• Title/Summary/Keyword: Fatal syndrome

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CASE REPORTS OF FASCIAL SPACE ABSCESS CAUSED BY ODONTOGENIC INFECTION (치성 감염에 의한 근막간극 농양의 치험례)

  • Choi, Ji-Eun;Yang, Kyu-Ho;Choi, Nam-Ki;Kim, Sun-Mi
    • Journal of the korean academy of Pediatric Dentistry
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    • v.35 no.1
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    • pp.136-143
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    • 2008
  • Infections involved with the oral and maxillofacial area are associated with various anatomical structures. If the proper treatment is not done in an immediate period, the infections will be quite fatal. The causes of the infections are numerous, but the most common cause of odontogenic infections in children is a dental caries. It is known to lead to some kinds of diseases such as periapical abscess, cellulitis, osteomyelitis, Ludwig's angina, toxic shock syndrome and so on. The common pathogenic sequence of fascial abscess is a necrotic pulpal inflammation in the form of dentoalvelor abscess which spreads over and gradually penetrates into the fascial membranes through the cortical bones and finally contracts the potential fascial spaces. If the infections of oral maxillofacial area were penetrated into the surrounding soft tissues, then they would diffuse into the directions of the least tissue resistance along with the connective tissues and the fascial spaces. These infections can be properly cured by tooth extraction, endodontic therapy, surgical treatment including Incision & drainage and antibiotics. The purpose of the cases is to report the satisfactory treatment results in the patients derived from the canine fascial space abscesss or buccal fascial space ones of the odontogenic origin.

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A Case of Mitochondrial Myopathy Showing Severe Hypoxemia during REM Sleep (렘수면중 심한 저산소혈증을 보인 사립체근병증 1례)

  • Kim, Ju-Sang;Kim, Sung-Kyung;Lee, Sang-Haak;Ahn, Joong-Hyun;Kim, Chi-Hong;Moon, Hwa-Sik
    • Sleep Medicine and Psychophysiology
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    • v.14 no.1
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    • pp.49-53
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    • 2007
  • Mitochondrial myopathy is characterized by variable clinical manifestations from mild limb weakness to fatal respiratory failure and central nervous system sequela. But it is a rare event that sleep disordered breathing become a clue of diagnosis for mitochondrial myopathy. We report a case of a 21 year-old man who was diagnosed as mitochondrial myopathy during the investigation for the possible cause of chronic hypoventilation syndrome. Before being admitted to our hospital, he was suspected as having sleep apnea syndrome in another hospital. We re-evaluated the history, physical examination, laboratoy findings and polysomnography in detail. Severe hypoxemia was noted during REM sleep on nocturnal polysomnography and the diagnosis of mitochondrial myopathy was made by muscle biopsy in rectus abdominis muscle. We treated him with bilevel positive airway pressure therapy during sleep and it could reverse the hypoxemia during REM sleep. He could be discharged with improved condition and is being well with the use of this ventilatory assistance.

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A Case of Spontaneous Hemothorax Due to Rupture of Pseudoaneurysm in Type 1 Neurofibromatosis (신경섬유종증에 동반된 가성동맥류 파열로 발생한 자연 혈흉 1예)

  • Kim, Sun-Jong;Jeong, Hoon;Lee, Sung-Soon;Lim, Chae-Man;Lee, Sang-Do;Koh, Youn-Suck;Kim, Woo-Sung;Kim, Dong-Soon;Kim, Won-Dong;Shim, Tae-Sun
    • Tuberculosis and Respiratory Diseases
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    • v.50 no.1
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    • pp.122-126
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    • 2001
  • A non-traumatic, spontaneous hemothorax is rare. The most common causes are coagulopathy, due to anticoagulation treatment, and cancers with a metastasis to the pleural surface. Other unusual causes include thoracic endometriosis, ruptured aortic aneurysm, pulmonary arterio-venous malformation, coagulopathy, Osler-Rendeu-Weber syndrome, Ehlers-Danlos syndrome et cetera. A type 1 neurofibromatosis(Von Recklinghausen's disease) is an autosomal dominant disease that is characterized by multiple skin tumors(neurofibroma) and abnormal skin pigmentation(caf$\acute{e}$-au-lait spots). Some are accompanied by vasculopathy, and are present with a spontaneous hemothorax. Such cases are unusual but fatal. We have recently experienced a case where a young male patient with neurofibromatosis initially presented with hypovolemic shock due to a spontaneous hemothorax. Later, aortography revealed that the cause of the hemothorax was a rupture of a pseudoaneurysm of the right internal mammary artery and as a result, an embolization was performed. Here we report this case with a review of the appropriate literature.

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Functional Dyspepsia (기능성 소화불량증)

  • Song, Kyung Ho
    • Korean Journal of Psychosomatic Medicine
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    • v.24 no.1
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    • pp.3-8
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    • 2016
  • Functional dyspepsia is one of the most common bowel disorders as prevalent of 7.7% Korean population. The cardinal manifestations include bothersome postprandial fullness, early satiation, epigastric burning or pain. These features are chronic and should be presented recurrently with no other compatible organic disease to explain the symptoms. Even though it is not life-shortening, functional dyspepsia usually make the health-related quality of life worse especially if other functional bowel disorder coexist. The coexistence of functional bowel disorders is called as 'overlap syndrome'. Anxiety, somatization and insomnia is more prevalent in overlap syndrome compared with sole functional bowel disorder. Therefore, it is worthwhile that physician interviews and elucidates whether the dyspeptic patient had other kinds of functional bowel disorders, and manages the underlying psychotic pathology. Placebo effect is large in functional dyspepsia, and there is only four kinds of prokinetics that is proven to be superior to placebo. Adverse events relating prolonged administration of prokinetics sometimes fatal or irreversible, physician willing to describe prokinetics should be familiar to the possible adverse effects and the relating risk factors. Pathologic acid reflux is not uncommon in functional dyspepsia, and acid-suppressant is equivalent to the prokientics in most of dyspeptic patients.

A Review on the Cause of Fever During Clozapine Treatment (클로자핀 투약시 나타나는 발열의 원인)

  • Jihye, Song;Sungsuk, Je;Jaejong, Lee;Seungyun, Lee;Seung-Hoon, Lee;Eunyoung, Lee;Hyungseok, So;Hayun, Choi;Jinhee, Choi
    • Korean Journal of Psychosomatic Medicine
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    • v.30 no.2
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    • pp.66-72
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    • 2022
  • Clozapine is accepted as the "gold standard" antipsychotics for treatment-resistant schizophrenia. Clozapine rarely causes extrapyramidal syndrome and tardive dyskinesia, which are common with other antipsychotics, and only a transient elevation of hyperprolactinemia has been reported. Despite such clinical usefulness, there are limitations to the use of clozapine due to adverse drug reactions (ADR). Fever is a common in adverse drug reactions associated with clozapine. At initiation of clozapine most fatal ADR such as agranulocytosis and neuroleptic malignant syndrome associated with fever, in which case clozapine should be discontinued immediately. However, as benign causes of fever are much more frequent than life-threatening ADR, clozapine should not be discontinued unconditionally in the event of fever during clozapine initiation. In addition, fever may occur at any time during the maintenance of clozapine treatment. In particular, since the risk of pneumonia does not decrease over time, and clozapine has a higher risk of pneumonia than other antipsychotic drugs, it is recommended to adjust clozapine dosage through therapeutic drug monitoring.

COVID-19 in a 16-Year-Old Adolescent With Mucopolysaccharidosis Type II: Case Report and Review of Literature

  • Park, So Yun;Kim, Heung Sik;Chu, Mi Ae;Chung, Myeong-Hee;Kang, Seokjin
    • Pediatric Infection and Vaccine
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    • v.29 no.2
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    • pp.70-76
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    • 2022
  • Coronavirus disease 2019 (COVID-19) in patients with underlying diseases, is associated with high infection and mortality rates, which may result in acute respiratory distress syndrome and death. Mucopolysaccharidosis (MPS) type II is a progressive metabolic disorder that stems from cellular accumulation of the glycosaminoglycans, heparan, and dermatan sulfate. Upper and lower airway obstruction and restrictive pulmonary diseases are common complaints of patients with MPS, and respiratory infections of bacterial or viral origin could result in fatal outcomes. We report a case of COVID-19 in a 16-year-old adolescent with MPS type II, who had been treated with idursulfase since 5 years of age. Prior to infection, the patient's clinical history included developmental delays, abdominal distension, snoring, and facial dysmorphism. His primary complaints at the time of admission included rhinorrhea, cough, and sputum without fever or increased oxygen demand. His heart rate, respiratory rate, and oxygen saturation were within the normal biological reference intervals, and chest radiography revealed no signs of pneumonia. Consequently, supportive therapy and quarantine were recommended. The patient experienced an uneventful course of COVID-19 despite underlying MPS type II, which may be the result of an unfavorable host cell environment and changes in expression patterns of proteins involved in interactions with viral proteins. Moreover, elevated serum heparan sulfate in patients with MPS may compete with cell surface heparan sulfate, which is essential for successful interaction between the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike protein and the host cell surface, thereby protecting against intracellular penetration by SARS-CoV-2.

Pathogenesis of Hantaan Virus Infection in Suckling Mice -Clinical, Virologic and Serologic Observations-

  • Kim, Gum-Ryong;Mckee, Jr, Kelly T.;Lee, Ho-Wang
    • The Journal of the Korean Society for Microbiology
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    • v.20 no.1
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    • pp.115-125
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    • 1985
  • Hemorrhagic fever with renal syndrome (HFRS) is a debilitating disease of humans caused by Hantaan virus (HV), the prototype member of a newly proposed genus of Bunyaviridae. Studies of HV pathogenesis have been limited by the absence of a well defined model for a virus-induced disease state. In an attempt to devise a model for HV pathogenesis in laboratory rodents, newborn outbred suckling ICR mice were shown to be uniformly susceptible to lethal infection with non- mouse adapted HV by intracerebral (IC), intraperitoneal (IP), intramuscular (IM), and subcutaneous (SC) inoculation routes. Clinical coures, mean time to death, and fatal outcome were age-dependent. With an inoculum of 10 $LD_{50}$, mortality was 100% in mice infected within 72h of birth, but declined to 50% by 7 days. By 2-2.5 weeks, animals developed complete resistance to clinical disease. Virus was consistently detected in serum by day 6 post-infection in IC- and IP- inoculated animals, and reached peak levels of $10^5\;PFU/ml$ by day 8 Mice infected IM and SC showed delays in onset of viremia, but achieved similar titers. Immunofluorescent antibody appeared by 17-18 days, and neutralizing antibody by 15 days, in all experimental groups. Two of 8 inbred mouse strains were identified as resistant to clinical disease : SJL/J and A/J. Manipulation of this model will allow investigation of natural rodent pathogenesis with HV, as well as offer insight into disease mechanisms and therapy of HFRS.

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Occult Gastric Cancer Presenting as Hypoxia from Pulmonary Tumor Thrombotic Microangiopathy

  • Mandaliya, Rohan;Farhat, Salman;Uprety, Dipesh;Balla, Mamtha;Gandhi, Apurva;Goldhahn, Richard;Auerbach, Herbert;Christensen, Chris;Reed, Conrad;Cohen, Sidney
    • Journal of Gastric Cancer
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    • v.14 no.2
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    • pp.142-146
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    • 2014
  • Pulmonary tumor thrombotic microangiopathy (PTTM) causing fatal pulmonary hypertension is a rare presentation of malignancy. In general, patients with PTTM rapidly succumb to death due to severe hypoxia. To date, very few cases of PTTM have been reported in the literature; and most of these cases were from gastric cancer and were diagnosed on post mortem autopsy, as it is extremely challenging to make an ante mortem diagnosis. We here report on a case of undiagnosed diffuse gastric cancer, presenting as worsening hypoxia. The clinical, radiographic, and echocardiographic features, and laboratory and pathological results were consistent with PTTM from gastric cancer. The patient was started on anticoagulation therapy, corticosteroids, and high-flow oxygen. However, her hypoxia worsened to the extent that she required ventilator support, and she died soon after intubation due to cardiac arrest. Since diffuse gastric cancer is associated with hereditary diffuse gastric cancer syndrome, cadherin 1 gene mutation analysis was performed to estimate the risk to her daughters. The test came back negative.

Distinct Humoral and Cellular Immunity Induced by Alternating Prime-boost Vaccination Using Plasmid DNA and Live Viral Vector Vaccines Expressing the E Protein of Dengue Virus Type 2

  • George, Junu A.;Eo, Seong-Kug
    • IMMUNE NETWORK
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    • v.11 no.5
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    • pp.268-280
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    • 2011
  • Background: Dengue virus, which belongs to the Flavivirus genus of the Flaviviridae family, causes fatal dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS) with infection risk of 2.5 billion people worldwide. However, approved vaccines are still not available. Here, we explored the immune responses induced by alternating prime-boost vaccination using DNA vaccine, adenovirus, and vaccinia virus expressing E protein of dengue virus type 2 (DenV2). Methods: Following immunization with DNA vaccine (pDE), adenovirus (rAd-E), and/or vaccinia virus (VV-E) expressing E protein, E protein-specific IgG and its isotypes were determined by conventional ELISA. Intracellular CD154 and cytokine staining was used for enumerating CD4+ T cells specific for E protein. E protein-specific CD8+ T cell responses were evaluated by in vivo CTL killing activity and intracellular IFN-${\gamma}$ staining. Results: Among three constructs, VV-E induced the most potent IgG responses, Th1-type cytokine production by stimulated CD4+ T cells, and the CD8+ T cell response. Furthermore, when the three constructs were used for alternating prime-boost vaccination, the results revealed a different pattern of CD4+ and CD8+ T cell responses. i) Priming with VV-E induced higher E-specific IgG level but it was decreased rapidly. ii) Strong CD8+ T cell responses specific for E protein were induced when VV-E was used for the priming step, and such CD8+ T cell responses were significantly boosted with pDE. iii) Priming with rAd-E induced stronger CD4+ T cell responses which subsequently boosted with pDE to a greater extent than VV-E and rAd-E. Conclusion: These results indicate that priming with live viral vector vaccines could induce different patterns of E protein-specific CD4+ and CD8+ T cell responses which were significantly enhanced by booster vaccination with the DNA vaccine. Therefore, our observation will provide valuable information for the establishment of optimal prime-boost vaccination against DenV.

Inhibitory Effect of Nicardipine on hERG Channel

  • Chung, Eun-Yong;Cho, Hea-Young;Cha, Ji-Hun;Kwon, Kyoung-Jin;Jeon, Seol-Hee;Jo, Su-Hyun;Kim, Eun-Jung;Kim, Hye-Soo;Chung, Hye-Ju
    • Biomolecules & Therapeutics
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    • v.18 no.4
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    • pp.448-453
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    • 2010
  • Drug-induced long QT syndrome is known to be associated with the onset of torsades de pointes (TdP), resulting in a fatal ventricular arrhythmia. QT interval prolongation can result from blocking the human ether-a-go-go-related gene (hERG) channel, which is important for the repolarization of cardiac action potential. Nicardipine, a Ca-channel blocker and antihypertensive agent, has been reported to increase the risk of occasional serious ventricular arrhythmias. We studied the effects of nicardipine on hERG $K^+$ channels expressed in HEK293 cells and Xenopus oocytes. The cardiac electrophysiological effect of nicardipine was also investigated in this study. Our results revealed that nicardipine dose-dependently decreased the tail current of the hERG channel expressed in HEK293 cells with an $IC_{50}$ of 0.43 ${\mu}M$. On the other hand, nicardipine did not affect hERG channel trafficking. Taken together, nicardipine inhibits the hERG channel by the mechanism of short-term channel blocking. Two S6 domain mutations, Y652A and F656A, partially attenuated (Y652A) or abolished (F656A) the hERG current blockade, suggesting that nicardipine blocks the hERG channel at the pore of the channel.