study (87 + 13%), but significantly decreased below the normal limit in the follow-up (81 + 13%). 5 These results indicate that survivors of paraquat poisoning may be left with a restrictive type of pulmonary dysfunction and suggest that a long-term follow-up of lung function may be necessary for survivors of paraquat poisoning.

CHEST Journal ◽  
2011 ◽  
Vol 140 (4) ◽  
pp. 951A
Author(s):  
Pedro Marcos ◽  
Isabel Otero ◽  
Maria Fernández-Marrube ◽  
Maria Rodriguez-Valcarcel ◽  
Luis Mariñas ◽  
...  

Author(s):  
Lene Maria Ørts ◽  
Bodil Hammer Bech ◽  
Torsten Lauritzen ◽  
Anders Helles Carlsen ◽  
Annelli Sandbæk ◽  
...  

2019 ◽  
Vol 78 (11) ◽  
pp. 1497-1504 ◽  
Author(s):  
Debbie M Boeters ◽  
Leonie E Burgers ◽  
René EM Toes ◽  
Annette van der Helm-van Mil

ObjectivesSustained disease-modifying antirheumatic drug (DMARD)-free status, the sustained absence of synovitis after cessation of DMARD therapy, is infrequent in autoantibody-positive rheumatoid arthritis (RA), but approximates cure (ie, disappearance of signs and symptoms). It was recently suggested that immunological remission, defined as disappearance of anti-citrullinated protein antibodies (ACPA) and rheumatoid factor (RF), underlies this outcome. Therefore, this long-term observational study determined if autoantibodies disappear in RA patients who achieved sustained DMARD-free remission.MethodsWe studied 95 ACPA-positive and/or RF-positive RA patients who achieved DMARD-free remission after median 4.8 years and kept this status for the remaining follow-up (median 4.2 years). Additionally, 21 autoantibody-positive RA patients with a late flare, defined as recurrence of clinical synovitis after a DMARD-free status of ≥1 year, and 45 autoantibody-positive RA patients who were unable to stop DMARD therapy (during median 10 years) were studied. Anti-cyclic citrullinated peptide 2 (anti-CCP2) IgG, IgM and RF IgM levels were measured in 587 samples obtained at diagnosis, before and after achieving DMARD-free remission.Results13% of anti-CCP2 IgG-positive RA patients had seroreverted when achieving remission. In RA patients with a flare and persistent disease this was 8% and 6%, respectively (p=0.63). For anti-CCP2 IgM and RF IgM, similar results were observed. Evaluating the estimated slope of serially measured levels revealed that RF levels decreased more in patients with than without remission (p<0.001); the course of anti-CCP2 levels was not different (p=0.66).ConclusionsSustained DMARD-free status in autoantibody-positive RA was not paralleled by an increased frequency of reversion to autoantibody negativity. This form of immunological remission may therefore not be a treatment target in patients with classified RA.


2014 ◽  
Vol 8 (1) ◽  
pp. 233-236 ◽  
Author(s):  
GUANGCAI YU ◽  
BAOTIAN KAN ◽  
XIANGDONG JIAN ◽  
JIERU WANG ◽  
JING SUN ◽  
...  

2020 ◽  
Author(s):  
Angela Vinturache ◽  
Lamiese Ismail ◽  
Stephen Damato ◽  
Hooman Soleymani Maid

Abstract Background: Leiomyomas are uncommon vulvar neoplasms often misdiagnosed as other Bartholin gland pathology. Due to their rarity and the absence of guidelines, their diagnosis and management remain challenging, largely based on expert opinion and evidence from case reports. Case Presentation: This case report describes a 44-year-old woman presenting with accelerating growth of a vulvar mass. Based on clinical signs and symptoms, the initial diagnosis was Bartholin cyst. Surgical excision was provided for symptom control and aesthetic reasons. The histopathologic diagnosis was vulvar leiomyoma. The postoperative recovery was complicated by secondary haematoma and dehiscence of the surgical site. There was no recurrence at two years follow up. Therefore, we discuss the dilemma posed by physical examination of a vulvar mass, the challenges of the management, and report on secondary morbidity and long-term follow up, aspects of care for patients with vulvar pathology not commonly addressed in the literature. Conclusions: Bartholin gland neoplasms are rare tumors, commonly misdiagnosed as Bartholin’s cysts. Excision is the treatment of choice. Short time follow up allows prompt management of potential postoperative complications. Continuing long term follow up is recommended due to recurrence risk.


1982 ◽  
Vol 16 (5) ◽  
pp. 404-407 ◽  
Author(s):  
Jerry L. Browne8 ◽  
Ming T. Tsuang ◽  
Paul J. Perry

A case of amoxapine (Asendin) overdose, in a 24-year-old female, is presented. The manifestations of amoxapine ingestion in this case are dissimilar to those of previously described tricyclic antidepressant (TCA) overdoses, and to those previously described for amoxapine. The signs and symptoms of TCA toxicity are discussed and contrasted with observations of this case. Impressions from this case indicate that amoxapine and other dibenzoxazepine derivatives possess a significantly different and greater toxic potential than other TCA agents.


PEDIATRICS ◽  
1981 ◽  
Vol 67 (2) ◽  
pp. 183-187
Author(s):  
Stephen P. Herman ◽  
Gunnar B. Stickler ◽  
Alexander R. Lucas

Records of 34 hyperventilating children aged 18 years or younger seen at the Mayo Clinic over a 25-year period were reviewed. Five different clinical subtypes were identified. Evaluation and treatment varied considerably. At follow-up, 40% were still hyperventilating as adults, and many had signs and symptoms of chronic anxiety. Hyperventilation in childhood can be a signal that the child is experiencing severe anxiety, which may persist into adulthood.


Author(s):  
Mehmet Gündüz ◽  
Özlem Ünal ◽  
Sumru Kavurt ◽  
Emrecan Türk ◽  
Neslihan Önenli Mungan

AbstractGlutathione synthetase (GS) deficiency is a rare inborn error of glutathione (GSH) metabolism manifested by severe metabolic acidosis, hemolytic anemia, neurological problems and massive excretion of pyroglutamic acid (5-oxoproline) in the urine. The disorder has mild, moderate, and severe clinical variants. We aimed to report clinical and laboratory findings of four patients, effect of sodium hydrogen carbonate treatment and long-term follow up of three patients.Urine organic acid analysis was performed with gas chromatography-mass spectrometry. Molecular genetic analysis was performed in three patients, mutation was found in two of them. Enzyme analysis was performed in one patient. Clinical and laboratory findings of four patients were evaluated.One patient died at 4 months old, one patient’s growth and development are normal, two patients have developed intellectual disability and seizures in the long term follow up period. Three patients benefited from sodium hydrogen carbonate treatment.The clinical picture varies from patient to patient, so it is difficult to predict the prognosis and the effectiveness of treatment protocols. We reported long term follow up of four patients and demonstrated that sodium hydrogen carbonate is effective for treatment of chronic metabolic acidosis in GS deficieny.


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