A rare case of newly diagnosed diabetes mellitus following COVID-19 infection

Abstract

Several reports showed the likelihood of a relationship between COVID-19 infection and the onset and prognosis of diabetes mellitus (DM) of all types. A 73-year-old female patient who presented to the clinic with respiratory symptoms and was tested positive for COVID-19 and treated for the next three days. Despite having neither a known history of hyperglycemia nor a family history of diabetes, she was unconscious and suffering from polyuria and polydipsia when she was brought to the emergency department. Once her condition was successfully stabilized, she was sent home with COVID-19 medications and oral anti-diabetic therapy. After subsequent viral recovery and continued anti-diabetic medication, the patient was monitored for the following seven months. DM might be linked to the SARS-CoV-2 infection. Further research is necessary to prove a relationship between COVID-19 and newly-onset diabetes.

1. Introduction

COVID-19 infection can lead to severe short- and long-term complications. After the pandemic started in 2020, many reports linked the viral infection to post-COVID-19 endocrine, musculoskeletal, cognitive, and sensorineural conditions that started after the infection [1]. Another link was found between COVID-19 infection and DM, as diabetic patients are at higher risk of having worse clinical outcomes after the infection [2]. Alternatively, new-onset type 1 diabetes (T1DM) was diagnosed in previously healthy subjects, and manifestations of diabetic ketoacidosis were observed in such cases [3,4]. It is unclear whether the infection unmasked pre-existing diabetes or if there is a role of the viral infection in the disease pathology [5]. We are discussing a new onset of DM following the COVID-19 virus in a 73-year-old female who was previously healthy. She was well treated, and her type II diabetes medicines were maintained.

2. Case presentation

A 73-year-old female Egyptian patient presented to the outpatient clinic with five days history of fever, mild dyspnea, fatigue, anorexia, loss of weight, and myalgia. She was hemodynamically stable but with mild tachycardia. Due to a history of contact with a confirmed positive COVID-19 patient three weeks before presentation, a nasopharyngeal swab was obtained, and a polymerase chain reaction (PCR) test confirmed she was positive for SARS-CoV-2. The physician prescribed her non-specific COVID-19 medications such as enoxaparin sodium, aspirin, budesonide, clarithromycin, and paracetamol and advised her to isolate herself at home. The patient was not in need of oxygen. During the following three days, she suffered from polyuria and polydipsia and presented comatose to the emergency department (ED). Random blood glucose was 442 mg/dl. The patient did not have ketone bodies. Intravenous fluids, electrolyte replacement solutions, and insulin drips were given for 8 hours until she became stable. She did not have any similar hyperglycemic crisis or any family history of diabetes, and the latest blood glucose in a regular check-up before COVID-19 symptoms was normal. Her medical history included mild left ventricular hypertrophy and cholecystectomy two years ago. The physician prescribed vildagliptin 50 mg/metformin 1000 mg daily, and she continued isolation and COVID-19 medications at home in addition to the anti-diabetic treatment for two weeks until she recovered. After two weeks of fasting, 2 h, postprandial blood glucose and glycosylated hemoglobin (HbA1C) were measured, and their values were 68mg/dl, 230 mg/dl, and 14.20%, respectively. Other laboratory results after admission are shown in Table 1 . The patient continued on the same anti-diabetic treatment, and two weeks later, fasting blood glucose and blood glucose 2 hours postprandial were repeated, and the results were 105 mg/dl and 129 mg/dl, respectively. The patient was followed up for the next seven months after recovery from the virus and was still taking the prescribed Vildagliptin 50 mg/Metformin 1000 mg daily.

Table 1.

Patient Laboratory results.

Parameter	Result	Normal range
Hemoglobin	11.3 g/dl	12.0–16.0
Neutrophils	76.0%	40–70
Lymphocytes	16%	20–45
ESR 1st hour	55.0 mm/hr	Up to 10.0
ESR 2nd hour	116.0 mm/hr	Up to 20.0
C-RP	Positive (27.9) mg/dl	Negative: less Than 6.0
Serum creatinine	0.57 mg/dl	(0.50–1.20)
Serum Albumin	3.5 g/dl	(3.5–5.5)
Albumin/creatinine ration	25.15 mg/dl	Normal: < 30
Serum T.S.H	2.420 uIU/ml	0.400–8.900

The consent for publication was obtained from the patient and will be provided upon request.

3. Discussion

It is already established that SARS-CoV-2 increases morbidity and mortality in old patients, especially those suffering from chronic diseases such as diabetes; however, the increasing number of newly-diagnosed diabetes mellitus (DM) after SARS-CoV-2 infection raises suspicion about the association between SARS-CoV-2 and developing DM [6]. The relationship between DM and the worsening of a patient's condition from other coronaviruses, such as severe acute respiratory syndrome coronavirus 1, has been the subject of numerous studies in the past [7] and Middle East respiratory syndrome coronavirus (MERS-CoV) [8]. Furthermore, many acute DM cases emerged following the SARS-CoV-1 outbreak, a strong prognostic factor for mortality, despite the absence of glucocorticoid use or relevant history [7]. Singh et al. suggested that SARS-CoV-2 may directly cause new-onset diabetes or aggravate the pre-existing DM due to acute metabolic decompensation, especially in severe cases requiring ICU admission [9]. Studies found that most cases present with diabetic ketoacidosis (DKA) either during or following the infection course despite having common predisposing factors for developing DM [10].

The suggested mechanisms include impaired insulin secretion caused by SARS-CoV-2 binding to angiotensin-converting enzyme 2 (ACE2) receptors on beta cells that lead to direct damage or trigger an autoimmune response against beta cells to their destruction, which can develop a new-onset DM or worsen a pre-existing DM [11]. Another mechanism that involves the cytokine storm impact on insulin function is the increased interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNFα) can cause insulin resistance and DM in patients with severe COVID-19 [12,13]. Most studies focused on T2DM, and others suggested that T1DM may have a worse COVID-19 course [14], but the suggested mechanisms of SARS-CoV-2 virus effect on beta cells and impaired insulin production and use indicate a relationship between COVID-19 and de novo T1DM, especially if evidence of T1DM is found in uncommon presentations. We discuss a case of newly diagnosed DM following COVID-19 in a 73-year-old female who was previously known to be healthy, her latest blood glucose and (HbA1C) tests were normal, and she never had a family history of diabetes. After recovering from COVID-19, the patient had a follow-up and continued to take Vildagliptin 50 mg/Metformin 1000 mg daily for the next seven months. Currently, there are different studies strongly suggesting that COVID-19 infection is diabetogenic. Chinese studies at the beginning of the pandemic reported new diabetes cases associated with COVID-19, who mostly presented with DKA or hyperglycemia associated with electrolyte disturbance and needed large insulin doses to control their condition [15]. Although ketoacidosis is a typical acute T1DM presenting symptom, a comprehensive study found that it also occurred in roughly 77% of COVID-19 patients with T2DM. Another systematic review found a higher mortality rate among new hyperglycemic patients, previously-diagnosed diabetics, and new-onset DM patients than non-diabetics. The characteristics of new-onset diabetes, identified by confirmed COVID-19, hyperglycemia without a prior history of diabetes, and previously normal HbA1C levels, are now being studied by an international registry. Furthermore, when another research attempted to categorize newly diagnosed hyperglycemic patients during the pandemic into those with proven COVID-19 infection and those without, they discovered that those with severe COVID-19 course had more significant hyperglycemia, which was largely connected with a mix of immunological mechanisms such as cytokine storm, iatrogenic variables such as corticosteroids treatment, and direct viral damage to beta cells.

4. Conclusion

DM can either originate from SARS-CoV-2 pathogenesis or be unmasked by the infection. Pre-existing diabetes may be confused with a new-onset type, so we need more research to clearly define types and factors associated with DM after infection and mind the different clinical presentations with varying severity.

Consent for publication

The consent for publication was obtained from the patients.

Availability of data and material

All data generated or analyzed during this study are included in this published article.

Funding

This study was not funded.

Authors' contributions

Data Collection: KRM.

Literature Search: KRM, FAM, KSA, YHA, RHE, SS.

Manuscript Preparation (draft and final editing): KRM, FAM, KSA, YHA, RHE, SS, AJN.

All authors read and approved the final manuscript.

Declaration of competing interest

The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Abdulqadir J. Nashwan reports a relationship with Hamad Medical Corporation that includes:.