Toxic Shock Syndrome: Clinical, Laboratory, and Pathologic Findings in Nine Fatal Cases

Larkin, Stephen M.; Williams, David N.; Osterholm, Michael T.; Tofte, Robert W.; Posalaky, Zoltan

doi:10.7326/0003-4819-96-6-858

Cited by 112 publications

(73 citation statements)

References 15 publications

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“…The authors noted that pathological findings in toxic shock syndrome include lymphocytic infiltration of the myocardium and vacuolar cellular degeneration of myocardial cells. 9 They suggested that tumor necrosis factor (TNF) may have caused the reversible heart block seen in their patient since TNF impairs muscle electrical activity. 10 TNF also decreases myocardial contractility.…”

Section: Discussionmentioning

confidence: 99%

Complete heart block in association with graft-versus-host disease

Gilman

Kooy

Atkins

et al. 1998

Bone Marrow Transplant

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Summary:An infant who received haploidentical BM for severe combined immunodeficiency (SCID) developed acute, reversible complete heart block in association with an exacerbation of GVHD. Respiratory distress and myocardial dysfunction were also seen with this and previous GVHD exacerbations. The patient had not received chemotherapy or radiation prior to BMT. The complete heart block resolved after 1 week of intensive immunosuppression. The association of complete heart block with GVHD is important because the heart block is potentially reversible with prompt, aggressive control of the GVHD. Keywords: cardiac; heart block; arrhythmia; graftversus-host disease; bone marrow transplantation Graft-versus-host disease is a major cause of morbidity and mortality after bone marrow transplantation. GVHD manifestations are predominantly limited to the skin, gastrointestinal tract, and liver. 1 However, severe GVHD is associated with a marked release of cytokines ('cytokine storm') 2 that may result in more widespread organ involvement. Cardiac involvement during acute or chronic GVHD has been reported to be infrequent, mild and generally asymptomatic. 3,4 We report the second case of complete atrioventricular block occurring in association with GVHD. A case of complete heart block has been reported in a patient with SCID who received an haploidentical parental marrow transplant. The patient had acute GVHD of the skin, liver and gut which was treated with high-dose steroids and monoclonal antibody. He had recurrent symptoms and signs of chronic GVHD and was maintained on low-dose steroids. Skin and liver biopsies were consistent with chronic GVHD. The patient developed complete heart block at day +97 and required a pacemaker. A myocardial biopsy showed interstitial edema, focal mononuclear cell infiltrate, and individual fiber degeneration. The lymphohistiocytic infiltrate resembled that from the skin biopsy. The patient Correspondence: Dr A Gilman, Pediatric Hematology/Oncology, The Children's Mercy Hospital, 2401 Gillham Road, Kansas City, MO 64108, USA Received 14 March 1997; accepted 14 July 1997 died 1 month later and autopsy results showed similar infiltrates with foci of necrosis and scarring present in the atrioventricular node, bundle of His and myocardium. No evidence of viral infection was found on the premortem biopsy specimen or at autopsy. 5 The patient in our report was treated with intensive immunosuppression, had reversal of his complete heart block, and remains well. Case reportThe patient was diagnosed with SCID when he presented at 4 months of age with Pneumocystis carinii pneumonia and failure to thrive. He had severe pneumonia and required a high-frequency ventilator and nitric oxide for 2 weeks. He had no clinical evidence of cardiac dysfunction. Immunophenotyping showed a lack of T lymphocytes and NK cells, and the presence of B lymphocytes. He received haploidentical T cell-depleted bone marrow from his father. T cell depletion was performed with OKT3 antibody and rabbit complement, which resulted...

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Section: Discussionmentioning

confidence: 99%

Complete heart block in association with graft-versus-host disease

Gilman

Kooy

Atkins

et al. 1998

Bone Marrow Transplant

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“…We (J. Q. Russell, unpublished observations) and others (2) have observed that Ag-activated T cells also traffic to the lung and kidneys, and we are examining the degree of tissue injury that results at these sites. This model might also serve to explain the liver dysfunction that is often observed after situations in which the immune system has been strongly activated largely outside the liver, such as by a superantigen in toxic shock syndrome (36,37). It also suggests that the normal number of resident liver lymphocytes in wild-type mice might induce tonic low levels of hepatocyte apoptosis in a Fas-dependent manner.…”

Section: Discussionmentioning

confidence: 99%

Liver Damage by Infiltrating CD8+ T Cells Is Fas Dependent

Kennedy

Russell

Michail

et al. 2001

The Journal of Immunology

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Ag stimulation of CD8+ lymphocytes in vivo results in their migration to various tissues as well as the activation of a cytolytic program involving perforin, TNF-α, and Fas ligand. The liver is one of the main sites for infiltration by activated CD8+ T cells, and this is followed by the death of hepatocytes. The contribution of the various cytolytic components to this process is unclear. Hepatocyte damage by CD8+ T cells was studied using the MHC class I-restricted OVA-specific TCR transgenic mouse (OT-1) to examine the contribution of Fas to hepatocyte death. Activated CD8+ T cells from both OT-1 and Fas-deficient OT-1lpr mice migrated to the liver in similar numbers after OVA administration, but only in OT-1 mice was there evidence of significant hepatocyte damage histologically and by elevation of serum aspartate transaminase. These differences were not the result of inefficient induction of cytolytic activity in OT-1lpr liver T cells, since they were as cytolytic in vitro as OT-1 liver T cells. This was supported by findings of similar high levels of message for perforin, TNF-α, and Fas ligand in liver lymphocytes from both mice. These findings demonstrate that following Ag activation, infiltrating liver CD8+ T lymphocytes induce hepatocyte damage in a Fas-dependent manner.

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“…Grossly abnormal liver function values with hyperbilirubinemia, markedly elevated transaminase enzyme activity, and normal alkaline phosphate levels, as seen in my patient, have been reported only for two fatal cases studied by Larkin et al 2 Physicians should be aware of this complication of hepatic dysfunction in toxic shock syndrome, as early diagnosis, adequate fluid replacement, vasopressor therapy, and appropriate antistaphylococcal antibiotics can prevent fatal outcome. …”

Section: Staphylococcus Aureusmentioning

confidence: 99%

Non-menstrual Toxic Shock Syndrome

Khan

1990

Ann Saudi Med

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Non-menstrual Toxic Shock Syndrome. 1990; 10(2): 221-222 To the Editor: I read with interest the letter by Fahim 1 and would like to describe my own observations in a patient with non-menstrual toxic shock syndrome, with an emphasis on severe hepatic dysfunctions as a complication of the syndrome. My patient made a complete recovery because of early diagnosis and effective treatment.A 28-year-old Saudi woman presented with abrupt onset of fever, sore throat, vomiting, confusion, generalized erythrodermic blanching rash, and hypotension, two weeks following a full-term vaginal delivery. On the seventh day following admission, her skin rash began to desquamate and she became deeply jaundiced with moderate ascites.Laboratory investigations showed the following values: hemoglobin, 84 g/L; white cell count, 24.0 × 10 9 /L; platelets, 100 × 10 9 /L; blood urea, 20.4 mmol/L; creatinine, 210 μmol/L; sodium, 120 mmol/L; calcium, 1.63 mmol/L; and magnesium, 0.5 mmol/L. Liver function tests showed bilirubin, 529 μmol/L; AST 18.1 μkat/L; and ALT, 19.6 μkat, with normal alkaline phosphatase activity. Abdominal ultrasound examination showed a normal gallbladder and biliary tree with moderate ascites. Culture from the vagina showed a concentrated growth of Staphylococcus aureusShe was treated with intravenous vancomycin, dopamine, calcium chloride, and fluids (normal saline and crystalloids), and she made a complete recovery. At the time of the patient's discharge, all laboratory values were normal.This case fulfilled the criteria for toxic shock syndrome. Grossly abnormal liver function values with hyperbilirubinemia, markedly elevated transaminase enzyme activity, and normal alkaline phosphate levels, as seen in my patient, have been reported only for two fatal cases studied by Larkin et al. 2 Physicians should be aware of this complication of hepatic dysfunction in toxic shock syndrome, as early diagnosis, adequate fluid replacement, vasopressor therapy, and appropriate antistaphylococcal antibiotics can prevent fatal outcome.

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Toxic Shock Syndrome: Clinical, Laboratory, and Pathologic Findings in Nine Fatal Cases

Cited by 112 publications

References 15 publications

Complete heart block in association with graft-versus-host disease

Complete heart block in association with graft-versus-host disease

Liver Damage by Infiltrating CD8+ T Cells Is Fas Dependent

Non-menstrual Toxic Shock Syndrome

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