- Case report
- Open Access
- Open Peer Review
Lung abscess without sepsis in a patient with diabetes with refractory episodes of spontaneous hypoglycemia: a case report and review of the literature
© Toda et al.; licensee BioMed Central Ltd. 2014
- Received: 6 April 2013
- Accepted: 16 December 2013
- Published: 13 February 2014
Hypoglycemia is a cause of considerable morbidity. Although hypoglycemia has been documented in the setting of septic shock and has been associated with higher mortality, hypoglycemia in infection without sepsis has not been reported in the literature.
A 72-year-old Japanese woman treated with high-dose glucocorticoids for autoimmune hemolytic anemia, as well as intensive insulin therapy for type 2 diabetes, presented with severe hypoglycemia. A lung abscess was diagnosed by imaging studies and treated with intravenous antibiotics. Hypoglycemia spontaneously recurred during lung abscess exacerbations, despite appropriate de-escalation of antidiabetic therapy. Only mild sporadic episodes of hypoglycemia occurred after the lung abscess was controlled. Infection accompanied with malnutrition and immunosuppression, although in the absence of sepsis, may have contributed to hypoglycemia.
Caution is warranted in the management of hypoglycemia in patients with diabetes with the conditions described here, that is malnutrition and immunosuppression, as infection may be a contributing factor.
- Type 2 diabetes
- Insulin resistance
Hypoglycemia is a cause of considerable morbidity, and is of major concern throughout the treatment of diabetes mellitus. Although infection is known to exacerbate insulin resistance and cause hyperglycemia, septic shock produces hypoglycemia. However, to the best of our knowledge, hypoglycemia in infection without sepsis has not been reported in the literature. Here, we present the case of a patient experiencing refractory episodes of spontaneous hypoglycemia in which lung abscess, although without sepsis, may have played a central role.
A 72-year-old Japanese woman presented to a neighboring hospital with loss of consciousness due to severe hypoglycemia (plasma glucose 10mg/dl). She was transferred to our facility the following day. She had had type 2 diabetes, treated with insulin (basal-supported oral therapy) for three years before admission. Three months before admission, she was diagnosed with autoimmune hemolytic anemia (AIHA) and was started on 70mg oral prednisolone per day, which exacerbated her diabetes, necessitating intensive insulin therapy. By two weeks before admission, oral prednisolone was tapered to 50mg as her hemoglobin concentration had stabilized around 10g/dl. She experienced no episodes of overt hypoglycemia prior to hospitalization.
Results of laboratory examinations on admission
White blood cells
Serum lactate dehydrogenase
Serum aspartate aminotransferase
Serum alanine aminotransferase
Serum blood urea nitrogen
Serum creatine kinase
Serum C-reactive protein
Fasting adrenocorticotropic hormone
Fasting plasma glucose
Fasting C-peptide reactivity
Postprandial plasma glucose
Postprandial C-peptide reactivity
Possible causative factors of recurrent hypoglycemia in the present case included insulin use, malnutrition, and severe infection resulting from the lung abscess. Insulin was unlikely to have played a central role, as no episodes of hypoglycemia were observed under administration of the same dosages of insulin before admission. Insulin dosages were appropriately skipped or tapered according to the amount of oral intake in unsuccessful attempts to avoid hypoglycemia during periods where hypoglycemia was observed. Oral intake was approximately 1000kcal/day, which was inadequate (21kcal per ideal body weight). However, we speculate malnutrition was not central to the pathogenesis of hypoglycemia, as oral intake was similar before and after the episodes of hypoglycemia. The infection was likely to be severe and prolonged, as suggested by low serum albumin levels and a rise in C-reactive protein to a maximum of 18.03mg/dl on day 24, though symptoms of infection in this patient may have been masked by glucocorticoid use. The normal levels of fasting ACTH and cortisol raised the possibility of very strong secretory stimuli, such as severe infection, and/or hypoglycemia causing a limited ACTH response even under high prednisolone doses. Moreover, the absence of hallmarks of adrenal insufficiency (stable systolic blood pressure at around 120mmHg, normal levels of potassium and eosinophils throughout the patient’s course) led us to believe adrenal insufficiency was not central in the pathogenesis of hypoglycemia. Supported by the observation that hypoglycemia and the lung abscess had exhibited parallel courses, severe infection may have played a central role in the pathogenesis of recurrent hypoglycemia in this patient.
Previous studies showed immunocompromised hosts with lung abscess to be more likely to develop lung abscesses with positive cultures for aerobes, as compared with immunocompetent hosts (63% vs. 20%; P = 0.057) , and that patients with lung abscess who have diabetes are at increased risk for lung abscess with positive cultures for Klebsiella pneumoniae compared to patients without diabetes (odds ratio 4.3, 95% confidence interval, 1.0 to 18.4, P = 0.039) . On these grounds, we speculate Gram-negative bacteria, such as K. pneumoniae, are candidates for the virulent organism in this patient receiving high-dose glucocorticoids in addition to having diabetes.
Hypoglycemia has been reported in 16.3% of patients with sepsis, and has been associated with higher mortality . Extensive research has been conducted to elucidate the mechanisms of hypoglycemia in infection, using animal models injected with lipopolysaccharide (LPS). LPS induces hyperglycemia approximately 1 hour after injection into mice  followed by hypoglycemia within 6 hours . Glycogen depletion, decreased gluconeogenesis, and increased glucose consumption have been suggested as mechanisms of hypoglycemia induction by LPS [5, 6]. LPS inhibits insulin signaling in vivo, which leads to decreased glycogen synthesis, increased glycogenolysis and also increased gluconeogenesis . Euglycemic hyperinsulinemic clamp studies on animal models of LPS-induced hyperglycemia support this view, revealing an increase in hepatic glucose output, possibly contributing to glycogen depletion . LPS-induced cytokines such as interleukin (IL)-1β and tumor necrosis factor (TNF) α impair the glucagon-induced increase in gluconeogenesis in animal models . LPS also downregulates cytoplasmic glucocorticoid receptors in the livers of mice, resulting in inhibition of the glucocorticoid-induced increase in hepatic gluconeogenesis . Negative blood cultures on multiple occasions in the present case were not suggestive of sepsis. However, taking the above observations together, we speculate that hypoglycemia can be induced by severe prolonged infection without signs of sepsis in settings of malnutrition and immunosuppression, even with high-dose glucocorticoid treatment, as in the present case.
Clinicians should exercise particular caution managing hypoglycemia in settings of malnutrition, immunosuppression, and glucocorticoid use, as severe bacterial infection may be involved in its pathogenesis.
Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.
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